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Fekete M, Lehoczki A, Szappanos Á, Zábó V, Kaposvári C, Horváth A, Farkas Á, Fazekas-Pongor V, Major D, Lipécz Á, Csípő T, Varga JT. Vitamin D and Colorectal Cancer Prevention: Immunological Mechanisms, Inflammatory Pathways, and Nutritional Implications. Nutrients 2025; 17:1351. [PMID: 40284214 PMCID: PMC12029991 DOI: 10.3390/nu17081351] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2025] [Revised: 04/10/2025] [Accepted: 04/11/2025] [Indexed: 04/29/2025] Open
Abstract
Vitamin D plays a crucial role in the regulation of the immune system, with immunomodulatory effects that are key in the prevention of colorectal cancer (CRC). Over the past decades, research has shown that this steroid hormone impacts much more than bone health, significantly influencing immune responses. Vitamin D enhances immune organ functions such as the spleen and lymph nodes, and boosts T-cell activity, which is essential in defending the body against tumors. Additionally, vitamin D mitigates inflammatory responses closely linked to cancer development, reducing the inflammation that contributes to CRC. It acts via vitamin D receptors (VDRs) expressed on immune cells, modulating immune responses. Adequate vitamin D levels influence gene expression related to inflammation and cell proliferation, inhibiting tumor development. Vitamin D also activates mechanisms that suppress cancer cell survival, proliferation, migration, and metastasis. Low levels of vitamin D have been associated with an increased risk of CRC, with deficiency correlating with higher disease incidence. Lifestyle factors, such as a diet high in red meat and calories but low in fiber, fruits, and vegetables, as well as physical inactivity, contribute significantly to CRC risk. Insufficient calcium and vitamin D intake are also linked to disease occurrence and poorer clinical outcomes. Maintaining optimal vitamin D levels and adequate dietary intake is crucial in preventing CRC and improving patient prognosis. This review explores the role of vitamin D in immune regulation and summarizes findings from randomized clinical trials assessing the effects of vitamin D supplementation on CRC outcomes.
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Affiliation(s)
- Mónika Fekete
- Institute of Preventive Medicine and Public Health, Faculty of Medicine, Semmelweis University, 1089 Budapest, Hungary; (M.F.); (A.L.); (C.K.); (V.F.-P.); (D.M.); (Á.L.); (T.C.)
| | - Andrea Lehoczki
- Institute of Preventive Medicine and Public Health, Faculty of Medicine, Semmelweis University, 1089 Budapest, Hungary; (M.F.); (A.L.); (C.K.); (V.F.-P.); (D.M.); (Á.L.); (T.C.)
- Health Sciences Division, Doctoral College, Semmelweis University, 1085 Budapest, Hungary;
| | - Ágnes Szappanos
- Heart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary;
- Department of Rheumatology and Clinical Immunology, Semmelweis University, 1023 Budapest, Hungary
| | - Virág Zábó
- Health Sciences Division, Doctoral College, Semmelweis University, 1085 Budapest, Hungary;
- Heart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary;
| | - Csilla Kaposvári
- Institute of Preventive Medicine and Public Health, Faculty of Medicine, Semmelweis University, 1089 Budapest, Hungary; (M.F.); (A.L.); (C.K.); (V.F.-P.); (D.M.); (Á.L.); (T.C.)
| | - Alpár Horváth
- Pulmonology Center of the Reformed Church in Hungary, 2045 Törökbálint, Hungary;
| | - Árpád Farkas
- HUN-REN Centre for Energy Research, 1121 Budapest, Hungary;
| | - Vince Fazekas-Pongor
- Institute of Preventive Medicine and Public Health, Faculty of Medicine, Semmelweis University, 1089 Budapest, Hungary; (M.F.); (A.L.); (C.K.); (V.F.-P.); (D.M.); (Á.L.); (T.C.)
| | - Dávid Major
- Institute of Preventive Medicine and Public Health, Faculty of Medicine, Semmelweis University, 1089 Budapest, Hungary; (M.F.); (A.L.); (C.K.); (V.F.-P.); (D.M.); (Á.L.); (T.C.)
| | - Ágnes Lipécz
- Institute of Preventive Medicine and Public Health, Faculty of Medicine, Semmelweis University, 1089 Budapest, Hungary; (M.F.); (A.L.); (C.K.); (V.F.-P.); (D.M.); (Á.L.); (T.C.)
| | - Tamás Csípő
- Institute of Preventive Medicine and Public Health, Faculty of Medicine, Semmelweis University, 1089 Budapest, Hungary; (M.F.); (A.L.); (C.K.); (V.F.-P.); (D.M.); (Á.L.); (T.C.)
| | - János Tamás Varga
- Department of Pulmonology, Semmelweis University, 1083 Budapest, Hungary
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Takasu A, Gotoda T, Suzuki S, Kusano C, Goto C, Ishikawa H, Kogure H. Daily Diet and Nutrition Risk Factors for Gastric Cancer Incidence in a Japanese Population. Gut Liver 2024; 18:602-610. [PMID: 38388181 PMCID: PMC11249943 DOI: 10.5009/gnl230354] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/06/2023] [Revised: 01/05/2024] [Accepted: 01/07/2024] [Indexed: 02/24/2024] Open
Abstract
Background/Aims : Nutritional factors associated with gastric cancer (GC) are not completely understood. We aimed to determine the effect of nutrient intake on the incidence of GC. Methods : This was a post hoc analysis of a prospective trial that evaluated modalities for GC screening in participants aged 30 to 74 years living in high-risk areas for GC in Japan between June 2011 and March 2013. The patients were followed up for GC incidence for 6 years. All participants completed a self-administered food frequency questionnaire (FFQ) upon enrollment before GC screening. Daily nutrient intake was calculated from the FFQ and dichotomized at each cutoff value using receiver operating characteristic analysis. Risk factors associated with GC incidence were investigated in terms of nutrient intake and participant characteristics using Cox proportional hazards regression analysis. Results : Overall, 1,147 participants were included in this analysis. The median age was 62 years, and 50.7% of the participants were men. The median follow-up period was 2,184 days. GC was detected in 25 participants during the follow-up. Multivariate Cox proportional hazards regression analysis revealed that the intake of sodium (adjusted hazards ratio [aHR], 3.905; 95% confidence interval [CI], 1.520 to 10.035; p=0.005) and vitamin D (aHR, 2.747; 95% CI, 1.111 to 6.788, p=0.029) were positively associated with GC incidence, whereas the intake of soluble dietary fiber (aHR, 0.104; 95% CI, 0.012 to 0.905; p=0.040) was inversely associated with GC incidence. Conclusions : Daily high intake of sodium and vitamin D and low soluble dietary fiber intake are associated with GC incidence.
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Affiliation(s)
- Ayaka Takasu
- Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
| | - Takuji Gotoda
- Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
- Department of Gastroenterology, Cancer Institute Hospital, Tokyo, Japan
| | - Sho Suzuki
- Department of Gastroenterology, International University of Health and Welfare Ichikawa Hospital, Ichikawa, Japan
| | - Chika Kusano
- Department of Gastroenterology, Kitasato University School of Medicine, Sagamihara, Japan
| | - Chiho Goto
- Department of Health and Nutrition, Nagoya Bunri University, Inazawa, Japan
| | - Hideki Ishikawa
- Department of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Osaka, Japan
| | - Hirofumi Kogure
- Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
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Kim M, Gunathilake M, Lee J, Oh JH, Chang HJ, Sohn DK, Shin A, Kim J. Sex-specific associations of empirically derived dietary patterns with colorectal cancer risk in a Korean population: a case‒control study. Sci Rep 2024; 14:6709. [PMID: 38509114 PMCID: PMC10954725 DOI: 10.1038/s41598-024-55524-5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/09/2023] [Accepted: 02/24/2024] [Indexed: 03/22/2024] Open
Abstract
Dietary patterns may be a crucial modifiable factor in colorectal cancer (CRC) risk. This study aimed to examine the associations of dietary patterns derived from two methods with CRC risk in Korea. In a study of 1420 CRC patients and 2840 control participants, we obtained dietary patterns by principal component analysis (PCA) and reduced rank regression (RRR) using 33 predefined food groups. The associations between dietary patterns and CRC risk were assessed using unconditional logistic regression models to calculate odds ratios (ORs) and 95% confidence intervals (CIs). We identified two similar dietary patterns, derived from PCA 1 (prudent) and RRR (healthy), characterized by higher consumption of green/yellow vegetables, light-colored vegetables, fruits, eggs, and milk in both men and women. In women, higher prudent and healthy pattern scores were significantly associated with a lower risk of CRC (prudent, ORQ4 vs. Q1 = 0.59, 95% CI 0.40-0.86, P for trend = 0.005; healthy, ORQ4 vs. Q1 = 0.62, 95% CI 0.43-0.89, P for trend = 0.007). In men, a significant inverse association between dietary pattern and risk of rectal cancer was found only for the healthy dietary pattern (ORQ4 vs. Q1 = 0.66, 95% CI 0.45-0.97, P for trend = 0.036). Compared with the dietary pattern derived by PCA, the RRR dietary pattern had a slightly stronger association with a lower risk of distal colon cancer (ORQ4 vs. Q1 = 0.58, 95% CI 0.35-0.97, P for trend = 0.025) and rectal cancer (ORQ4 vs. Q1 = 0.29, 95% CI 0.15-0.57, P for trend < 0.001) in women. Our findings suggest cancer prevention strategies focusing on a diet rich in vegetables, fruits, eggs, and milk. Moreover, the use of both PCA and RRR methods may be advantageous to explore the associations between dietary patterns and risk of CRC.
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Affiliation(s)
- Minji Kim
- Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi-do, South Korea
| | - Madhawa Gunathilake
- Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi-do, South Korea
| | - Jeonghee Lee
- Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi-do, South Korea
| | - Jae Hwan Oh
- Center for Colorectal Cancer, National Cancer Center Hospital, National Cancer Center, Goyang-si, Gyeonggi-do, South Korea
| | - Hee Jin Chang
- Center for Colorectal Cancer, National Cancer Center Hospital, National Cancer Center, Goyang-si, Gyeonggi-do, South Korea
| | - Dae Kyung Sohn
- Center for Colorectal Cancer, National Cancer Center Hospital, National Cancer Center, Goyang-si, Gyeonggi-do, South Korea
| | - Aesun Shin
- Department of Preventive Medicine, Seoul National University College of Medicine, Jongno-gu, Seoul, South Korea
| | - Jeongseon Kim
- Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi-do, South Korea.
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Xiao J, Ma J, Khan MZ, Alugongo GM, Chen T, Liu S, Li S, Cao Z. Unlocking the potential of milk whey protein components in colorectal cancer prevention and therapy. Crit Rev Food Sci Nutr 2023; 64:12961-12998. [PMID: 37846905 DOI: 10.1080/10408398.2023.2258970] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2023]
Abstract
Extensive research from large prospective cohort studies and meta-analytical investigations over recent decades have consistently indicated that dairy foods have protective effects, reducing the risk of colorectal cancer. Most of the literature has explored the potential role of milk minerals and vitamins in managing colorectal cancer. Yet, there is a paucity of a comprehensive summary of the anticancer attributes of milk protein components and their underlying mechanisms of action. Recent advancements have spotlighted the potential of whey proteins, including β-lactoglobulin, α-lactalbumin, serum albumin, and lactoferrin, as promising candidates for both the prevention and treatment of colorectal cancer. Notably, whey proteins have demonstrated a more pronounced capacity for suppressing carcinogen-induced tumors when compared to casein. Their strong binding affinity enables them to serve as effective carriers for small molecules or drugs targeting colon cancer therapy. Furthermore, numerous studies have underscored the anti-inflammatory and antioxidant prowess of whey proteins in cancer prevention. Additionally, whey proteins have been shown to trigger apoptosis, hinder tumor cell proliferation, and impede metastasis. This comprehensive review, therefore, not only substantiates the significance of incorporating whey protein components into a balanced daily diet but also underscores their potential in safeguarding against the onset and progression of colorectal cancer.
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Affiliation(s)
- Jianxin Xiao
- State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing, China
- Key Laboratory of Low Carbon Culture and Safety Production in Cattle in Sichuan, Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, China
| | - Jiaying Ma
- State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing, China
| | - Muhammad Zahoor Khan
- Faculty of Veterinary and Animal Sciences, University of Agriculture Dera Ismail Khan, Khyber Pakhtunkhwa, Pakistan
| | - Gibson Maswayi Alugongo
- State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing, China
| | - Tianyu Chen
- State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing, China
| | - Shuai Liu
- State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing, China
| | - Shengli Li
- State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing, China
| | - Zhijun Cao
- State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing, China
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Paulsen EM, Rylander C, Brustad M, Jensen TE. Pre-diagnostic intake of vitamin D and incidence of colorectal cancer by anatomical subsites: the Norwegian Women and Cancer Cohort Study (NOWAC). Br J Nutr 2023; 130:1047-1055. [PMID: 36620946 PMCID: PMC10442793 DOI: 10.1017/s0007114523000077] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/15/2022] [Revised: 12/12/2022] [Accepted: 01/03/2023] [Indexed: 01/10/2023]
Abstract
According to the World Cancer Research Fund International, vitamin D might decrease the risk of colorectal cancer (CRC). However, less is known about the association with cancers in different subsites of the colon and in the rectum. The aim of this study was to examine associations between pre-diagnostic intake of vitamin D and risk of CRC by anatomical subsites. Data from 95 416 participants in the Norwegian Women and Cancer Cohort Study was included, and vitamin D intake was estimated from two repeated FFQ. Associations between vitamin D intake and incidence of CRC were assessed using multivariable Cox regression. During follow-up, there were 1774 incident cases of CRC. A small but borderline significant inverse association was found for a 5-µg increase in vitamin D intake and risk of CRC (hazard ratio (HR) = 0·97; 95 % CI 0·93, 1·01) and colon cancer (HR = 0·96; 95 % CI 0·91, 1·01). High (≥ 20 µg) compared with low (< 10 µg) vitamin D intake was associated with 17 % borderline significant reduced risk of CRC (HR = 0·83; 95 % CI 0·68, 1·02). Medium (10-19 µg) v. low intake (< 10 µg) was associated with 27 % reduced risk of proximal colon cancer (HR = 0·73; 95 % CI 0·57, 0·94). No significant associations were observed between vitamin D intake and risk of distal colon or rectal cancer. Our study indicates that vitamin D may be differently associated with subsites of the colon. The association between vitamin D intake and proximal colon cancer is novel.
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Affiliation(s)
- Elise Marlen Paulsen
- Department of Community Medicine, University of Tromsø – The Arctic University of Norway, 9037Tromsø, Norway
| | - Charlotta Rylander
- Department of Community Medicine, University of Tromsø – The Arctic University of Norway, 9037Tromsø, Norway
| | - Magritt Brustad
- Department of Community Medicine, University of Tromsø – The Arctic University of Norway, 9037Tromsø, Norway
| | - Torill E Jensen
- Department of Community Medicine, University of Tromsø – The Arctic University of Norway, 9037Tromsø, Norway
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Boughanem H, Kompella P, Tinahones FJ, Macias-Gonzalez M. An overview of vitamins as epidrugs for colorectal cancer prevention. Nutr Rev 2023; 81:455-479. [PMID: 36018754 DOI: 10.1093/nutrit/nuac065] [Citation(s) in RCA: 5] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
Abstract
Gene expression altering epigenomic modifications such as DNA methylation, histone modification, and chromosome remodeling is crucial to regulating many biological processes. Several lifestyle factors, such as diet and natural, bioactive food compounds, such as vitamins, modify epigenetic patterns. However, epigenetic dysregulation can increase the risk of many diseases, including cancer. Various studies have provided supporting and contrasting evidence on the relationship between vitamins and cancer risk. Though there is a gap in knowledge about whether dietary vitamins can induce epigenetic modifications in the context of colorectal cancer (CRC), the possibility of using them as epidrugs for CRC treatment is being explored. This is promising because such studies might be informative about the most effective way to use vitamins in combination with DNA methyltransferase inhibitors and other approved therapies to prevent and treat CRC. This review summarizes the available epidemiological and observational studies involving dietary, circulating levels, and supplementation of vitamins and their relationship with CRC risk. Additionally, using available in vitro, in vivo, and human observational studies, the role of vitamins as potential epigenetic modifiers in CRC is discussed. This review is focused on the action of vitamins as modifiers of DNA methylation because aberrant DNA methylation, together with genetic alterations, can induce the initiation and progression of CRC. Although this review presents some studies with promising results, studies with better study designs are necessary. A thorough understanding of the underlying molecular mechanisms of vitamin-mediated epigenetic regulation of CRC genes can help identify effective therapeutic targets for CRC prevention and treatment.
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Affiliation(s)
- Hatim Boughanem
- are with the Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Institute of Biomedical Research in Malaga (IBIMA), University of Malaga, Malaga, Spain.,are with the Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
| | - Pallavi Kompella
- are with the Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Institute of Biomedical Research in Malaga (IBIMA), University of Malaga, Malaga, Spain.,is with the Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas, USA
| | - Francisco J Tinahones
- are with the Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Institute of Biomedical Research in Malaga (IBIMA), University of Malaga, Malaga, Spain.,are with the Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
| | - Manuel Macias-Gonzalez
- are with the Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Institute of Biomedical Research in Malaga (IBIMA), University of Malaga, Malaga, Spain.,are with the Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
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Islam MR, Akash S, Rahman MM, Nowrin FT, Akter T, Shohag S, Rauf A, Aljohani AS, Simal-Gandara J. Colon cancer and colorectal cancer: Prevention and treatment by potential natural products. Chem Biol Interact 2022; 368:110170. [DOI: 10.1016/j.cbi.2022.110170] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/26/2022] [Revised: 08/24/2022] [Accepted: 09/03/2022] [Indexed: 11/29/2022]
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Is Season of Diagnosis a Predictor of Cancer Survival? Results from the Zurich Cancer Registry. Nutrients 2022; 14:nu14204291. [PMID: 36296975 PMCID: PMC9608958 DOI: 10.3390/nu14204291] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/23/2022] [Revised: 10/10/2022] [Accepted: 10/11/2022] [Indexed: 11/17/2022] Open
Abstract
In Switzerland, there is a large seasonal variation in sunlight, and vitamin D deficiency is relatively common during winter. The season of diagnosis may be linked to cancer survival via vitamin D status. Using data from the Cancer Registry of Zurich, Zug, Schaffhausen, and Schwyz with more than 171,000 cancer cases registered since 1980, we examined the association of the season of diagnosis with survival for cancers including prostate (ICD10 code C61; International Categorization of Diseases, version 10), breast (C50), colorectal (C18-21), lung (C34), melanoma (C43), and all sites combined. Cox proportional hazards regression models were used to assess the differences in the all-cause mortality by the season of the diagnosis. Winter was used as the reference season. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated for all the cancers combined (excluding nonmelanoma skin cancer) and for prostate (in men), breast (in women), colorectal, lung cancer, and melanomas, separately. A diagnosis in summer and/or autumn was associated with improved survival in all the sites combined for both sexes (men: HR 0.97 [95% CI 0.96-0.99]; women: HR 0.97 [95% CI 0.94-0.99]) and in colorectal (HR 0.91 [95% CI 0.84-0.99]), melanoma (HR 0.81 [95% CI 0.65-1.00]), and breast cancer (HR 0.91 [95% CI 0.94-0.99]) in women. Our study results suggest that a cancer diagnosis in summer and/or autumn is associated with a better prognosis. The improved seasonal survival coincides with the seasonal variation of sun-induced vitamin D, and vitamin D may play a protective and beneficial role in cancer survival.
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Hernández-Alonso P, Canudas S, Boughanem H, Toledo E, Sorlí JV, Estruch R, Castañer O, Lapetra J, Alonso-Gómez AM, Gutiérrez-Bedmar M, Fiol M, Serra-Majem L, Pintó X, Ros E, Fernandez-Lazaro CI, Ramirez-Sabio JB, Fitó M, Portu-Zapirain J, Macias-González M, Babio N, Salas-Salvadó J. Dietary vitamin D intake and colorectal cancer risk: a longitudinal approach within the PREDIMED study. Eur J Nutr 2021; 60:4367-4378. [PMID: 34050394 DOI: 10.1007/s00394-021-02585-1] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/03/2021] [Accepted: 05/11/2021] [Indexed: 12/31/2022]
Abstract
PURPOSE We evaluated whether the intake of dietary vitamin D is associated with the incidence of both colorectal cancer (CRC) and colon cancer in the framework of the PREDIMED cohort of older adults at high cardiovascular risk. METHODS We analyzed data from 7216 men and women (55-80 years) without CRC at baseline from the PREvención con DIeta MEDiterránea study. Baseline consumption of vitamin D was assessed using a validated 137-item food frequency questionnaire. Cox proportional hazards ratios (HRs) of CRC and colon cancer incidence were estimated for quartiles and per 1-SD of baseline vitamin D intake. RESULTS During a median follow-up of 6 years, we documented 97 incident CRC cases after the exclusion of subjects with no baseline dietary data and/or outliers of energy intake. A non-significant HRs and 95% confidence intervals (CIs) of CRC for the comparison of extreme quartiles (4th vs 1st) of vitamin D intake were observed [0.55 (0.30-1.00), P for trend = 0.072], whereas it was significant for colon cancer incidence alone [0.44 (0.22-0.90), P for trend = 0.032]. However, this association became significant in CRC and colon cancer incidence, after excluding 391 subjects consuming baseline vitamin D and/or calcium medication or prescribed supplements [0.52 (0.28-0.96) and 0.41 (0.12-0.85), respectively]. CONCLUSION A higher dietary intake of vitamin D was significantly associated with a reduced CRC risk in individuals at high cardiovascular risk.
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Affiliation(s)
- Pablo Hernández-Alonso
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, C/Sant Llorenç 21, 43201, Reus, Spain
- Institut d'Investigació Sanitària Pere Virgili (IISPV), Hospital Universitari San Joan de Reus, 43204, Reus, Spain
- Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Institute of Biomedical Research in Malaga (IBIMA), University of Malaga, 29016, Málaga, Spain
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
| | - Silvia Canudas
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, C/Sant Llorenç 21, 43201, Reus, Spain
- Institut d'Investigació Sanitària Pere Virgili (IISPV), Hospital Universitari San Joan de Reus, 43204, Reus, Spain
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
| | - Hatim Boughanem
- Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Institute of Biomedical Research in Malaga (IBIMA), University of Malaga, 29016, Málaga, Spain
| | - Estefanía Toledo
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Department of Preventive Medicine and Public Health, Universidad de Navarra, 31008, Pamplona, Spain
- IdiSNA, Navarra Institute for Health Research, 31008, Pamplona, Spain
| | - Jose V Sorlí
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Department of Preventive Medicine, Universidad de Valencia, 46010, Valencia, Spain
| | - Ramón Estruch
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Cardiovascular Risk, Nutrition and Aging Research Unit, August Pi i Sunyer Biomedical Research Institute (IDIBAPS), 08003, Barcelona, Spain
- Internal Medicine Service, Hospital Clínic, 08036, Barcelona, Spain
| | - Olga Castañer
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Cardiovascular Risk and Nutrition Research Group, Hospital del Mar Medical Research Institute (IMIM), 08003, Barcelona, Spain
| | - José Lapetra
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Department of Family Medicine, Research Unit, Distrito Sanitario Atención Primaria Sevilla, 41013, Sevilla, Spain
| | - Angel M Alonso-Gómez
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Bioaraba Health Research Institute, Osakidetza Basque Health Service, Araba University Hospital, University of the Basque Country UPV/EHU, 01002, Vitoria-Gasteiz, Spain
| | - Mario Gutiérrez-Bedmar
- Department of Preventive Medicine and Public Health, School of Medicine, Instituto de Investigación Biomédica de Málaga-IBIMA, Universidad de Málaga, 29010, Málaga, Spain
| | - Miquel Fiol
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Health Research Institute of the Balearic Islands (IdISBa), Hospital Son Espases, 07120, Palma de Mallorca, Spain
| | - Lluis Serra-Majem
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Institute for Biomedical and Health Research, Universidad de Las Palmas de Gran Canaria, 35016, Las Palmas, Spain
| | - Xavier Pintó
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Lipids and Vascular Risk Unit, Internal Medicine, Hospital Universitario de Bellvitge-Idibell, 08907, L'Hospitalet de Llobregat, Spain
| | - Emilio Ros
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Lipid Clinic, Department of Endocrinology and Nutrition Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), Hospital Clinic, University of Barcelona, Barcelona, Spain
| | - Cesar I Fernandez-Lazaro
- Department of Preventive Medicine and Public Health, Universidad de Navarra, 31008, Pamplona, Spain
| | | | - Montse Fitó
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
- Cardiovascular Risk and Nutrition Research Group, Hospital del Mar Medical Research Institute (IMIM), 08003, Barcelona, Spain
| | - Joseba Portu-Zapirain
- Bioaraba, Infectious Diseases Research Group, Vitoria-Gasteiz, Spain
- Internal Medicine Department, Osakidetza Basque Health Service, Araba University Hospital, Vitoria-Gasteiz, Spain
| | - Manuel Macias-González
- Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Institute of Biomedical Research in Malaga (IBIMA), University of Malaga, 29016, Málaga, Spain.
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain.
| | - Nancy Babio
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, C/Sant Llorenç 21, 43201, Reus, Spain.
- Institut d'Investigació Sanitària Pere Virgili (IISPV), Hospital Universitari San Joan de Reus, 43204, Reus, Spain.
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain.
| | - Jordi Salas-Salvadó
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, C/Sant Llorenç 21, 43201, Reus, Spain
- Institut d'Investigació Sanitària Pere Virgili (IISPV), Hospital Universitari San Joan de Reus, 43204, Reus, Spain
- Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III (ISCIII), 28029, Madrid, Spain
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The effect of vitamin D on the occurrence and development of colorectal cancer: a systematic review and meta-analysis. Int J Colorectal Dis 2021; 36:1329-1344. [PMID: 33598751 DOI: 10.1007/s00384-021-03879-w] [Citation(s) in RCA: 12] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 02/03/2021] [Indexed: 02/04/2023]
Abstract
PURPOSE There has been a lot of controversies about the correlation between vitamin D and colorectal cancer (CRC). In this meta-analysis, we purposed to explore the relationship between vitamin D and the incidence of CRC/the prognosis of CRC. METHODS A systematic search for articles in databases (Pubmed, Web of Science, EBSCO and Cochrane Library) was terminated in April 2020. The primary outcomes were the incidence rate of CRC and the long-term survival of patients with CRC. RESULTS According to the estimated pooled OR from 21 eligible studies, covering 904,152 people, the use of vitamin D was inversely associated with the incidence of CRC [OR = 0.87, (0.82-0.92)]. Among the four studies included in this meta-analysis, covering 7486 patients, compared the overall survival (OS) of CRC between the vitamin D users and the non-users. Based on the estimated pooled HR, vitamin D potentially improved the long-term survival of CRC patients [HR = 0.91, (0.83-0.98)]. CONCLUSION This meta-analysis demonstrates that vitamin D not only has a positive impact on the incidence of CRC from either the dietary or supplemental sources but also benefits clinical outcomes and improves the long-term survival of CRC patients. However, further studies are recommended to clarify the above phenomena.
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11
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Liang PS, Shaukat A, Crockett SD. AGA Clinical Practice Update on Chemoprevention for Colorectal Neoplasia: Expert Review. Clin Gastroenterol Hepatol 2021; 19:1327-1336. [PMID: 33581359 DOI: 10.1016/j.cgh.2021.02.014] [Citation(s) in RCA: 26] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/05/2020] [Revised: 02/02/2021] [Accepted: 02/08/2021] [Indexed: 02/07/2023]
Abstract
DESCRIPTION The purpose of this expert review is to describe the role of medications for the chemoprevention of colorectal neoplasia. Neoplasia is defined as precancerous lesions (e.g., adenoma and sessile serrated lesion) or cancer. The scope of this review excludes dietary factors and high-risk individuals with hereditary syndromes or inflammatory bowel disease. METHODS The best practice advice statements are based on a review of the literature to provide practical advice. A formal systematic review and rating of the quality of evidence or strength of recommendation were not performed. BEST PRACTICE ADVICE 1: In individuals at average risk for CRC who are (1) younger than 70 years with a life expectancy of at least 10 years, (2) have a 10-year cardiovascular disease risk of at least 10%, and (3) not at high risk for bleeding, clinicians should use low-dose aspirin to reduce CRC incidence and mortality. BEST PRACTICE ADVICE 2: In individuals with a history of CRC, clinicians should consider using aspirin to prevent recurrent colorectal neoplasia. BEST PRACTICE ADVICE 3: In individuals at average risk for CRC, clinicians should not use non-aspirin NSAIDs to prevent colorectal neoplasia because of a substantial risk of cardiovascular and gastrointestinal adverse events. BEST PRACTICE ADVICE 4: In individuals with type 2 diabetes, clinicians may consider using metformin to prevent colorectal neoplasia. BEST PRACTICE ADVICE 5: In individuals with CRC and type 2 diabetes, clinicians may consider using metformin to reduce mortality. BEST PRACTICE ADVICE 6: Clinicians should not use calcium or vitamin D (alone or together) to prevent colorectal neoplasia. BEST PRACTICE ADVICE 7: Clinicians should not use folic acid to prevent colorectal neoplasia. BEST PRACTICE ADVICE 8: In individuals at average risk for CRC, clinicians should not use statins to prevent colorectal neoplasia. BEST PRACTICE ADVICE 9: In individuals with a history of CRC, clinicians should not use statins to reduce mortality.
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Affiliation(s)
- Peter S Liang
- NYU Langone Health, New York, New York; VA New York Harbor Health Care System, New York, New York.
| | - Aasma Shaukat
- University of Minnesota, Minneapolis, Minnesota; Minneapolis VA Health Care System, Minneapolis, Minnesota
| | - Seth D Crockett
- University of North Carolina School of Medicine, Chapel Hill, North Carolina
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12
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Boughanem H, Canudas S, Hernandez-Alonso P, Becerra-Tomás N, Babio N, Salas-Salvadó J, Macias-Gonzalez M. Vitamin D Intake and the Risk of Colorectal Cancer: An Updated Meta-Analysis and Systematic Review of Case-Control and Prospective Cohort Studies. Cancers (Basel) 2021; 13:2814. [PMID: 34200111 PMCID: PMC8201292 DOI: 10.3390/cancers13112814] [Citation(s) in RCA: 16] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/06/2021] [Accepted: 05/31/2021] [Indexed: 12/15/2022] Open
Abstract
Obesity, a sedentary lifestyle, high red meat consumption and alcohol, and tobacco are considered the driving factors behind colorectal cancer (CRC) worldwide. Both diet and lifestyle are recognized to play an important role in the prevention of CRC. Forty years later, the vitamin D-cancer hypothesis is considered consistent. However, the relationship between low vitamin D intake and CRC is still controversial. The aim of this meta-analysis is to determine the associations between Vitamin D intake and CRC. MEDLINE-PubMed and Cochrane databases were searched up to May 2020 for studies evaluating the association between vitamin D intake (from foods and supplements) and CRC. Two reviewers, working independently, screened all titles and abstracts to identify the studies that met the inclusion criteria (case-control or prospective cohort (PC) studies published in English). Data were pooled by the generic inverse variance method using a random or fixed effect model. Heterogeneity was identified using the Cochran Q-test and quantified by the I2 statistic. A total of 31 original studies were included for the quantitative meta-analysis, comprising a total 47.540 cases and 70.567 controls in case-control studies, and a total of 14.676 CRC-incident cases (out of 808.130 subjects in PC studies) from 17 countries. A significant 25% lower risk was reported comparing the highest vs. the lowest dietary vitamin D consumption and CRC risk (odds ratio (95% confidence interval): 0.75 (0.67; 0.85)) in case-control studies, whereas a non-significant association was reported in case of prospective studies (hazard ratio (95% confidence interval): 0.94 (0.79; 1.11). The present meta-analysis demonstrates that high dietary vitamin D is associated to CRC prevention. However, larger and high-quality prospective studies and clinical trials are warranted to confirm this association.
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Affiliation(s)
- Hatim Boughanem
- Instituto de Investigación Biomédica de Málaga (IBIMA), Unidad de Gestión Clínica de Endocrinología y Nutrición del Hospital Virgen de la Victoria, 29010 Málaga, Spain; (H.B.); (M.M.-G.)
| | - Silvia Canudas
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, Hospital Universitari San Joan de Reus, 43201 Reus, Spain; (S.C.); (N.B.); (J.S.-S.)
- Institut d’Investigació Sanitària Pere Virgili (IISPV), 43204 Reus, Spain
- Instituto de Salud Carlos III (ISCIII), Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), 28220 Madrid, Spain
- Department of Nutrition, Food Sciences and Gastronomy, Food Torribera Campus, School of Pharmacy and Food Sciences, University of Barcelona, Santa Coloma de Gramenet, 08921 Barcelona, Spain
| | - Pablo Hernandez-Alonso
- Instituto de Investigación Biomédica de Málaga (IBIMA), Unidad de Gestión Clínica de Endocrinología y Nutrición del Hospital Virgen de la Victoria, 29010 Málaga, Spain; (H.B.); (M.M.-G.)
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, Hospital Universitari San Joan de Reus, 43201 Reus, Spain; (S.C.); (N.B.); (J.S.-S.)
- Institut d’Investigació Sanitària Pere Virgili (IISPV), 43204 Reus, Spain
- Instituto de Salud Carlos III (ISCIII), Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), 28220 Madrid, Spain
- Biochemical and Biotechnology Department, Faculty of Medicine and Health Sciences Human Nutrition Unit, Rovira and Virgili University, C/Sant Llorenç, 21, 43201 Reus, Spain
- Open Evidence Research Group, Universitat Oberta de Catalunya, 08018 Barcelona, Spain
| | - Nerea Becerra-Tomás
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, Hospital Universitari San Joan de Reus, 43201 Reus, Spain; (S.C.); (N.B.); (J.S.-S.)
- Institut d’Investigació Sanitària Pere Virgili (IISPV), 43204 Reus, Spain
- Instituto de Salud Carlos III (ISCIII), Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), 28220 Madrid, Spain
- Biochemical and Biotechnology Department, Faculty of Medicine and Health Sciences Human Nutrition Unit, Rovira and Virgili University, C/Sant Llorenç, 21, 43201 Reus, Spain
- Department of Preventive Medicine and Public Health, School of Medicine, University of Valencia, 46010 Valencia, Spain
- MRC Centre for Environment and Health, Department of Epidemiology & Biostatistics, School of Public Health, Faculty of Medicine, Imperial College London, St Mary’s Campus, Norfolk Place, London W2 1PG, UK
| | - Nancy Babio
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, Hospital Universitari San Joan de Reus, 43201 Reus, Spain; (S.C.); (N.B.); (J.S.-S.)
- Institut d’Investigació Sanitària Pere Virgili (IISPV), 43204 Reus, Spain
- Instituto de Salud Carlos III (ISCIII), Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), 28220 Madrid, Spain
| | - Jordi Salas-Salvadó
- Universitat Rovira i Virgili, Departament de Bioquímica i Biotecnologia, Unitat de Nutrició Humana, Hospital Universitari San Joan de Reus, 43201 Reus, Spain; (S.C.); (N.B.); (J.S.-S.)
- Institut d’Investigació Sanitària Pere Virgili (IISPV), 43204 Reus, Spain
- Instituto de Salud Carlos III (ISCIII), Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), 28220 Madrid, Spain
| | - Manuel Macias-Gonzalez
- Instituto de Investigación Biomédica de Málaga (IBIMA), Unidad de Gestión Clínica de Endocrinología y Nutrición del Hospital Virgen de la Victoria, 29010 Málaga, Spain; (H.B.); (M.M.-G.)
- Instituto de Salud Carlos III (ISCIII), Consorcio CIBER, M.P. Fisiopatología de la Obesidad y Nutrición (CIBERObn), 28220 Madrid, Spain
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13
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Abbasnezhad A, Falahi E, Ghavamzadeh S, Beiranvand R, Talaiezadeh A, Hasanvand A, Angali KA, Choghakhori R. Association between deficient levels of circulating vitamin D, dietary intake of vitamin D, calcium and retinol, and risk of colorectal cancer in an Iranian population: A case control study. Asia Pac J Clin Oncol 2021; 18:118-126. [PMID: 33852772 DOI: 10.1111/ajco.13524] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/31/2019] [Accepted: 10/11/2020] [Indexed: 11/30/2022]
Abstract
AIM We aimed to assess the association between deficient levels of circulating vitamin D, dietary intake of vitamin D, calcium and retinol, and risk of colorectal cancer in an Iranian population. METHODS In this retrospective case-control study that was conducted between 2012 and 2015, 278 first incident colorectal cancer cases (colon cancer = 103; rectal cancer = 175), and 278 sex and age matched healthy controls (HCs) were recruited. Serum 25(OH)D, dietary vitamin D, and calcium intake were assessed. Logistic regression was used to estimate the odds ratio (OR) between studied factors and colorectal cancer. Estimates of OR were calculated according to both bivariate analyses based on the matching factors and multivariate analyses, with additional adjustment for potential confounders. RESULTS A strong inverse linear dose-response association was seen between serum 25(OH)D and colorectal cancer (P for trend = .002). In comparison to serum 25(OH)D more than 40 nmol/L, lower serum concentrations were significantly associated with an increased OR of colorectal cancer. When analyzing anatomical subsites separately, lower circulating 25(OH)D was associated with higher OR for both colon and rectum cancers. Dietary vitamin D and calcium intake were not associated with colorectal cancer. Interaction analysis between serum 25(OH)D and the amount of calcium intake demonstrated that the lowest level of both factors was associated with an increased OR of colorectal cancer. The highest OR of colorectal cancer that was associated with lowest circulating 25(OH)D was stronger at the highest retinol intakes. CONCLUSION This study demonstrated an inverse strong association between 25(OH)D concentration and colorectal cancer in an Iranian population.
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Affiliation(s)
- Amir Abbasnezhad
- Nutritional Health Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran.,Nutrition and Metabolic Diseases Research Center, Department of Nutrition, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
| | - Ebrahim Falahi
- Nutritional Health Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran
| | - Saeid Ghavamzadeh
- Department of Human Nutrition, Medicine Faculty, Urmia University of Medical Sciences, Urmia, Iran
| | - Ramin Beiranvand
- Social Determinants of Health Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran
| | | | - Amin Hasanvand
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran
| | - Kambiz Ahmadi Angali
- Biostatistics Division, Health Faculty, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
| | - Razieh Choghakhori
- Razi Herbal Medicines Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran
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Liu X, Wu P, Shen L, Jiao B, Liao X, Wang H, Peng J, Lin Z. DHCR7 rs12785878 T>C Polymorphism Is Associated With an Increased Risk of Early Onset of Alzheimer's Disease in Chinese Population. Front Genet 2021; 12:583695. [PMID: 33692822 PMCID: PMC7938861 DOI: 10.3389/fgene.2021.583695] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/15/2020] [Accepted: 01/08/2021] [Indexed: 01/08/2023] Open
Abstract
Background: Vitamin D insufficiency has been considered a risk factor for Alzheimer's disease (AD) in several studies. Recently, four single-nucleotide polymorphisms (SNPs) to be genome-wide significant for 25-hydroxyvitamin D [25(OH)D] were identified to have an association with the risk of AD. These include GC rs2282679 A>C, CYP2R1 rs10741657 T>C, DHCR7 rs12785878 T>C, and CYP24A1 rs6013897 T>A. However, the association between these polymorphisms and AD susceptibility in the Chinese population remains unclear. Methods: A case-control cohort study was conducted in 676 AD patients (mean age at onset was 69.52 ± 10.90 years, male: 39.2%) and 551 healthy controls (mean age was 67.73 ± 6.02 years, male: 44.8%). Genotyping was determined by PCR and SNaPshot sequencing. To determine whether the four SNPs account for risks in AD in Chinese population, multivariate logistic regression models were performed. Stratified analysis was performed based on gender and age of onset of AD, separately. Statistical significance was set at 0.0125 (0.05/4) based on Bonferroni correction. Findings:DHCR7 rs12785878 T>C was found to be significantly associated with an increased risk of early-onset Alzheimer's disease (EOAD) (n = 300, risk allele C, adjusted OR = 1.542, adjusted 95% CI = 1.176–2.023, p = 0.002). There was no statistical significance of the other three SNPs between the two groups. Interpretation: Our results suggested that DHCR7 rs12785878 T>C might be associated with an increased risk of EOAD in the Chinese population, while other polymorphisms related to vitamin D insufficiency might not be. However, due to the limited data in this study, replication studies in a larger sample are required.
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Affiliation(s)
- Xixi Liu
- Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
| | - Pengfei Wu
- Hunan Provincial Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, Changsha, China
| | - Lu Shen
- Department of Neurology, Xiangya Hospital, Central South University, Changsha, China.,Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, China.,National Clinical Research Center for Geriatric Diseases, Changsha, China.,Key Laboratory of Organ Injury, Aging and Regenerative Medicine of Hunan Province, Changsha, China
| | - Bin Jiao
- Department of Neurology, Xiangya Hospital, Central South University, Changsha, China.,Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, China
| | - Xinxin Liao
- Department of Geriatrics Neurology, Xiangya Hospital, Central South University, Changsha, China
| | - Haochen Wang
- Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, China
| | - Jiangnan Peng
- Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, China
| | - Zhangyuan Lin
- Key Laboratory of Organ Injury, Aging and Regenerative Medicine of Hunan Province, Changsha, China.,Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, China
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15
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Jin S, Kim Y, Je Y. Dairy Consumption and Risks of Colorectal Cancer Incidence and Mortality: A Meta-analysis of Prospective Cohort Studies. Cancer Epidemiol Biomarkers Prev 2020; 29:2309-2322. [DOI: 10.1158/1055-9965.epi-20-0127] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/28/2020] [Revised: 05/02/2020] [Accepted: 08/19/2020] [Indexed: 12/24/2022] Open
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16
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Kim H, Giovannucci E. Vitamin D Status and Cancer Incidence, Survival, and Mortality. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY 2020; 1268:39-52. [DOI: 10.1007/978-3-030-46227-7_3] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
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17
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Huang D, Lei S, Wu Y, Weng M, Zhou Y, Xu J, Xia D, Xu E, Lai M, Zhang H. Additively protective effects of vitamin D and calcium against colorectal adenoma incidence, malignant transformation and progression: A systematic review and meta-analysis. Clin Nutr 2019; 39:2525-2538. [PMID: 31784301 DOI: 10.1016/j.clnu.2019.11.012] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/10/2019] [Revised: 10/26/2019] [Accepted: 11/07/2019] [Indexed: 02/07/2023]
Abstract
BACKGROUND Colorectal cancer (CRC) exhibits a linear progression from normal colonic epithelium, adenoma initiation, carcinoma transformation and even to metastasis. Diet changes might influence carcinogenesis and prognosis. We aimed to determine the effects of vitamin D and calcium on colorectal adenoma incidence, malignancy development and prognosis. METHODS Systematic literature searches (PubMed, Embase, and Cochrane Library databases) and hand searches were performed by September 30, 2019. A random-effects model was adopted to pool relative ratios (RRs) for colorectal tumour incidence or hazard ratios (HRs) for CRC mortality. Stratified analyses were performed by gender, tumour location, calcium intake level and ethnic group. RESULTS Total 854,195 cases from 166 studies were included. The colorectal adenoma incidence was inversely correlated with the circulating 25-hydroxyvitamin D [25(OH)D] level (RR: 0.80, 95% CI: 0.71-0.89), vitamin D intake (RR: 0.87, 95% CI: 0.82-0.92) and calcium intake (RR: 0.86, 95% CI: 0.81-0.91). The CRC incidence was decreased by circulating 25(OH)D (RR: 0.67, 95% CI: 0.59-0.77), vitamin D intake (RR: 0.85, 95% CI: 0.78-0.93) and calcium intake (RR: 0.75, 95% CI: 0.70-0.79). High-level circulating 25(OH)D triggered better overall survival (HR: 0.67, 95% CI: 0.57-0.79) and CRC-specific survival (HR: 0.63, 95% CI: 0.53-0.74). Stratified analyses showed that vitamin D and calcium significantly suppressed colorectal tumour incidence among women. Left-sided CRC risk was reversely related to circulating 25(OH)D (RR: 0.60, 95% CI: 0.41-0.88) and vitamin D intake (RR: 0.73, 95% CI: 0.57-0.93). Circulating 25(OH)D decreased colorectal adenoma (RR: 0.63, 95% CI: 0.48-0.82) and CRC (RR: 0.69, 95% CI: 0.56-0.86) risk in populations with higher calcium intake. European and American populations benefited more from vitamin D intake against colorectal tumour. A significant dose-response relationship was observed between intake of vitamin D or calcium and colorectal tumour incidence. CONCLUSIONS Vitamin D and calcium play additively chemopreventive roles in colorectal adenoma incidence, malignant transformation and progression, especially for women and left-sided CRC patients.
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Affiliation(s)
- Dongdong Huang
- Department of Pathology and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; Key Laboratory of Disease Proteomics of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Pathology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
| | - Siqin Lei
- Department of Pathology and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; Key Laboratory of Disease Proteomics of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Yihua Wu
- Department of Toxicology, School of Public Health and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Menghan Weng
- Department of Pathology and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; Key Laboratory of Disease Proteomics of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Pathology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
| | - Yuwei Zhou
- Department of Pathology and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Jiawei Xu
- Department of Toxicology, School of Public Health and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Dajing Xia
- Department of Toxicology, School of Public Health and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Enping Xu
- Department of Pathology and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; Key Laboratory of Disease Proteomics of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Maode Lai
- Key Laboratory of Disease Proteomics of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Honghe Zhang
- Department of Pathology and Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; Key Laboratory of Disease Proteomics of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China.
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18
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Milk and risk of colorectal, colon and rectal cancer in the Norwegian Women and Cancer (NOWAC) Cohort Study. Br J Nutr 2019; 119:1274-1285. [PMID: 29770759 DOI: 10.1017/s0007114518000752] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
According to World Cancer Research Fund International/American Institute for Cancer Research, it is 'probable' that dairy products decrease the risk of colorectal cancer (CRC). However, meta-analyses restricted to women have not shown associations between milk intake and risk of CRC. The aim of this study was to examine the association between milk intake and risk of CRC, colon cancer and rectal cancer among women. Data from 81 675 participants in the Norwegian Women and Cancer Cohort Study were included, and multivariable Cox proportional hazard regression models were used to investigate milk intake using two different analytical approaches: one that included repeated measurements and one that included baseline measurements only (872 and 1084 CRC cases, respectively). A weak inverse association between milk intake and risk of colon cancer may be indicated both in repeated measurements analyses and in baseline data analyses. Hazard ratios (HR) for colon cancer of 0·80 (95 % CI 0·62, 1·03, P trend 0·07) and 0·81 (95 % CI 0·64, 1·01, P trend 0·03) and HR for rectal cancer of 0·97 (95 % CI 0·67, 1·42, P trend 0·92) and 0·71 (95 % CI 0·50, 1·01, P trend 0·03) were found when comparing the high with the no/seldom milk intake group in energy-adjusted multivariable models. Our study indicates that there may be a weak inverse association between milk intake and risk of colon cancer among women. The two analytical approaches yielded different results for rectal cancer and hence CRC. Our study indicates that the use of single or repeated measurements in analyses may influence the results.
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19
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Suzuki N, Niikura R, Ihara S, Hikiba Y, Kinoshita H, Higashishima N, Hayakawa Y, Yamada A, Hirata Y, Nakata R, Okamoto M, Sano M, Kushiyama A, Ichinose M, Woods SL, Worthley D, Iwamoto Y, Koike K. Alpha-Blockers As Colorectal Cancer Chemopreventive: Findings from a Case-Control Study, Human Cell Cultures, and In Vivo Preclinical Testing. Cancer Prev Res (Phila) 2019; 12:185-194. [PMID: 30700439 DOI: 10.1158/1940-6207.capr-18-0288] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/13/2018] [Revised: 12/17/2018] [Accepted: 01/18/2019] [Indexed: 11/16/2022]
Abstract
A retrospective case-controlled analysis was performed to identify drug candidates in the current use that may prevent colorectal cancer, outside of aspirin. A total of 37,510 patients aged ≥20 years were assessed to identify subjects who had been diagnosed with colorectal cancer by colonoscopy without a previous diagnosis of colorectal cancer, inflammatory bowel disease (IBD), or gastrointestinal symptoms; 1,560 patients were identified who were diagnosed with colorectal cancer by colonoscopy. The patients with colorectal cancer were matched with 1,560 age, gender, family history of colorectal cancer and comorbidity-matched control patients who were not diagnosed with colorectal cancer at colonoscopy. The medication histories were compared between the two groups. Next, candidate drugs that were more frequently used by the control patients were selected and their effects on human colorectal cancer cell lines in vitro and an inflammation-induced mouse model of colorectal cancer were tested. Putative colorectal cancer preventative agents were identified, including aspirin, vitamin D, vitamin B, vitamin C, vitamin E, xanthine oxidase inhibitor, alpha-blockers, angiotensin receptor blocker, nateglinide, probiotics, thienopyridine, folic acid, nitrovasodilators, bisphosphonates, calcium channel blockers, steroids, and statins (P < 0.05). Alpha-blockers and xanthine oxidase inhibitors were selected for further study because these agents have not been analyzed previously as factors that may affect colorectal cancer outcomes. In vitro doxazosin (alpha-blocker), but not febuxostat (xanthine oxidase inhibitor), suppressed the proliferation of human colorectal cancer cells. Doxazosin also decreased tumorigenesis in an AOM/DSS mouse colorectal cancer model. Alpha-blockers may prevent colorectal cancer.
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Affiliation(s)
- Nobumi Suzuki
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. .,Division of Gastroenterology, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.,School of Medicine, University of Adelaide and South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
| | - Ryota Niikura
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
| | - Sozaburo Ihara
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.,Division of Gastroenterology, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan
| | - Yohko Hikiba
- Division of Gastroenterology, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan
| | - Hiroto Kinoshita
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.,Division of Gastroenterology, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan
| | - Naoko Higashishima
- Division of Gastroenterology, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan
| | - Yoku Hayakawa
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
| | - Atsuo Yamada
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
| | - Yoshihiro Hirata
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
| | - Ryo Nakata
- Department of Gastroenterology, Japanese Red Cross Medical Center, Tokyo, Japan
| | - Makoto Okamoto
- Department of Gastroenterology, JR Tokyo General Hospital, Tokyo, Japan
| | - Munetaka Sano
- Department of Gastroenterology, Yaizu City Hospital, Shizuoka, Japan
| | - Akifumi Kushiyama
- Division of Diabetes and Metabolism, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan
| | - Mari Ichinose
- School of Medicine, University of Adelaide and South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
| | - Susan L Woods
- School of Medicine, University of Adelaide and South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
| | - Daniel Worthley
- School of Medicine, University of Adelaide and South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
| | - Yasuhiko Iwamoto
- Division of Diabetes and Metabolism, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan
| | - Kazuhiko Koike
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
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20
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Haidari F, Abiri B, Iravani M, Razavi SM, Vafa M. The Effects of UVB and Vitamin D on Decreasing Risk of Colorectal Cancer Incidence and Mortality: A Review of the Epidemiology, Clinical Trials, and Mechanisms. Nutr Cancer 2018; 71:709-717. [PMID: 30588844 DOI: 10.1080/01635581.2018.1521444] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
The solar ultraviolet B-vitamin D-cancer hypothesis was first suggested in 1980 based on a geographical ecological study. Since then, several ecological and observational studies, as well as researches of mechanisms have supported the hypothesis. Also, the association between vitamin D condition and cancer risk has been assessed in a number of epidemiologic studies, while data from interventional studies remain scant. In regard of cancer locations, the body of evidence is most substantial for colorectal cancer, for which support comes from studies of 25(OH)D, vitamin D intake, and region of residence in a sunny weather. Collectively evidence demonstrates that vitamin D has a potent and beneficial effect at antagonizing and blocking several mitogenic mechanisms related to tumorigenesis. Taken together with the epidemiological studies and limited clinical trials, individuals may need to consider elevating 25(OH)D levels via sun exposure and/or vitamin D supplementation to decrease risk of colorectal cancer, in addition to standard care, treat cancer.
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Affiliation(s)
- Fatemeh Haidari
- a Department of Nutritional Sciences, Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences , Ahvaz , Iran
| | - Behnaz Abiri
- b Department of Nutrition, Faculty of Paramedicine , Ahvaz Jundishapur University of Medical Sciences , Ahvaz , Iran
| | - Masood Iravani
- c Department of Medical Oncology and Hematology , Tehran University of Medical Sciences , Tehran , Iran
| | - Seyyed-Mohsen Razavi
- d Department of Medical Oncology and Hematology , Iran University of Medical Sciences , Tehran , Iran
| | - Mohammadreza Vafa
- e Department of Nutrition, School of Public Health , Iran University of Medical Sciences , Tehran , Iran
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21
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Yang W, Liu L, Masugi Y, Qian ZR, Nishihara R, Keum N, Wu K, Smith-Warner SA, Ma Y, Nowak JA, Momen-Heravi F, Zhang L, Bowden M, Morikawa T, da Silva A, Wang M, Chan AT, Fuchs CS, Meyerhardt JA, Ng K, Giovannucci E, Ogino S, Zhang X. Calcium intake and risk of colorectal cancer according to expression status of calcium-sensing receptor (CASR). Gut 2018; 67:1475-1483. [PMID: 28676564 PMCID: PMC5754263 DOI: 10.1136/gutjnl-2017-314163] [Citation(s) in RCA: 39] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/16/2017] [Revised: 05/08/2017] [Accepted: 05/15/2017] [Indexed: 01/01/2023]
Abstract
OBJECTIVE Although evidence suggests an inverse association between calcium intake and the risk of colorectal cancer, the mechanisms remain unclear. The calcium-sensing receptor (CASR) is expressed abundantly in normal colonic epithelium and may influence carcinogenesis. We hypothesized that calcium intake might be associated with lower risk of CASR-positive, but not CASR-negative, colorectal cancer. DESIGN We assessed tumour CASR protein expression using immunohistochemistry in 779 incident colon and rectal cancer cases that developed among 136 249 individuals in the Nurses' Health Study and Health Professionals Follow-Up Study. Duplication method Cox proportional hazards regression analysis was used to assess associations of calcium intake with incidence of colorectal adenocarcinoma subtypes by CASR status. RESULTS Total calcium intake was inversely associated with the risk of developing colorectal cancer (ptrend=0.01, comparing ≥1200 vs <600 mg/day: multivariable HR=0.75, 95% CI 0.60 to 0.95). For the same comparison, higher total calcium intake was associated with a lower risk of CASR-positive tumours (ptrend=0.003, multivariable HR=0.67, 95% CI 0.51 to 0.86) but not with CASR-negative tumours (ptrend=0.67, multivariable HR=1.15, 95% CI 0.75 to 1.78; pheterogeneity=0.06 between the CASR subtypes). The stronger inverse associations of calcium intake with CASR-positive but not CASR-negative tumours generally appeared consistent regardless of sex, tumour location and source of calcium. CONCLUSIONS Our molecular pathological epidemiology data suggest a causal relationship between higher calcium intake and lower colorectal cancer risk, and a potential role of CASR in mediating antineoplastic effect of calcium.
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Affiliation(s)
- Wanshui Yang
- Department of Social Science and Public Health, School of Basic Medical Science, Jiujiang University, Jiujiang, Jiangxi, P.R. China
| | - Li Liu
- Department of Oncologic Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA,Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Department of Epidemiology and Biostatistics, and the Ministry of Education Key Lab of Environment and Health, School of Public Health, Huazhong University of Science and Technology, Wuhan, P.R. China
| | - Yohei Masugi
- Department of Oncologic Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
| | - Zhi Rong Qian
- Department of Oncologic Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
| | - Reiko Nishihara
- Department of Oncologic Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA,Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Division of MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School Boston, MA, USA
| | - NaNa Keum
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA
| | - Kana Wu
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA
| | - Stephanie A. Smith-Warner
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA
| | - Yanan Ma
- Department of Biostatistics and Epidemiology, School of Public Health, China Medical University, Shenyang, Liaoning, PR China
| | - Jonathan A Nowak
- Division of MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School Boston, MA, USA
| | - Fatemeh Momen-Heravi
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA,Section of Oral and Diagnostic Sciences, Division of Periodontics, Columbia University College of Dental Medicine, New York, NY, USA
| | - Libin Zhang
- Institute for Community Inclusion, University of Massachusetts Boston, MA, USA
| | - Michaela Bowden
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
| | - Teppei Morikawa
- Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
| | - Annacarolina da Silva
- Department of Oncologic Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
| | - Molin Wang
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA
| | - Andrew T. Chan
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA,Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA,Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
| | - Charles S. Fuchs
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA,Yale Cancer Center, New Haven, CT, USA,Department of Medicine, Yale School of Medicine, New Haven, CT, USA,Smilow Cancer Hospital, New Haven, CT, USA
| | - Jeffrey A. Meyerhardt
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
| | - Kimmie Ng
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
| | - Edward Giovannucci
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
| | - Shuji Ogino
- Department of Oncologic Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA,Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA,Division of MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School Boston, MA, USA
| | - Xuehong Zhang
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
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22
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Abstract
In many cells throughout the body, vitamin D is converted into its active form calcitriol and binds to the vitamin D receptor (VDR), which functions as a transcription factor to regulate various biological processes including cellular differentiation and immune response. Vitamin D-metabolising enzymes (including CYP24A1 and CYP27B1) and VDR play major roles in exerting and regulating the effects of vitamin D. Preclinical and epidemiological studies have provided evidence for anti-cancer effects of vitamin D (particularly against colorectal cancer), although clinical trials have yet to prove its benefit. In addition, molecular pathological epidemiology research can provide insights into the interaction of vitamin D with tumour molecular and immunity status. Other future research directions include genome-wide research on VDR transcriptional targets, gene-environment interaction analyses and clinical trials on vitamin D efficacy in colorectal cancer patients. In this study, we review the literature on vitamin D and colorectal cancer from both mechanistic and population studies and discuss the links and controversies within and between the two parts of evidence.
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23
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Lee DH, Keum N, Giovannucci EL. Colorectal Cancer Epidemiology in the Nurses' Health Study. Am J Public Health 2016; 106:1599-607. [PMID: 27459444 DOI: 10.2105/ajph.2016.303320] [Citation(s) in RCA: 42] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
OBJECTIVES To review the contribution of the Nurses' Health Study (NHS) to identifying risk and protective factors for colorectal adenomas and colorectal cancer (CRC). METHODS We performed a narrative review of the publications using the NHS between 1976 and 2016. RESULTS Existing epidemiological studies using the NHS have reported that red and processed meat, alcohol, smoking, and obesity were associated with an increased risk of CRC, whereas folate, calcium, vitamin D, aspirin, and physical activity were associated with decreased risk of CRC. Moreover, modifiable factors, such as physical activity, vitamin D, folate, insulin and insulin-like growth factor binding protein-1, and diet quality, were identified to be associated with survival among CRC patients. In recent years, molecular pathological epidemiological studies have been actively conducted and have shown refined results by molecular subtypes of CRC. CONCLUSIONS The NHS has provided new insights into colorectal adenomas, CRC etiology, and pathogenic mechanisms. With its unique strengths, the NHS should continue to contribute to the field of CRC epidemiology and play a major role in public health.
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Affiliation(s)
- Dong Hoon Lee
- All authors are with the Departments of Nutrition and Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA. Edward L. Giovannucci is also with the Department of Medicine, Harvard Medical School, Boston
| | - NaNa Keum
- All authors are with the Departments of Nutrition and Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA. Edward L. Giovannucci is also with the Department of Medicine, Harvard Medical School, Boston
| | - Edward L Giovannucci
- All authors are with the Departments of Nutrition and Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA. Edward L. Giovannucci is also with the Department of Medicine, Harvard Medical School, Boston
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24
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Proportion of colon cancer attributable to lifestyle in a cohort of US women. Cancer Causes Control 2015; 26:1271-1279. [PMID: 26092381 DOI: 10.1007/s10552-015-0619-z] [Citation(s) in RCA: 38] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/12/2014] [Accepted: 06/11/2015] [Indexed: 12/13/2022]
Abstract
BACKGROUND Many modifiable lifestyle factors have been associated with colon cancer risk, but less is known about their effect on disease when considered together. Estimating the proportion of colon cancer cases that could be prevented by the adoption of combined modifiable lifestyle behaviors will provide important insights into disease prevention. METHODS In the Nurses' Health Study, we defined a low-risk group according to a combination of six factors: body mass index < 25 kg/m(2), physical activity of ≥ 21 metabolic equivalent of task per week, alcohol consumption ≤ 30 g/day, cigarette smoking <10 pack-years before the age of 30, current use of multivitamins for ≥ 15 years, and total calcium intake ≥ 700 mg/day. A composite risk score index was created and the population attributable risk (PAR%) was calculated after accounting for other known risk or protective factors. RESULTS We documented 1,127 colon cancer cases among 81,092 over 24 years of follow-up. Compared with women in the lowest risk category, the women at all other exposure levels had a hazard ratio of colon cancer of 1.81 (95% confidence interval 1.15-2.85). The score index was significantly and linearly related to an increasing risk of colon cancer (p value for trend <0.0001). The PAR% of the six risk factors considered together in relation to colon cancer was 0.37 (95% CI 0.09-0.60). When regular aspirin use (two tablets/week for six or more years) was included with the other low-risk behaviors, the PAR% increased to 0.43 (95% CI 0.14-0.65). CONCLUSIONS Beyond the known benefit from colonoscopy/sigmoidoscopy, key behavior modifications and adherence to a healthy lifestyle could avoid approximately 37% of colon cancer cases among women.
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25
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Song M, Garrett WS, Chan AT. Nutrients, foods, and colorectal cancer prevention. Gastroenterology 2015; 148:1244-60.e16. [PMID: 25575572 PMCID: PMC4409470 DOI: 10.1053/j.gastro.2014.12.035] [Citation(s) in RCA: 456] [Impact Index Per Article: 45.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/06/2014] [Revised: 11/26/2014] [Accepted: 12/01/2014] [Indexed: 02/07/2023]
Abstract
Diet has an important role in the development of colorectal cancer. In the past few decades, findings from extensive epidemiologic and experimental investigations have linked consumption of several foods and nutrients to the risk of colorectal neoplasia. Calcium, fiber, milk, and whole grains have been associated with a lower risk of colorectal cancer, and red meat and processed meat have been associated with an increased risk. There is substantial evidence for the potential chemopreventive effects of vitamin D, folate, fruits, and vegetables. Nutrients and foods also may interact, as a dietary pattern, to influence colorectal cancer risk. Diet likely influences colorectal carcinogenesis through several interacting mechanisms. These include the direct effects on immune responsiveness and inflammation, and the indirect effects of overnutrition and obesity-risk factors for colorectal cancer. Emerging evidence also implicates the gut microbiota as an important effector in the relationship between diet and cancer. Dietary modification therefore has the promise of reducing colorectal cancer incidence.
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Affiliation(s)
- Mingyang Song
- Department of Nutrition, Harvard School of Public Health, Boston, MA,Department of Epidemiology, Harvard School of Public Health, Boston, MA
| | - Wendy S. Garrett
- Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA,Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA,Department of Medicine, Harvard Medical School, Boston, MA,Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA
| | - Andrew T. Chan
- Department of Medicine, Harvard Medical School, Boston, MA,Channing Division of Network Medicine, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA,Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA
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26
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Chacko L, Macaron C, Burke CA. Colorectal cancer screening and prevention in women. Dig Dis Sci 2015; 60:698-710. [PMID: 25596719 DOI: 10.1007/s10620-014-3452-4] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/15/2014] [Accepted: 11/16/2014] [Indexed: 02/07/2023]
Abstract
Colorectal cancer (CRC) is one of the leading cancers and cause of cancer deaths in American women and men. Females and males share a similar lifetime cumulative risk of CRC however, substantial differences in risk factors, tumor biology, and effectiveness of cancer prevention services have been observed between them. This review distills the evidence documenting the unique variation observed between the genders relating to CRC risk factors, screening and prevention. Consistent evidence throughout the world demonstrates that women reach equivalent levels of adenomas and CRC as men but it occurs nearly a decade later in life than in their male counterparts. Women have a higher proportion of tumors which are hypermethylated, have microsatellite instability and located in the proximal colon suggesting the serrated pathway may be of greater consequence in them than in men. Other CRC risk factors such as smoking, diet and obesity have been shown to have disparate effects on women which may related to interactions between estrogen exposure, body fat distribution, and the biologic underpinnings of their tumors. There is data showing the uptake, choice, and efficacy of different CRC screening methods in women is dissimilar to that in men. The mortality benefit from FOBT, sigmoidoscopy, and protection from interval CRC by colonoscopy appears to be lower in women than men. A greater understanding of these gender idiosyncrasies will facilitate an personalized approach to CRC prevention and should ultimately lead to a reduced burden of disease.
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Affiliation(s)
- Lyssa Chacko
- Department of Gastroenterology and Hepatology, Denver Veterans Affairs Medical Center, Denver, CO, USA
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27
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Liu Y, Yu Q, Zhu Z, Zhang J, Chen M, Tang P, Li K. Vitamin and multiple-vitamin supplement intake and incidence of colorectal cancer: a meta-analysis of cohort studies. Med Oncol 2015; 32:434. [PMID: 25491145 DOI: 10.1007/s12032-014-0434-5] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2014] [Accepted: 12/03/2014] [Indexed: 02/06/2023]
Abstract
This paper systematically evaluated the association of intake of different vitamins and multiple-vitamin supplements and the incidence of colorectal cancer. Relevant studies were identified in MEDLINE via PubMed (published up to April 2014). We extracted data from articles on vitamins A, C, D, E, B9 (folate), B2, B3, B6, and B12 and multiple-vitamin supplements. We used multivariable-adjusted relative risks (RRs) and a random-effects model for analysis and random effects. With heterogeneity, we looked for the source of heterogeneity or performed sensitivity and stratified analyses. We found 47 articles meeting the inclusion criteria. The multivariable-adjusted RR for pooled studies for the association between the highest versus lowest vitamin B9 (folate) intake and colorectal cancer was 0.88 [95 % confidence interval (95 % CI) 0.81-0.95]. Vitamin D was 0.87 (95 % CI 0.77-0.99); vitamin B6, 0.88 (95 % CI 0.79-0.99); vitamin B2, 0.86 (95 % CI, 0.76-0.97); vitamin A, 0.87 (95 % CI, 0.75-1.03); vitamin C, 0.92 (95 % CI, 0.80-1.06); vitamin E, 0.94 (95 % CI, 0.82-1.07); vitamin B12, 1.10 (95 % CI, 0.92-1.32); vitamin B3, 1.18 (95 % CI, 0.76-1.84). Vitamin B9 (folate), D, B6, and B2 intake was inversely associated with risk of colorectal cancer, but further study is needed. Our study featured unacceptable heterogeneity for studies of multiple-vitamin supplements, so findings were inconclusive.
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Affiliation(s)
- Yan Liu
- Department of Public Health, Shantou University Medical College, No. 22 Xinling Road, Shantou, 515041, Guangdong, China,
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28
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Heine-Bröring RC, Winkels RM, Renkema JMS, Kragt L, van Orten-Luiten ACB, Tigchelaar EF, Chan DSM, Norat T, Kampman E. Dietary supplement use and colorectal cancer risk: a systematic review and meta-analyses of prospective cohort studies. Int J Cancer 2014; 136:2388-401. [PMID: 25335850 DOI: 10.1002/ijc.29277] [Citation(s) in RCA: 82] [Impact Index Per Article: 7.5] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/18/2014] [Accepted: 09/19/2014] [Indexed: 12/31/2022]
Abstract
Use of dietary supplements is rising in countries where colorectal cancer is prevalent. We conducted a systematic literature review and meta-analyses of prospective cohort studies on dietary supplement use and colorectal cancer risk. We identified relevant studies in Medline, Embase and Cochrane up to January 2013. Original and peer-reviewed papers on dietary supplement use and colorectal cancer, colon cancer, or rectal cancer incidence were included. "Use-no use"(U-NU), "highest-lowest"(H-L) and "dose-response"(DR) meta-analyses were performed. Random-effects models were used to estimate summary estimates. In total, 24 papers were included in the meta-analyses. We observed inverse associations for colorectal cancer risk and multivitamin (U-NU: RR = 0.92; 95% CI: 0.87,0.97) and calcium supplements (U-NU: RR = 0.86; 95% CI: 0.79,0.95; H-L: RR = 0.80; 95% CI: 0.70,0.92; DR: for an increase of 100 mg/day, RR = 0.96; 95% CI: 0.94,0.99). Inconsistent associations were found for colon cancer risk and supplemental vitamin A and vitamin C, and for colorectal cancer risk and supplemental vitamin D, vitamin E, garlic and folic acid. Meta-analyses of observational studies suggest a beneficial role for multivitamins and calcium supplements on colorectal cancer risk, while the association with other supplements and colorectal cancer risk is inconsistent. Residual confounding of lifestyle factors might be present. Before recommendations can be made, an extensive assessment of dietary supplement use and a better understanding of underlying mechanisms is needed.
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29
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Ralston RA, Truby H, Palermo CE, Walker KZ. Colorectal cancer and nonfermented milk, solid cheese, and fermented milk consumption: a systematic review and meta-analysis of prospective studies. Crit Rev Food Sci Nutr 2014; 54:1167-79. [PMID: 24499149 DOI: 10.1080/10408398.2011.629353] [Citation(s) in RCA: 50] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
Colorectal cancer is the second most prevalent cancer worldwide. A systematic review and meta-analysis of prospective studies was conducted to examine the association between intake of different types of dairy foods during adulthood and the development of colorectal cancer, specifically comparing nonfermented milk, solid cheese, and fermented milk. Seven databases were systematically searched and 15 cohort studies selected for inclusion, involving over 900,000 subjects and over 5200 colorectal cancer cases. Meta-analysis resulted in an overall relative risk of colon cancer of 0.74 (95% confidence interval 0.60-0.91) in men consuming nonfermented milk (highest intake category averaging 525 g/day). No association was found between consumption of nonfermented milk and rectal cancer in men or nonfermented milk and colon or rectal cancer in women. No protective association was found between consumption of solid cheese or fermented milk and colorectal cancer. Reasons for the differences in the impact of nonfermented milk, solid cheese, and fermented milk in the colon are discussed. This meta-analysis supports the inverse association between nonfermented milk consumption and risk of colon cancer in men, and provides an evidence base to assist in the formulation of dietary guidelines involving dairy foods.
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Affiliation(s)
- Robin A Ralston
- a Department of Nutrition and Dietetics, Southern Clinical School of Medicine, Monash Medical Centre , Monash University , Victoria , Australia
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Kuppusamy P, Yusoff MM, Maniam GP, Ichwan SJA, Soundharrajan I, Govindan N. Nutraceuticals as potential therapeutic agents for colon cancer: a review. Acta Pharm Sin B 2014; 4:173-81. [PMID: 26579381 PMCID: PMC4629076 DOI: 10.1016/j.apsb.2014.04.002] [Citation(s) in RCA: 70] [Impact Index Per Article: 6.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2013] [Revised: 01/14/2014] [Accepted: 03/27/2014] [Indexed: 12/27/2022] Open
Abstract
Colon cancer is a world-wide health problem and the second-most dangerous type of cancer, affecting both men and women. The modern diet and lifestyles, with high meat consumption and excessive alcohol use, along with limited physical activity has led to an increasing mortality rate for colon cancer worldwide. As a result, there is a need to develop novel and environmentally benign drug therapies for colon cancer. Currently, nutraceuticals play an increasingly important role in the treatment of various chronic diseases such as colon cancer, diabetes and Alzheimer׳s disease. Nutraceuticals are derived from various natural sources such as medicinal plants, marine organisms, vegetables and fruits. Nutraceuticals have shown the potential to reduce the risk of colon cancer and slow its progression. These dietary substances target different molecular aspects of colon cancer development. Accordingly, this review briefly discusses the medicinal importance of nutraceuticals and their ability to reduce the risk of colorectal carcinogenesis.
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Key Words
- 5-FU, 5-fluorouracil
- ACC, acetyl CoA carboxylase
- ACF, aberrant crypt foci
- ACL, ATP-citrate lyase
- ASTX, astaxanthin
- COX-2, cyclooxygenase 2
- Colon cancer
- DHA, decahexaenoic acid
- DMH, 1,2-dimethylhydrazine
- DR, death receptor
- EGCG, epigallocatechingallate
- EPA, eicosapentaenoic acid
- FAS, fatty acid synthase
- GADD, growth arrest and DNA damage
- HMG-CoA, 3-hydroxy-3-methyl-glutaryl CoA
- HUVEC, human umbilical vein endothelial cell
- IGF, insulin-like growth factor
- IL, interleukin
- LDH, lactate dehydrogenase
- MMP, matrix metallo-proteins
- Marine organisms
- NF-κB, nuclear factor-kappa B
- Nutraceuticals
- PRAP, prolactin receptor associated protein
- Plant derivatives
- TCA, tricarboxylic acid cycle
- TNF, tumor necrosis factor
- TRAIL, tumor necrosis factor-related apoptosis-induced ligand
- Therapeutics
- VEGF, vascular endothelial growth factor
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Affiliation(s)
- Palaniselvam Kuppusamy
- Mammalian Cell Technology Laboratory, Faculty of Industrial Sciences and Technology, Universiti Malaysia Pahang, Lebuhraya Tun Razak 26300, Gambang, Kuantan, Pahang, Malaysia
| | - Mashitah M. Yusoff
- Mammalian Cell Technology Laboratory, Faculty of Industrial Sciences and Technology, Universiti Malaysia Pahang, Lebuhraya Tun Razak 26300, Gambang, Kuantan, Pahang, Malaysia
| | - Gaanty Pragas Maniam
- Mammalian Cell Technology Laboratory, Faculty of Industrial Sciences and Technology, Universiti Malaysia Pahang, Lebuhraya Tun Razak 26300, Gambang, Kuantan, Pahang, Malaysia
| | | | - Ilavenil Soundharrajan
- Department of Biochemistry, National Institute of Animal Science, Suwon-si, Gyeonggi-do 441706, South Korea
| | - Natanamurugaraj Govindan
- Mammalian Cell Technology Laboratory, Faculty of Industrial Sciences and Technology, Universiti Malaysia Pahang, Lebuhraya Tun Razak 26300, Gambang, Kuantan, Pahang, Malaysia
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Hiraki LT, Joshi AD, Ng K, Fuchs CS, Ma J, Hazra A, Peters U, Karlson EW, Giovannucci E, Kraft P, Chan AT. Joint effects of colorectal cancer susceptibility loci, circulating 25-hydroxyvitamin D and risk of colorectal cancer. PLoS One 2014; 9:e92212. [PMID: 24670869 PMCID: PMC3966783 DOI: 10.1371/journal.pone.0092212] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/17/2013] [Accepted: 01/25/2014] [Indexed: 11/26/2022] Open
Abstract
Background Genome wide association studies (GWAS) have identified several SNPs associated with colorectal cancer (CRC) susceptibility. Vitamin D is also inversely associated with CRC risk. Methods We examined main and joint effects of previously GWAS identified genetic markers of CRC and plasma 25-hydroxyvitamin D (25(OH)D) on CRC risk in three prospective cohorts: the Nurses' Health Study (NHS), the Health Professionals Follow-up Study (HPFS), and the Physicians' Health Study (PHS). We included 1895 CRC cases and 2806 controls with genomic DNA. We calculated odds ratios and 95% confidence intervals for CRC associated with additive genetic risk scores (GRSs) comprised of all CRC SNPs and subsets of these SNPs based on proximity to regions of increased vitamin D receptor binding to vitamin D response elements (VDREs), based on published ChiP-seq data. Among a subset of subjects with additional prediagnostic 25(OH)D we tested multiplicative interactions between plasma 25(OH)D and GRS's. We used fixed effects models to meta-analyze the three cohorts. Results The per allele multivariate OR was 1.12 (95% CI, 1.06–1.19) for GRS-proximalVDRE; and 1.10 (95% CI, 1.06–1.14) for GRS-nonproxVDRE. The lowest quartile of plasma 25(OH)D compared with the highest, had a multivariate OR of 0.63 (95% CI, 0.48–0.82) for CRC. We did not observe any significant interactions between any GRSs and plasma 25(OH)D. Conclusions We did not observe evidence for the modification of genetic susceptibility for CRC according to vitamin D status, or evidence that the effect of common CRC risk alleles differed according to their proximity to putative VDR binding sites.
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Affiliation(s)
- Linda T. Hiraki
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America
| | - Amit D. Joshi
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America
| | - Kimmie Ng
- Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
| | - Charles S. Fuchs
- Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America
| | - Jing Ma
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America
| | - Aditi Hazra
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America
| | - Ulrike Peters
- Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America
| | - Elizabeth W. Karlson
- Division of Rheumatology, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America
| | - Edward Giovannucci
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America
- Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts, United States of America
| | - Peter Kraft
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America
| | - Andrew T. Chan
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America
- Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, United States of America
- * E-mail:
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Pericleous M, Mandair D, Caplin ME. Diet and supplements and their impact on colorectal cancer. J Gastrointest Oncol 2013; 4:409-23. [PMID: 24294513 DOI: 10.3978/j.issn.2078-6891.2013.003] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/14/2012] [Accepted: 01/17/2013] [Indexed: 12/23/2022] Open
Abstract
BACKGROUND Colorectal cancer is the third commonest cancer and the third leading cause of cancer death among men and women. It has been proposed that dietary factors are responsible for 70-90% of colorectal cancer and diet optimization may prevent most cases. AIM To evaluate the role of dietary components and supplements in colorectal cancer. METHODS Bibliographical searches were performed in Pubmed for the terms "diet and colorectal cancer", "diet and colon cancer", "diet and rectal cancer", "nutrition and colorectal cancer", "probiotics and colorectal cancer", "prebiotics and colorectal cancer", "alcohol and cancer" and "colorectal cancer epidemiology". RESULTS Consumption of processed or red meat, especially when cooked at high temperatures may be associated with increased risk of colorectal cancer. The evidence for dietary fibre is unclear but foods that contain high amounts of fibre are usually rich in polyphenols which have been shown to alter molecular processes that can encourage colorectal carcinogenesis. Meta-analyses provide evidence on the benefits of circulating, diet-derived and supplemented, vitamin D and Calcium. We also found that diets rich in Folate may prevent colorectal carcinoma. The evidence on dietary micronutrients such as Zinc and Selenium in association with colorectal cancer is not conclusive. It has been suggested that there may be a direct association between alcohol intake and colorectal cancer. In vitro and in vivo studies have highlighted a possible protective role of prebiotics and probiotics. CONCLUSIONS The lack of randomized trials and the presence of confounding factors including smoking, physical activity, obesity and diabetes may often yield inconclusive results. Carefully designed randomized trials are recommended.
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Hiraki LT, Qu C, Hutter CM, Baron JA, Berndt SI, Bézieau S, Brenner H, Caan BJ, Casey G, Chang-Claude J, Chanock SJ, Conti DV, Duggan D, Fuchs CS, Gallinger S, Giovannucci E, Harrison TA, Hayes R, Hazra A, Henderson B, Hoffmeister M, Hopper JL, Hudson TJ, Jenkins MA, Küry S, Le Marchand L, Lemire M, Ma J, Manson JE, Nan H, Newcomb PA, Ng K, Potter JD, Schoen RE, Schumacher F, Seminara D, Slattery ML, Wactawski-Wende J, White E, Wu K, Zanke BW, Kraft P, Peters U, Chan AT. Genetic predictors of circulating 25-hydroxyvitamin d and risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev 2013; 22:2037-46. [PMID: 23983240 PMCID: PMC3818310 DOI: 10.1158/1055-9965.epi-13-0209] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
BACKGROUND Experimental evidence has demonstrated an antineoplastic role for vitamin D in the colon, and higher circulating 25-hydroxyvitamin D [25(OH)D] levels are consistently associated with a lower risk of colorectal cancer. Genome-wide association studies have identified loci associated with levels of circulating 25(OH)D. The identified single-nucleotide polymorphisms (SNPs) from four gene regions collectively explain approximately 5% of the variance in circulating 25(OH)D. METHODS We investigated whether five polymorphisms in GC, CYP2R1, CYP24A1, and DHCR7/NADSYN1, genes previously shown to be associated with circulating 25(OH)D levels, were associated with colorectal cancer risk in 10,061 cases and 12,768 controls drawn from 13 studies included in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) and Colon Cancer Family Registry (CCFR). We conducted a meta-analysis of crude and multivariate-adjusted logistic regression models to calculate odds ratios and associated confidence intervals for SNPs individually, SNPs simultaneously, and for a vitamin D additive genetic risk score (GRS). RESULTS We did not observe a statistically significant association between the 25(OH)D-associated SNPs and colorectal cancer marginally, conditionally, or as a GRS, or for colon or rectal cancer separately. CONCLUSIONS Our findings do not support an association between SNPs associated with circulating 25(OH)D and risk of colorectal cancer. Additional work is warranted to investigate the complex relationship between 25(OH)D and colorectal cancer risk. IMPACT There was no association observed between genetic markers of circulating 25(OH)D and colorectal cancer. These genetic markers account for a small proportion of the variance in 25(OH)D.
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Affiliation(s)
- Linda T Hiraki
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health
| | - Conghui Qu
- Public Health Sciences Division, Fred Hutchinson Cancer Research Center
| | - Carolyn M Hutter
- Public Health Sciences Division, Fred Hutchinson Cancer Research Center
| | - John A Baron
- Division of Gastroenterology and Hepatology, UNC School of Medicine
| | - Sonja I Berndt
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health
| | | | - Hermann Brenner
- Division of Clinical Epidemiology and Aging Research, German Cancer Research Center
| | - Bette J Caan
- Division of Research, Kaiser Permanente Medical Care Program
| | - Graham Casey
- Department of Preventive Medicine, University of Southern California, Keck School of Medicine
| | | | - Stephen J Chanock
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health
| | - David V Conti
- Department of Preventive Medicine, Keck School of Medicine, University of Southern California
| | | | - Charles S Fuchs
- Department of Medicine, Brigham and Women's Hospital
- Gastrointestinal Malignancy Program, Dana-Farber Cancer Institute
- Department of Medicine, Harvard Medical School
| | | | - Edward Giovannucci
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health
- Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School
- Department of Nutrition, Harvard School of Public Health
| | | | - Richard Hayes
- Department of Environmental Medicine, Division of Epidemiology, New York University School of Medicine
| | - Aditi Hazra
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health
- Department of Medicine, Harvard Medical School
| | - Brian Henderson
- Department of Preventive Medicine, University of Southern California, Keck School of Medicine
| | - Michael Hoffmeister
- Division of Clinical Epidemiology and Aging Research, German Cancer Research Center
| | - John L Hopper
- Melborne School of Population Health, The University of Melborne
| | - Thomas J Hudson
- Ontario Institute for Cancer Research
- Departments of Medical Biophysics and Molecular Genetics, University of Toronto
| | - Mark A Jenkins
- Melborne School of Population Health, The University of Melborne
| | | | | | | | - Jing Ma
- Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School
| | - JoAnn E Manson
- Department of Medicine, Brigham and Women's Hospital
- Department of Medicine, Harvard Medical School
| | | | - Polly A Newcomb
- Public Health Sciences Division, Fred Hutchinson Cancer Research Center
- Department of Epidemiology, University of Washington School of Public Health
| | - Kimmie Ng
- Department of Medicine, Harvard Medical School
- Medical-Oncology, Dana-Farber Cancer Institute
| | - John D Potter
- Public Health Sciences Division, Fred Hutchinson Cancer Research Center
| | - Robert E Schoen
- Department of Epidemiology, University of Pittsburgh Medical Center
| | - Fredrick Schumacher
- Department of Preventive Medicine, University of Southern California, Keck School of Medicine
| | - Daniela Seminara
- Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health
| | - Martha L Slattery
- Department of Internal Medicine, University of Utah Health Sciences Center
| | | | - Emily White
- Public Health Sciences Division, Fred Hutchinson Cancer Research Center
- Department of Epidemiology, University of Washington School of Public Health
| | - Kana Wu
- Department of Nutrition, Harvard School of Public Health
| | | | - Peter Kraft
- Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health
- Department of Biostatistics, Harvard School of Public Health
| | - Ulrike Peters
- Public Health Sciences Division, Fred Hutchinson Cancer Research Center
- Department of Epidemiology, University of Washington School of Public Health
| | - Andrew T Chan
- Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School
- Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School
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Kim SY, Son J, Lo YM, Lee C, Moon B. Effects of Light-Emitting Diode (LED) Lighting on the Ergosterol Content of Beech Mushrooms (L
yophyllum ulmarium
). J FOOD PROCESS PRES 2013. [DOI: 10.1111/jfpp.12165] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/20/2023]
Affiliation(s)
- Su-Yeon Kim
- Department of Food and Nutrition; Chung-Ang University; Anseong-si 456-756 Korea
| | - Jihye Son
- Department of Food and Nutrition; Chung-Ang University; Anseong-si 456-756 Korea
| | - Y. Martin Lo
- Department of Nutrition and Food; University of Maryland; College Park MD
| | - Chan Lee
- Department of Food Science and Technology; Chung-Ang University; Anseong-si Korea
| | - Bokyung Moon
- Department of Food and Nutrition; Chung-Ang University; Anseong-si 456-756 Korea
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Abstract
Some evidence suggests that Ca and vitamin D supplements affect cancer risk; however, it is uncertain whether the effects are due to Ca, vitamin D or the combination. We investigated the effect of Ca supplements without co-administered vitamin D on cancer risk. Medline, Embase and the Cochrane Central Register of Controlled Trials, reference lists of meta-analyses and two clinical trial registries were searched for randomised, placebo-controlled trials of Ca supplements ( ≥ 500 mg/d), with ≥ 100 participants and duration >1 year. The lead authors of eligible trials supplied data on cancer outcomes. Trial-level data were analysed using random-effects meta-analyses and patient-level data using Cox proportional hazards models. A total of sixteen trials were eligible, six had no data available, ten provided trial-level data (n 10 496, mean duration 3·9 years), and of these, four provided patient-level data (n 7221, median duration 3·5 years). In the meta-analysis of trial-level data, allocation to Ca did not alter the risk of total cancer (relative risk 0·95, 95 % CI 0·76, 1·18, P= 0·63), colorectal cancer (relative risk 1·38, 95 % CI 0·89, 2·15, P= 0·15), breast cancer (relative risk 1·01, 95 % CI 0·64, 1·59, P= 0·97) or cancer-related mortality (relative risk 0·96, 95 % CI 0·74, 1·24, P= 0·75), but reduced the risk of prostate cancer (relative risk 0·54, 95 % CI 0·30, 0·96, P= 0·03), although there were few events. The meta-analysis of patient-level data showed similar results, with no effect of Ca on the risk of total cancer (hazard ratio 1·07, 95 % CI 0·89, 1·28, P= 0·50). Ca supplements without co-administered vitamin D did not alter total cancer risk over 4 years, although the meta-analysis lacked power to detect very small effects, or those with a longer latency.
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Vitamin D and Colorectal Cancer Prevention: A Review of Epidemiologic Studies. Curr Nutr Rep 2013. [DOI: 10.1007/s13668-012-0037-8] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/27/2022]
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Biancuzzo RM, Clarke N, Reitz RE, Travison TG, Holick MF. Serum concentrations of 1,25-dihydroxyvitamin D2 and 1,25-dihydroxyvitamin D3 in response to vitamin D2 and vitamin D3 supplementation. J Clin Endocrinol Metab 2013; 98:973-9. [PMID: 23386645 PMCID: PMC3590486 DOI: 10.1210/jc.2012-2114] [Citation(s) in RCA: 85] [Impact Index Per Article: 7.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
OBJECTIVE The purpose of this study was to determine 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and 1,25-dihydroxyvitamin D2 [1,25(OH)2D2] levels in healthy adults consuming 1000 IU vitamin D2 or vitamin D3 per day for 11 weeks. SUBJECTS AND DESIGN Blood from 34 healthy male and female adults, aged 18 to 79 years, from a placebo-controlled, double-blind study who received a placebo, 1000 IU vitamin D3, or 1000 IU vitamin D2 daily for 11 weeks at end of winter was analyzed. Serum levels of 25-hydroxyvitamin D2, 25-hydroxyvitamin D3, 1,25(OH)2D2, and 1,25(OH)2D3 were determined by liquid chromatography-tandem mass spectroscopy. RESULTS Of the adults, 82% were vitamin D insufficient (serum 25-hydroxyvitamin D [25(OH)D <30 ng/mL]) at the start of the study. Administration of vitamin D2 and vitamin D3 induced similar increases in total 25(OH)D as well as in 25-hydroxyvitamin D2 and 25-hydroxyvitamin D3, respectively. Compared with placebo and adjusting for baseline levels, 1000 IU daily of vitamin D2 was associated with a mean increase of 7.4 pg/mL (95% confidence interval, 4.4-10.3) in 1,25(OH)2D2, which was accompanied by a mean decrease of 9.9 pg/mL (-15.8 to -4.0) in 1,25(OH)2D3. No such differences accompanied administration of 1000 IU daily of vitamin D3. CONCLUSION Vitamin D2 and vitamin D3 were effective in raising and maintaining total serum concentrations of 25(OH)D. Ingestion of vitamin D2 also resulted in an increase in serum concentrations of 1,25(OH)2D2. This increase was accompanied by a comparable decrease in serum concentrations of 1,25(OH)2D3; therefore, the total 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations did not significantly change after 11 weeks compared with baseline levels. Ingestion of vitamin D3 did not alter serum concentrations of 1,25(OH)2D3 or total 1,25(OH)2D. Therefore, ingestion of 1000 IU vitamin D2 or vitamin D3 for 11 weeks was effective in raising total serum concentrations of 25(OH)D as well as sustaining serum concentrations of total 1,25(OH)2D.
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Affiliation(s)
- Rachael M Biancuzzo
- Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118, USA
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Dastani Z, Li R, Richards B. Genetic regulation of vitamin D levels. Calcif Tissue Int 2013; 92:106-17. [PMID: 23114382 DOI: 10.1007/s00223-012-9660-z] [Citation(s) in RCA: 65] [Impact Index Per Article: 5.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/08/2012] [Accepted: 10/01/2012] [Indexed: 01/08/2023]
Abstract
Vitamin D plays several roles in the body, influencing bone health as well as serum calcium and phosphate levels. Further, vitamin D may modify immune function, cell proliferation, differentiation, and apoptosis. Vitamin D deficiency has been associated with numerous health outcomes, including bone disease, cancer, autoimmune disease, infectious disease, type 1 and type 2 diabetes, hypertension, and heart disease, although it is unclear whether or not these associations are causal. Various twin and family studies have demonstrated moderate to high heritability for circulating vitamin D levels. Accordingly, many studies have investigated the genetic determinants of this hormone. Recent advances in the methodology of large-scale genetic association studies, including coordinated international collaboration, have identified associations of CG, DHCR1, CYP2R1, VDR, and CYP24A1 with serum levels of vitamin D. Here, we review the genetic determinants of vitamin D levels by focusing on new findings arising from candidate gene and genomewide association studies.
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Affiliation(s)
- Zari Dastani
- Department of Epidemiology, Biostatistics and Occupational Health, Jewish General Hospital, Lady Davis Institute, McGill University, Montreal, QC, H3T 1E2, Canada
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Sunlight, vitamin D and the prevention of cancer: a systematic review of epidemiological studies. Eur J Cancer Prev 2013; 18:458-75. [PMID: 19730382 DOI: 10.1097/cej.0b013e32832f9bb1] [Citation(s) in RCA: 58] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
The number of studies reporting beneficial effects of sunlight and vitamin D on several types of cancer with a high mortality rate is growing rapidly. Present health recommendations on sun exposure are mainly based on the increased risks for skin cancer. We reviewed all published studies concerning cancer and sun exposure and vitamin D, respectively, excluding those about skin cancer. Most identified ecological, case-control and prospective studies on the incidence and mortality of colorectal, prostate, breast carcinoma and non-Hodgkin lymphoma reported a significantly inverse association with sun exposure. The results of the included studies on the association between cancer risk and vitamin D were much less consistent. Only those studies that prospectively examined the 25-hydroxyvitamin D serum levels in relation to risk of colorectal cancer are homogeneous: they all reported inverse associations, although not all reaching statistical significance. The results of the intervention studies are suggestive of a protective role of high doses of vitamin D in cancer, but they have been criticized in the literature. We, therefore, conclude that there is accumulating evidence for sunlight as a protective factor for several types of cancer. The same conclusion can be made concerning high vitamin D levels and the risk of colorectal cancer. This evidence, however, is not conclusive, because the number of (good quality) studies is still limited and publication biases cannot be excluded. The discrepancies between the epidemiological evidence for a possible preventive effect of sunlight and vitamin D and the question of how to apply the findings on the beneficial effects of sunlight to (public) health recommendations are discussed.
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Yu XF, Wang YQ, Zou J, Dong J. A meta-analysis of the effects of energy intake on risk of digestive cancers. World J Gastroenterol 2012; 18:7362-7370. [PMID: 23326146 PMCID: PMC3544043 DOI: 10.3748/wjg.v18.i48.7362] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/13/2012] [Revised: 10/04/2012] [Accepted: 11/13/2012] [Indexed: 02/06/2023] Open
Abstract
AIM: To quantitatively assess the relationship between energy intake and the incidence of digestive cancers in a meta-analysis of cohort studies.
METHODS: We searched MEDLINE, EMBASE, Science Citation Index Expanded, and the bibliographies of retrieved articles. Studies were included if they reported relative risks (RRs) and corresponding 95% CIs of digestive cancers with respect to total energy intake. When RRs were not available in the published article, they were computed from the exposure distributions. Data were extracted independently by two investigators and discrepancies were resolved by discussion with a third investigator. We performed fixed-effects meta-analyses and meta-regressions to compute the summary RR for highest versus lowest category of energy intake and for per unit energy intake and digestive cancer incidence by giving each study-specific RR a weight that was proportional to its precision.
RESULTS: Nineteen studies consisting of 13 independent cohorts met the inclusion criteria. The studies included 995 577 participants and 5620 incident cases of digestive cancer with an average follow-up of 11.1 years. A significant inverse association was observed between energy intake and the incidence of digestive cancers. The RR of digestive cancers for the highest compared to the lowest caloric intake category was 0.90 (95% CI 0.81-0.98, P < 0.05). The RR for an increment of 239 kcal/d energy intake was 0.97 (95% CI 0.95-0.99, P < 0.05) in the fixed model. In subgroup analyses, we noted that energy intake was associated with a reduced risk of colorectal cancer (RR 0.90, 95% CI 0.81-0.99, P < 0.05) and an increased risk of gastric cancer (RR 1.19, 95% CI 1.08-1.31, P < 0.01). There appeared to be no association with esophageal (RR 0.96, 95% CI 0.86-1.07, P > 0.05) or pancreatic (RR 0.79, 95% CI 0.49-1.09, P > 0.05) cancer. Associations were also similar in studies from North America and Europe. The RR was 1.02 (95% CI 0.79-1.25, P > 0.05) when considering the six studies conducted in North America and 0.87 (95% CI 0.77-0.98, P < 0.05) for the five studies from Europe.
CONCLUSION: Our findings suggest that high energy intake may reduce the total digestive cancer incidence and has a preventive effect on colorectal cancer.
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Aggarwal A, Monsivais P, Drewnowski A. Nutrient intakes linked to better health outcomes are associated with higher diet costs in the US. PLoS One 2012; 7:e37533. [PMID: 22662168 PMCID: PMC3360788 DOI: 10.1371/journal.pone.0037533] [Citation(s) in RCA: 83] [Impact Index Per Article: 6.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2011] [Accepted: 04/20/2012] [Indexed: 12/26/2022] Open
Abstract
PURPOSE Degrees of nutrient intake and food groups have been linked to differential chronic disease risk. However, intakes of specific nutrients may also be associated with differential diet costs and unobserved differences in socioeconomic status (SES). The present study examined degrees of nutrient intake, for every key nutrient in the diet, in relation to diet cost and SES. METHODS Socio-demographic data for a stratified random sample of adult respondents in the Seattle Obesity Study were obtained through telephone survey. Dietary intakes were assessed using food frequency questionnaire (FFQ) (n = 1,266). Following standard procedures, nutrient intakes were energy-adjusted using the residual method and converted into quintiles. Diet cost for each respondent was estimated using Seattle supermarket retail prices for 384 FFQ component foods. RESULTS Higher intakes of dietary fiber, vitamins A, C, D, E, and B12, beta carotene, folate, iron, calcium, potassium, and magnesium were associated with higher diet costs. The cost gradient was most pronounced for vitamin C, beta carotene, potassium, and magnesium. Higher intakes of saturated fats, trans fats and added sugars were associated with lower diet costs. Lower cost lower quality diets were more likely to be consumed by lower SES. CONCLUSION Nutrients commonly associated with a lower risk of chronic disease were associated with higher diet costs. By contrast, nutrients associated with higher disease risk were associated with lower diet costs. The cost variable may help somewhat explain why lower income groups fail to comply with dietary guidelines and have highest rates of diet related chronic disease.
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Affiliation(s)
- Anju Aggarwal
- Center for Public Health Nutrition, School of Public Health, University of Washington, Seattle, Washington, United States of America.
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Neuhouser ML, Manson JE, Millen A, Pettinger M, Margolis K, Jacobs ET, Shikany JM, Vitolins M, Adams-Campbell L, Liu S, LeBlanc E, Johnson KC, Wactawski-Wende J. The influence of health and lifestyle characteristics on the relation of serum 25-hydroxyvitamin D with risk of colorectal and breast cancer in postmenopausal women. Am J Epidemiol 2012; 175:673-84. [PMID: 22362582 DOI: 10.1093/aje/kwr350] [Citation(s) in RCA: 42] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022] Open
Abstract
The authors' objective was to discern whether lifestyle or health-related factors were confounders, effect modifiers, or irrelevant with regard to understanding observational associations of serum 25-hydroxyvitamin D (25(OH)D) with colorectal and breast cancer. The authors conducted nested case-control studies of colorectal cancer (310 cases, 310 controls) and breast cancer (1,080 cases, 1,080 controls) in the Women's Health Initiative Calcium and Vitamin D Clinical Trial (1994-2005). Case-control matching factors included age, latitude, race/ethnicity, and blood collection date. Serum 25(OH)D was assayed in baseline fasting blood. Conditional logistic regression was used to estimate odds ratios for each cancer by serum 25(OH)D concentration, comparing the relative effects of successively adding body mass index, physical activity, and other health and lifestyle characteristics particular to each cancer. In models with matching factors only, low (vs. high) serum 25(OH)D was associated with a colorectal cancer odds ratio of 2.72 (95% confidence interval (CI): 1.55, 4.77) and a breast cancer odds ratio of 1.33 (95% CI: 1.02, 1.72). In multivariate-adjusted models for colorectal cancer, the association strengthened (OR = 4.45, 95% CI: 1.96, 10.10). However, in multivariate-adjusted breast cancer models, associations were no longer significant (OR = 1.06, 95% CI: 0.78, 1.43). Adjusting for health and lifestyle characteristics has differential effects depending on the cancer site; when modeling such relations, investigators should take these factors into account.
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Affiliation(s)
- Marian L Neuhouser
- Cancer Prevention Program, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109-1024, USA.
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Dart H, Wolin KY, Colditz GA. Commentary: eight ways to prevent cancer: a framework for effective prevention messages for the public. Cancer Causes Control 2012; 23:601-8. [PMID: 22367724 PMCID: PMC3685578 DOI: 10.1007/s10552-012-9924-y] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/29/2011] [Accepted: 02/14/2012] [Indexed: 12/14/2022]
Abstract
Research over the past 40 years has convincingly shown that lifestyle factors play a huge role in cancer incidence and mortality. The public, though, can often discount the preventability of cancer. That health information on the Internet is a vast and often scientifically suspect commodity makes promoting important and sound cancer prevention messages to the public even more difficult. To help address these issues and improve the public's knowledge of, and attitudes toward, cancer prevention, there need to be concerted efforts to create evidence-based, user-friendly information about behaviors that could greatly reduce overall cancer risk. Toward this end, we condensed the current scientific evidence on the topic into eight key behaviors. While not an end in themselves, "Eight Ways to Stay Healthy and Prevent Cancer" forms an evidence-based and targeted framework that supports broader cancer prevention efforts.
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Affiliation(s)
- Hank Dart
- Department of Surgery, Alvin J. Siteman Cancer Center, Washington University School of Medicine in St. Louis, St. Louis, MO, USA.
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Determinants of plasma 25-hydroxyvitamin D and development of prediction models in three US cohorts. Br J Nutr 2012; 108:1889-96. [PMID: 22264926 DOI: 10.1017/s0007114511007409] [Citation(s) in RCA: 108] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/21/2023]
Abstract
Epidemiological and other evidence suggests that vitamin D may be protective against several chronic diseases. Assessing vitamin D status in epidemiological studies, however, is challenging given finite resources and limitations of commonly used approaches. Using multivariable linear regression, we derived predicted 25-hydroxyvitamin D (25(OH)D) scores based on known determinants of circulating 25(OH)D, including age, race, UV-B radiation flux at residence, dietary and supplementary vitamin D intakes, BMI, physical activity, alcohol intake, post-menopausal hormone use (women only) and season of blood draw, in three nationwide cohorts: the Nurses' Health Study, Nurses' Health Study II and the Health Professionals Follow-up Study. The model r 2 for each cohort ranged from 0·25 to 0·33. We validated the prediction models in independent samples of participants from these studies. Mean measured 25(OH)D levels rose with increasing decile of predicted 25(OH)D score, such that the differences in mean measured 25(OH)D between the extreme deciles of predicted 25(OH)D were in the range 8·7-12·3 ng/ml. Substituting predicted 25(OH)D scores for measured 25(OH)D in a previously published case-control analysis of colorectal cancer yielded similar effect estimates with OR of approximately 0·8 for a 10 ng/ml difference in either plasma or predicted 25(OH)D. We conclude that these data provide reasonable evidence that a predicted 25(OH)D score is an acceptable marker for ranking individuals by long-term vitamin D status and may be particularly useful in research settings where biomarkers are not available for the majority of a study population.
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Calcium and vitamin D and risk of colorectal cancer: results from a large population-based case-control study in Newfoundland and Labrador and Ontario. Canadian Journal of Public Health 2012. [PMID: 22032106 DOI: 10.1007/bf03404181] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
BACKGROUND Previous epidemiological studies have been suggestive but inconclusive in demonstrating inverse associations of calcium, vitamin D, dairy product intakes with risk of colorectal cancer (CRC). We conducted a large population-based comparison of such associations in Newfoundland and Labrador (NL) and Ontario (ON). METHODS A case control study design was used. Colorectal cancer cases were new CRC patients aged 20-74 years. Controls were a sex and age-group matched random sample of the population in each province. 1760 cases and 2481 controls from NL and ON were analyzed. Information on dietary intake and lifestyle was collected using self-administered food frequency and personal history questionnaires. RESULTS Controls reported higher mean daily intakes of total calcium and total vitamin D than cases in both provinces. In ON, significant reduced CRC risk was associated with intakes of total calcium (OR of highest vs. lowest quintiles was 0.57, 95% CI 0.42-0.77, p(trend) = 0.03), total vitamin D (OR = 0.73, 95% CI 0.54-1.00), dietary calcium (OR = 0.76, 95% CI 0.60-0.97), dietary vitamin D (OR = 0.77, 95% CI 0.61-0.99), total dairy products and milk (OR = 0.78, 95% CI 0.60-1.00), calcium-containing supplements use (OR = 0.76). In NL, the inverse associations of calcium, vitamin D with CRC risk were most pronounced among calcium- or vitamin D-containing supplement users (OR = 0.67, 0.68, respectively). CONCLUSIONS Results of this study add to the evidence that total calcium, dietary calcium, total vitamin D, dietary vitamin D, calcium- or vitamin D-containing supplement use may reduce the risk of CRC. The inverse associations of CRC risk with intakes of total dairy products and milk may be largely due to calcium and vitamin D.
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Aune D, Lau R, Chan DSM, Vieira R, Greenwood DC, Kampman E, Norat T. Dairy products and colorectal cancer risk: a systematic review and meta-analysis of cohort studies. Ann Oncol 2012; 23:37-45. [PMID: 21617020 DOI: 10.1093/annonc/mdr269] [Citation(s) in RCA: 222] [Impact Index Per Article: 17.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022] Open
Abstract
BACKGROUND Previous studies of the association between intake of dairy products and colorectal cancer risk have indicated an inverse association with milk, however, the evidence for cheese or other dairy products is inconsistent. METHODS We conducted a systematic review and meta-analysis to clarify the shape of the dose-response relationship between dairy products and colorectal cancer risk. We searched the PubMed database for prospective studies published up to May 2010. Summary relative risks (RRs) were estimated using a random effects model. RESULTS Nineteen cohort studies were included. The summary RR was 0.83 (95% CI [confidence interval]: 0.78-0.88, I2=25%) per 400 g/day of total dairy products, 0.91 (95% CI: 0.85-0.94, I2=0%) per 200 g/day of milk intake and 0.96 (95% CI: 0.83-1.12, I2=28%) per 50 g/day of cheese. Inverse associations were observed in both men and women but were restricted to colon cancer. There was evidence of a nonlinear association between milk and total dairy products and colorectal cancer risk, P<0.001, and the inverse associations appeared to be the strongest at the higher range of intake. CONCLUSION This meta-analysis shows that milk and total dairy products, but not cheese or other dairy products, are associated with a reduction in colorectal cancer risk.
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Affiliation(s)
- D Aune
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London.
| | - R Lau
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London
| | - D S M Chan
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London
| | - R Vieira
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London
| | - D C Greenwood
- Biostatistics Unit, Centre for Epidemiology and Biostatistics, University of Leeds, Leeds, UK
| | - E Kampman
- Division of Human Nutrition, Wageningen University and Research Centre, Wageningen, The Netherlands
| | - T Norat
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London
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Ma Y, Zhang P, Wang F, Yang J, Liu Z, Qin H. Association between vitamin D and risk of colorectal cancer: a systematic review of prospective studies. J Clin Oncol 2011; 29:3775-82. [PMID: 21876081 DOI: 10.1200/jco.2011.35.7566] [Citation(s) in RCA: 281] [Impact Index Per Article: 20.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
PURPOSE To conduct a systematic review of prospective studies assessing the association of vitamin D intake or blood levels of 25-hydroxyvitamin D [25(OH)D] with the risk of colorectal cancer using meta-analysis. METHODS Relevant studies were identified by a search of MEDLINE and EMBASE databases before October 2010 with no restrictions. We included prospective studies that reported relative risk (RR) estimates with 95% CIs for the association between vitamin D intake or blood 25(OH)D levels and the risk of colorectal, colon, or rectal cancer. Approximately 1,000,000 participants from several countries were included in this analysis. RESULTS Nine studies on vitamin D intake and nine studies on blood 25(OH)D levels were included in the meta-analysis. The pooled RRs of colorectal cancer for the highest versus lowest categories of vitamin D intake and blood 25(OH)D levels were 0.88 (95% CI, 0.80 to 0.96) and 0.67 (95% CI, 0.54 to 0.80), respectively. There was no heterogeneity among studies of vitamin D intake (P = .19) or among studies of blood 25(OH)D levels (P = .96). A 10 ng/mL increment in blood 25(OH)D level conferred an RR of 0.74 (95% CI, 0.63 to 0.89). CONCLUSION Vitamin D intake and blood 25(OH)D levels were inversely associated with the risk of colorectal cancer in this meta-analysis.
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Affiliation(s)
- Yanlei Ma
- The Sixth People's Hospital affiliated with Shanghai Jiao Tong University, 600 Yishan Rd, Shanghai 200233, People's Republic of China
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Calcium, vitamin D and colorectal cancer chemoprevention. Best Pract Res Clin Gastroenterol 2011; 25:485-94. [PMID: 22122765 DOI: 10.1016/j.bpg.2011.10.001] [Citation(s) in RCA: 36] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/25/2011] [Revised: 10/12/2011] [Accepted: 10/13/2011] [Indexed: 02/06/2023]
Abstract
Identifying modifiable risk factors, particularly dietary factors, which have been hypothesized to play an important role in colorectal carcinogenesis, remains crucial in developing primary prevention strategies. Calcium and vitamin D have been shown consistently in experimental studies to have anti-cancerous properties including but not limited to stimulating differentiation, reducing proliferation, and inducing apoptosis. The majority of epidemiologic studies consistently support an approximately 20-30% reduction in risk of colorectal cancer and adenomas comparing high to low intake categories of both calcium and vitamin D, although independent effects may not be adequately separated. Less consistency exists on the dose-response relation for both nutrients. Intake of calcium of not more than 1000 mg/d and intake of vitamin D of 1000-2000 IU/d, achieving a level of at least 30 ng/mL, appear important for colorectal cancer prevention. More study is warranted to determine the optimal intake levels and duration to reduce the colorectal cancer risk.
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Touvier M, Chan DSM, Lau R, Aune D, Vieira R, Greenwood DC, Kampman E, Riboli E, Hercberg S, Norat T. Meta-analyses of vitamin D intake, 25-hydroxyvitamin D status, vitamin D receptor polymorphisms, and colorectal cancer risk. Cancer Epidemiol Biomarkers Prev 2011; 20:1003-16. [PMID: 21378269 DOI: 10.1158/1055-9965.epi-10-1141] [Citation(s) in RCA: 158] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
BACKGROUND Our objective was to conduct a systematic review and meta-analysis of prospective studies on colorectal cancer (CRC) and vitamin D intake and 25-hydroxyvitamin D status, as part of the World Cancer Research Fund Continuous Update Project. We also aimed at conducting meta-analysis of all studies on CRC and vitamin D receptor (VDR) single-nucleotide polymorphisms. METHODS Relevant studies were identified in PubMed (up to June 2010). Inclusion criteria were original and peer-reviewed publications with a prospective design (for studies on vitamin D intake or status). Random effects of dose-response meta-analyses were performed on cancer incidence. RESULTS We observed inverse associations of CRC risk with dietary vitamin D [summary relative risk (RR) per 100 IU/day = 0.95, 95% CI: 0.93-0.98; 10 studies; range of intake (midpoints) = 39-719 IU/day] and serum/plasma 25-hydroxyvitamin D (RR per 100 IU/L = 0.96, 0.94-0.97; 6 studies; range = 200-1,800 IU/L), but not with total vitamin D (5 studies). Supplemental (2 studies; range = 0-600 IU/day) and total (4 studies; range = 79-732 IU/day) vitamin D intake and 25-hydroxyvitamin D status (6 studies; range = 200-1,800 IU/L) were inversely associated with colon cancer risk. We did not observe statistically significant associations between FokI, PolyA, TaqI, Cdx2, and ApaI VDR polymorphisms and CRC risk. The BsmI polymorphism was associated with a lower CRC risk (RR = 0.57, 0.36-0.89 for BB versus bb, 8 studies). CONCLUSIONS These meta-analyses support the evidence of an inverse association between vitamin D intake, 25-hydroxyvitamin D status, and the BsmI VDR polymorphism and CRC risk. IMPACT Improving vitamin D status could be potentially beneficial against CRC incidence.
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Affiliation(s)
- Mathilde Touvier
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
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Karasik D. How pleiotropic genetics of the musculoskeletal system can inform genomics and phenomics of aging. AGE (DORDRECHT, NETHERLANDS) 2011; 33:49-62. [PMID: 20596786 PMCID: PMC3063644 DOI: 10.1007/s11357-010-9159-3] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 03/10/2010] [Accepted: 06/14/2010] [Indexed: 04/16/2023]
Abstract
Genetic study can provide insight into the biologic mechanisms underlying inter-individual differences in susceptibility to (or resistance to) organisms' aging. Recent advances in molecular genetics and genetic epidemiology provide the necessary tools to perform a study of the genetic sources of biological aging. However, to be successful, the genetic study of a complex condition requires a heritable phenotype to be developed and validated. Genome-wide association studies offer an unbiased approach to identify new candidate genes for human diseases. It is hypothesized that convergent results from multiple aging-related traits will point out the genes responsible for the general aging of the organism. This perspective focuses on the musculoskeletal aging as an example of an approach to identify a downstream common pathway that summarizes aging processes. Since the musculoskeletal traits are linked to the state of many vital functions, disability, and ultimately survival rates, we postulate that there is significance in studying musculoskeletal aging. Construction of an integrated phenotype of aging can be achieved based on shared genetics among multiple musculoskeletal biomarkers. Valid biomarkers from other systems of the organism should be similarly explored. The new composite aging score needs to be validated by determining whether it predicts all-cause mortality, incidences of major chronic diseases, and disability late in life. Comprehensive databases on biomarkers of musculoskeletal aging in multiple large cohort studies, along with information on various health outcomes, are needed to validate the proposed measure of biological aging.
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Affiliation(s)
- David Karasik
- Institute for Aging Research, Hebrew SeniorLife, Harvard Medical School, 1200 Centre Street, Boston, MA 02131, USA.
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