Wed, May 8, 2024
[Archive]
Volume 7, Issue 4 (NOV 2022)
JNFS 2022, 7(4): 474-483 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Toorang F, Narmcheshm S, Sasanfar B, Amini N, Hadji M, Mortazavi M et al . Vitamins and Stomach Cancer: A Hospital Based Case-Control Study in Iran. JNFS 2022; 7 (4) :474-483
URL: http://jnfs.ssu.ac.ir/article-1-507-en.html
URL: http://jnfs.ssu.ac.ir/article-1-507-en.html
Fatemeh Toorang 
, Saba Narmcheshm , Bahareh Sasanfar , Neda Amini , Maryam Hadji , Mahshid Mortazavi , Kazem Zendehdel *
, Saba Narmcheshm , Bahareh Sasanfar , Neda Amini , Maryam Hadji , Mahshid Mortazavi , Kazem Zendehdel *
Cancer Biology Research Center, Cancer Institute of Iran, Tehran University of Medical Science, Tehran, Iran.
Full-Text [PDF 649 kb]
(243 Downloads)
| Abstract (HTML) (1537 Views)
Full-Text: (167 Views)
Vitamins and Stomach Cancer: A Hospital Based Case-Control Study in Iran
Fatemeh Toorang; MSc 1,2, Saba Narmcheshm; MSc 1, Bahareh Sasanfar; MSc2,3,4, Neda Amini; MD5,
Maryam Hadji; MSc6, Mahshid Mortazavi; MD 2 & Kazem Zendehdel; MD, PhD *2,7
Fatemeh Toorang; MSc 1,2, Saba Narmcheshm; MSc 1, Bahareh Sasanfar; MSc2,3,4, Neda Amini; MD5,
Maryam Hadji; MSc6, Mahshid Mortazavi; MD 2 & Kazem Zendehdel; MD, PhD *2,7
1 Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran; 2 Cancer Research Institute, Tehran University of Medical Science, Tehran, Iran; 3 Nutrition and Food Security Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran; 4 Department of Nutrition, School of Public Health, Shahid Sadoughi University of Medical Sciences, Yazd, Iran; 5 Northwell health, Long Island Jewish hospital; 6 Health Unites, Faculty of Social Sciences, Tampere University, Tampere, Finland; 7 Cancer Biology Research Center, Cancer Institute of Iran, Tehran University of Medical Science, Tehran, Iran.
| ARTICLE INFO | ABSTRACT | |
| ORIGINAL ARTICLE | Background: This study investigated the association between vitamins intakes and risk of gastric cancer (GC) among Iranian population. Methods: In this hospital-based case-control study, 178 pathologically confirmed GC patients and 276 healthy controls were interviewed to answer a valid diet history questionnaire. Unconditional logistic regression, in which potential confounders were taken into account, was applied to determine the association of vitamin intakes and odds of GC in total population and in stratums of body mass index (BMI), helicobacter pylori (H-pylori) infection, and smoking. Results: GC was directly associated with vitamin D (OR 1.59; CI 95% 1.07, 2.36) and cobalamin (OR 1.25; CI 95% 1.08, 1.44). Thiamin (OR 0.50; 95%CI 0.30, 0.83), pantothenic acid (OR 0.71; 95%CI 0.58, 0.87), folate (OR 0.99; 95%CI 0.99, 0.99) and vitamin E (OR 0.98; 95%CI 0.96, 0.99) were inversely associated with GC. In 231 H-pylori infected participants, consumption of thiamin (OR 0.3; 95% CI 0.59, 0.86), pyridoxine (OR 0.52; 95%CI 0.31, 0.85), and folate (OR 0.99; 95%CI 0.99, 0.99) reduced GC risk. In H-pylori negative participants, only vitamin E (OR 0.96; 95%CI 0.93, 0.99) reduced the risk and vitamin D (OR 1.99; 95%CI 1.18, 3.36), riboflavin (OR 1.91; 95%CI 1.37, 2.66), pantothenic acid (OR 1.34; 95%CI 1.13, 1.64), biotin (OR 1.03; 95%CI 1.01, 1.05), and cobalamin (OR 1.36; 95%CI 1.13, 1.64) increased the risk. In BMI stratums, only vitamin D (OR 1.81; 95%CI 1.07, 3.08) was associated with the risk of GC among normal weight participants. Vitamin E was associated with lower risk of GC in ever smokers (OR 0.97; 95%CI 0.95, 0.99) and thiamin (OR 0.41; 95%CI 0.19, 0.86) and niacin (OR 0.93; 95%CI 0.87, 0.99) were associated with lower risk in never smokers. Positive associations were observed by increasing vitamin D (OR 2.08; 95%CI 1.12, 3.85) and cobalamin (OR 1.33; 95%CI 1.08, 1.65) in never smokers. Conclusion: This study provided support for a possible protective effect of vitamin E, thiamin, pantothenic acid, and folate on GC risk. Vitamin D and cobalamin intake increased the risk. Keywords: Vitamin; Stomach cancer; Nutrition; Dietary Intake; Hospital-based case-control study |
|
| Article history: Received: 27 Oct 2021 Revised: 5 Dec 2021 Accepted: 5 Jan 2022 |
||
| *Corresponding author: kzendeh@tums.ac.ir Cancer Research Center, Cancer Institute of IR. Iran | 3rd Fl. of Radiotherapy Bldg., Cancer Institute, Imam Khomeini Hospital, Tehran, Iran. Postal code: 13145-158 Tel: +98 2166581638 |
Introduction
Gastric cancer (GC) is the fifth most common malignancy and the third leading cause of cancer related death in both sexes worldwide (Fock, 2014). Its incidence has substantially decreased in developed countries, but it remained a major public health problem in developing countries, such as Iran. GC remained an important public health burden in Iran and its incidence rate is higher than the global average (Alireza et al., 2005). Its age standardized incidence rate in Iran was 26.1 in 100,000 men and 11.1 in women (Mehrabian et al., 2010), and 7300 new cases (10.5 per 100000 individual) are diagnosed annually (Akbari et al., 2008).
Although medical and surgical treatment have significantly improved the gastrointestinal cancers surveillance (Guyot et al., 2005, Ono et al., 2009); total survival rate of GC has not shown any significant improvement in two past decades (Kong et al., 2014). Therefore, primary prevention and early detection are the most sensible strategies in GC control (Lambert et al., 2012). It is clear that prevention requires identification of risk factors (Lee and Derakhshan, 2013).
GC is a complex and multifactorial disease (Piazuelo and Correa, 2013). Helicobacter pylori (H-pylori) is recognized as a main risk factor for GC (Fock, 2014). However, only 1% of individuals affected with H-pylori develop GC (Fock, 2014). Genetic factors (González et al., 2013), tobacco smoking (Sasco et al., 2004), and heavy alcohol drinking (Duell et al., 2011, Tramacere et al., 2011) are also considered as provoking factors. Diet is a modifiable risk factor for GC (Thomson et al., 2003). The effect of nutritional intake on GC development has been investigated in several studies (Berretta et al., 2012, Buiatti et al., 1990, Gonz et al., 1994, Hansson et al., 1994, López‐Carrillo et al., 1999, Marmot et al., 2007, Mayne et al., 2001, Palli et al., 2001, Qiu et al., 2005). Intake of salty foods and red or processed meat might provoke formation of GC enhancing factors (Liu and Russell, 2008, Malekzadeh, 2013). In this regard, fruit and vegetable intakes are explored as protecting factors (Liu and Russell, 2008).
Some studies have investigated the association of several vitamins intakes with GC; however, they ended to inconclusive results and there is still an open question (Berretta et al., 2012). Vitamin D intake has been considered as a risk factor of several cancers (Goyal et al., 2019). This vitamin has a substantial role in immune system and could modify tumor microenvironment. Several studies have reported the association of vitamin D intake or status with gastrointestinal cancers (Camara and Brandao, 2019, Goyal et al., 2019). Moreover, higher intake of antioxidant components, such as vitamin C and E is proposed to reduce GC in some studies but these associations need more clarification (Key et al., 2020, Rawla and Barsouk, 2019). The most important group of vitamins in GC etiology is vitamins which are involved in One-carbon metabolism. It is considered that lower intake of these B vitamins or lower serum levels could initiate tumorigenic reaction. Several studies examined the association of folate, cobalamin or pyridoxine intakes with GC (Miranti et al., 2017, Xiao et al., 2014). American cancer society and world cancer fund, in their recent review, reported that there are limited evidence on the association between GC and vitamin intake (Rock et al., 2020). Accordingly, the data of a hospital based case-control study conducted in cancer institute of Iran were used to provide further evidence on the relation of vitamins intake and GC.
Materials and Methods
Study protocol: It is a hospital-based case-control study conducted in Cancer Institute of Iran between May 2010 and June 2012. Cancer Institute of Iran is a referral teaching hospital which is located in Imam Khomeini complex in Tehran, capital city of Iran. The standard questionnaire which includes questions related to socio-demographic characteristics of participants was completed by face-to-face interview. Interviewers were trained bachelors of health. Blood samples were obtained in both cases and controls for evaluation of H-pylori infections status. IgG antibody were evaluated in serum samples by ELISA kits and the seropositivity > 0.87 was considered positive.
Participants: Cases were histopathologically confirmed GC patients. All newly admitted patients, who were 40 years or older, were asked to take part the study if they fulfill the inclusion criteria. The main criterion was no more than six month of cancer diagnosis and no previous diagnosis of any cancers. Controls were frequently matched to cases by 5-year age group, sex, and geographic area. They were healthy people who came to visit their relatives in the hospital.
Dietary assessment: A trained nutritionist interviewed the participants by Persian version of Diet History Questionnaire (DHQ). Its validity was reported previously (Toorang et al., 2019). Complete description of this DHQ and its analysis process was explained elsewhere (Toorang et al., 2019). The questionnaire questions were about consumption of 146 foods and mixed dishes in the preceding year. Moreover, it covers information on cooking methods and adding oil or sauces during cooking. It is clear that, interviewers reminded the patients to recall their dietary habits before the presence of cancer symptoms. Daily intakes of foods were computed in a program made by authors in STATA. Food intakes were converted to energy and nutrients intakes using food composition table in Access program. The translated version of McCance and Widdowson's Food composition table was used (Dorosti and Tabatabaei, 2007) and integrated with Iranian food composition table (Movahedi and Roosta, 2000) in case of special Iranian food which were not covered by the mentioned food composition table.
Ethical considerations: The research protocol was approved by Ethics Committee of Tehran University of Medical Science (no.17198) and was in accordance with the Declaration of Helsinki Ethical Principles. All the participants signed an informed written consent after oral description of the study protocol.
Data analysis: Odd ratios (OR) and 95% confidence intervals (CIs) of GC according to energy adjusted intakes of vitamins were reported using unconditional multiple logistic regression models. The residual method explained by Willett was used to adjust vitamin intakes based on energy intakes (Willett et al., 1997). Two models were considered, including model A which was adjusted for age, sex, and energy and model B which was adjusted for age, sex, smoking, H-pylori, and residential place. Stratified OR and 95% CIs of GC according to energy adjusted intakes of vitamins in different Strata of H-pylori infection, body mass index (BMI), and smoking status were also reported. All statistical analyses were carried out using STATA 14 (State Corp., College station, TX).
Results
A total of 188 GC patients and 284 controls were recruited in this study. People with implausible energy intakes (± 2SD) were considered as under and over-reporting and were excluded from analysis. Finally, 178 GC patients and 276 controls were selected. General characteristics of the participants are shown in Table 1. Most of the participants in both groups were men (132, 74.2% in the case group and 176, 63.8% in the control group). GC patients smoked more (45.5% vs. 38.8%, P = 0.001) had lower education level, so that 62.4% of the participants in the case group and 26.1% in the control group were illiterate. Obesity was more frequent in cases, so that BMI in 57.3% of the participants in the case group and 48.6% the control group was over 25 kg/m2 or more.
Table 2 shows daily intakes of vitamins in GC patients and controls. It also represents ORs for the case group compared to the control group in two different models: A, partially adjusted (age, sex, and energy) and B, fully adjusted (age, sex, energy, education, ever smoking, H-pylori, and residence). GC patients consumed slightly more vitamin A (1250 vs. 1198 µg/day), vitamin D (1.7 vs. 1.6 µg/day), riboflavin (3.6 vs. 3.2 mg/day), pantothenic acid (8.6 vs. 8.4 mg/day), biotin (54.7 vs. 53.8 µg/day), folate (446.9 vs. 440.9 µg/day), and cobalamin (4.8 vs. 4.1 µg/day). In full adjusting model, GC showed a positive association with vitamin D (OR 1.59; 95%CI 1.07, 2.36) and cobalamin (OR 1.25; 95%CI 1.08, 1.44). An inversely significant association was found for vitamin E (OR 0.98; 95%CI 0.96, 0.99), thiamin (OR 0.50; 95%CI 0.30, 0.83), pantothenic acid (OR 0.71; 95%CI 0.58, 0.87), and folate (OR 0.99; 95%CI 0.99, 0.99).
Table 3 shows ORs and the corresponding 95% CIs of vitamin intakes in three subgroups according to H-pylori infection, BMI, and smoking status. In 231 H-pylori infected participants, consumption of thiamin (OR 0.3; 95% CI 0.59, 0.86), pyridoxine (OR 0.52; 95%CI 0.31, 0.85), and folate (OR 0.99; 95%CI 0.99, 0.99) was associated with lower risk of GC; however, only vitamin E intake reduced the risk (OR 0.96; 95%CI 0.93, 0.99) in H-pylori negative subjects. Vitamin D (OR 1.99; 95%CI 1.18, 3.36), riboflavin (OR 1.91; 95%CI 1.37, 2.66), pantothenic acid (OR 1.34; 95%CI 1.13, 1.64), biotin (OR 1.03; 95%CI 1.01, 1.05), and cobalamin (OR 1.36; 95%CI 1.13, 1.64) consumption increased the risk of GC in this group.
In the present study, totally 235 (51.8%) participants were overweight or obese (BMI ≥ 25 kg/m2). In this stratum, there was no significant association between vitamin intakes and risk of GC. Among normal weight participants defined as BMI < 25 kg/m2 (n = 212), only vitamin D intake affected the risk of GC (OR 1.81; 95%CI 1.07, 3.08).
Vitamin E reduced the risk of GC (OR 0.97; 95%CI 0.95, 0.99) in ever smokers. Thiamin (OR 0.41; 95%CI 0.19, 0.86) and niacin (OR 0.93; 95%CI 0.87, 0.99) reduced the risk of GC in never smokers. A positive association was observed with increasing intakes in vitamin D (OR 2.08; 95%CI 1.12, 3.85) and cobalamin (OR 1.33; 95%CI 1.08, 1.65) intakes in never smoker.
Although medical and surgical treatment have significantly improved the gastrointestinal cancers surveillance (Guyot et al., 2005, Ono et al., 2009); total survival rate of GC has not shown any significant improvement in two past decades (Kong et al., 2014). Therefore, primary prevention and early detection are the most sensible strategies in GC control (Lambert et al., 2012). It is clear that prevention requires identification of risk factors (Lee and Derakhshan, 2013).
GC is a complex and multifactorial disease (Piazuelo and Correa, 2013). Helicobacter pylori (H-pylori) is recognized as a main risk factor for GC (Fock, 2014). However, only 1% of individuals affected with H-pylori develop GC (Fock, 2014). Genetic factors (González et al., 2013), tobacco smoking (Sasco et al., 2004), and heavy alcohol drinking (Duell et al., 2011, Tramacere et al., 2011) are also considered as provoking factors. Diet is a modifiable risk factor for GC (Thomson et al., 2003). The effect of nutritional intake on GC development has been investigated in several studies (Berretta et al., 2012, Buiatti et al., 1990, Gonz et al., 1994, Hansson et al., 1994, López‐Carrillo et al., 1999, Marmot et al., 2007, Mayne et al., 2001, Palli et al., 2001, Qiu et al., 2005). Intake of salty foods and red or processed meat might provoke formation of GC enhancing factors (Liu and Russell, 2008, Malekzadeh, 2013). In this regard, fruit and vegetable intakes are explored as protecting factors (Liu and Russell, 2008).
Some studies have investigated the association of several vitamins intakes with GC; however, they ended to inconclusive results and there is still an open question (Berretta et al., 2012). Vitamin D intake has been considered as a risk factor of several cancers (Goyal et al., 2019). This vitamin has a substantial role in immune system and could modify tumor microenvironment. Several studies have reported the association of vitamin D intake or status with gastrointestinal cancers (Camara and Brandao, 2019, Goyal et al., 2019). Moreover, higher intake of antioxidant components, such as vitamin C and E is proposed to reduce GC in some studies but these associations need more clarification (Key et al., 2020, Rawla and Barsouk, 2019). The most important group of vitamins in GC etiology is vitamins which are involved in One-carbon metabolism. It is considered that lower intake of these B vitamins or lower serum levels could initiate tumorigenic reaction. Several studies examined the association of folate, cobalamin or pyridoxine intakes with GC (Miranti et al., 2017, Xiao et al., 2014). American cancer society and world cancer fund, in their recent review, reported that there are limited evidence on the association between GC and vitamin intake (Rock et al., 2020). Accordingly, the data of a hospital based case-control study conducted in cancer institute of Iran were used to provide further evidence on the relation of vitamins intake and GC.
Materials and Methods
Study protocol: It is a hospital-based case-control study conducted in Cancer Institute of Iran between May 2010 and June 2012. Cancer Institute of Iran is a referral teaching hospital which is located in Imam Khomeini complex in Tehran, capital city of Iran. The standard questionnaire which includes questions related to socio-demographic characteristics of participants was completed by face-to-face interview. Interviewers were trained bachelors of health. Blood samples were obtained in both cases and controls for evaluation of H-pylori infections status. IgG antibody were evaluated in serum samples by ELISA kits and the seropositivity > 0.87 was considered positive.
Participants: Cases were histopathologically confirmed GC patients. All newly admitted patients, who were 40 years or older, were asked to take part the study if they fulfill the inclusion criteria. The main criterion was no more than six month of cancer diagnosis and no previous diagnosis of any cancers. Controls were frequently matched to cases by 5-year age group, sex, and geographic area. They were healthy people who came to visit their relatives in the hospital.
Dietary assessment: A trained nutritionist interviewed the participants by Persian version of Diet History Questionnaire (DHQ). Its validity was reported previously (Toorang et al., 2019). Complete description of this DHQ and its analysis process was explained elsewhere (Toorang et al., 2019). The questionnaire questions were about consumption of 146 foods and mixed dishes in the preceding year. Moreover, it covers information on cooking methods and adding oil or sauces during cooking. It is clear that, interviewers reminded the patients to recall their dietary habits before the presence of cancer symptoms. Daily intakes of foods were computed in a program made by authors in STATA. Food intakes were converted to energy and nutrients intakes using food composition table in Access program. The translated version of McCance and Widdowson's Food composition table was used (Dorosti and Tabatabaei, 2007) and integrated with Iranian food composition table (Movahedi and Roosta, 2000) in case of special Iranian food which were not covered by the mentioned food composition table.
Ethical considerations: The research protocol was approved by Ethics Committee of Tehran University of Medical Science (no.17198) and was in accordance with the Declaration of Helsinki Ethical Principles. All the participants signed an informed written consent after oral description of the study protocol.
Data analysis: Odd ratios (OR) and 95% confidence intervals (CIs) of GC according to energy adjusted intakes of vitamins were reported using unconditional multiple logistic regression models. The residual method explained by Willett was used to adjust vitamin intakes based on energy intakes (Willett et al., 1997). Two models were considered, including model A which was adjusted for age, sex, and energy and model B which was adjusted for age, sex, smoking, H-pylori, and residential place. Stratified OR and 95% CIs of GC according to energy adjusted intakes of vitamins in different Strata of H-pylori infection, body mass index (BMI), and smoking status were also reported. All statistical analyses were carried out using STATA 14 (State Corp., College station, TX).
Results
A total of 188 GC patients and 284 controls were recruited in this study. People with implausible energy intakes (± 2SD) were considered as under and over-reporting and were excluded from analysis. Finally, 178 GC patients and 276 controls were selected. General characteristics of the participants are shown in Table 1. Most of the participants in both groups were men (132, 74.2% in the case group and 176, 63.8% in the control group). GC patients smoked more (45.5% vs. 38.8%, P = 0.001) had lower education level, so that 62.4% of the participants in the case group and 26.1% in the control group were illiterate. Obesity was more frequent in cases, so that BMI in 57.3% of the participants in the case group and 48.6% the control group was over 25 kg/m2 or more.
Table 2 shows daily intakes of vitamins in GC patients and controls. It also represents ORs for the case group compared to the control group in two different models: A, partially adjusted (age, sex, and energy) and B, fully adjusted (age, sex, energy, education, ever smoking, H-pylori, and residence). GC patients consumed slightly more vitamin A (1250 vs. 1198 µg/day), vitamin D (1.7 vs. 1.6 µg/day), riboflavin (3.6 vs. 3.2 mg/day), pantothenic acid (8.6 vs. 8.4 mg/day), biotin (54.7 vs. 53.8 µg/day), folate (446.9 vs. 440.9 µg/day), and cobalamin (4.8 vs. 4.1 µg/day). In full adjusting model, GC showed a positive association with vitamin D (OR 1.59; 95%CI 1.07, 2.36) and cobalamin (OR 1.25; 95%CI 1.08, 1.44). An inversely significant association was found for vitamin E (OR 0.98; 95%CI 0.96, 0.99), thiamin (OR 0.50; 95%CI 0.30, 0.83), pantothenic acid (OR 0.71; 95%CI 0.58, 0.87), and folate (OR 0.99; 95%CI 0.99, 0.99).
Table 3 shows ORs and the corresponding 95% CIs of vitamin intakes in three subgroups according to H-pylori infection, BMI, and smoking status. In 231 H-pylori infected participants, consumption of thiamin (OR 0.3; 95% CI 0.59, 0.86), pyridoxine (OR 0.52; 95%CI 0.31, 0.85), and folate (OR 0.99; 95%CI 0.99, 0.99) was associated with lower risk of GC; however, only vitamin E intake reduced the risk (OR 0.96; 95%CI 0.93, 0.99) in H-pylori negative subjects. Vitamin D (OR 1.99; 95%CI 1.18, 3.36), riboflavin (OR 1.91; 95%CI 1.37, 2.66), pantothenic acid (OR 1.34; 95%CI 1.13, 1.64), biotin (OR 1.03; 95%CI 1.01, 1.05), and cobalamin (OR 1.36; 95%CI 1.13, 1.64) consumption increased the risk of GC in this group.
In the present study, totally 235 (51.8%) participants were overweight or obese (BMI ≥ 25 kg/m2). In this stratum, there was no significant association between vitamin intakes and risk of GC. Among normal weight participants defined as BMI < 25 kg/m2 (n = 212), only vitamin D intake affected the risk of GC (OR 1.81; 95%CI 1.07, 3.08).
Vitamin E reduced the risk of GC (OR 0.97; 95%CI 0.95, 0.99) in ever smokers. Thiamin (OR 0.41; 95%CI 0.19, 0.86) and niacin (OR 0.93; 95%CI 0.87, 0.99) reduced the risk of GC in never smokers. A positive association was observed with increasing intakes in vitamin D (OR 2.08; 95%CI 1.12, 3.85) and cobalamin (OR 1.33; 95%CI 1.08, 1.65) intakes in never smoker.
| Table 1. Characteristics of the participants in the case-control study of gastric cancer and vitamin intake. | |||
| Characteristics | Cases (n=178) | Control (n=276) | P-valuea |
| Age (year) | 60.8 ± 12.0b | 53.2 ± 11.9 | <0.001 |
| Gender (Males) | 132 (74.2)c | 176 (63.8) | 0.021 |
| Education level Illiterate |
111 (62.4) |
72 (26.1) |
<0.001 |
| Literate | 67 (37.6) | 204 (73.9) | |
| Smoking Never smokers |
97 (54.5) |
191 (69.2) |
0.001 |
| Ever smokers | 81 (45.5) | 85 (30.8) | |
| Body mass index (kg/m2) < 25 |
76 (42.7) |
142 (51.4) |
0.068 |
| >= 25 | 102 (57.3) | 134 (48.6) | |
| H-pylori infection Positive |
110 (61.8) |
121 (43.8) |
<0.001 |
| Negative | 68 (38.2) | 155 (56.2) | |
| Residential places Capital city |
93 (52.3) |
140 (50.7) |
0.753 |
| Others | 85 (47.7) | 136 (49.3) | |
| a: Chi-square test for categorical variables and independent student's t-test for continuous variables; b: Mean ± SD; c: n (%) | |||
| Table 2. Daily intake of vitamins and OR and 95% CIs of gastric cancer. | ||||||
| Vitamins | Cases (n=178) | Controls (n=276) | Model Aa | Model Bb | ||
| OR | 95%CI | OR | 95%CI | |||
| Vitamin A (µg) | 1250.02 ± 636.70 | 1197.80 ± 607.12 | 1.00 | 0.99-1.00 | 1.00 | 0.99-1.00 |
| Carotene (µg) | 5634.72 ± 3630.24 | 5635.63 ± 3571.34 | 0.99 | 0.99-1.00 | 1.00 | 0.99-1.00 |
| Vitamin D(µg) | 1.71 ± 0.63 | 1.66 ± 0.69 | 1.05 | 0.77-1.43 | 1.59 | 1.07-2.36 |
| Vitamin E (mg) | 24.42 ± 14.19 | 29.48 ± 19.56 | 0.97 | 0.96-0.99 | 0.98 | 0.96-0.99 |
| Thiamin (mg) | 2.09 ± 0.44 | 2.17 ± 0.54 | 0.67 | 0.43-1.05 | 0.50 | 0.30-0.83 |
| Riboflavin (mg) | 3.56 ± 1.23 | 3.24 ± 1.42 | 1.18 | 1.01-1.38 | 0.87 | 0.63-1.21 |
| Niacin (mg) | 17.58 ± 7.26 | 18.57 ± 7.23 | 0.98 | 0.95-1.01 | 0.98 | 0.95-1.02 |
| Pantothenic acid (mg) | 8.62 ± 2.13 | 8.38 ± 2.37 | 1.04 | 0.95-1.14 | 0.71 | 0.58-0.87 |
| Pyridoxine(mg) | 2.47 ± 0.51 | 2.52 ± 0.65 | 0.79 | 0.55-1.14 | 0.79 | 0.53-1.19 |
| Biotin(µg) | 54.65 ± 19.14 | 53.78 ± 23.57 | 1.00 | 0.99-1.01 | 1.00 | 1.00-1.02 |
| Folate(µg) | 446.91 ± 98.47 | 440.85 ± 114.03 | 1.00 | 0.99-1.00 | 0.99 | 0.99-0.99 |
| Cobalamin(µg) | 4.77 ± 1.71 | 4.05 ± 1.79 | 1.29 | 1.14-1.46 | 1.25 | 1.08-1.44 |
| Ascorbic acid (mg) | 224.51 ± 98.23 | 227.57 ± 109.13 | 0.99 | 0.99-1.00 | 0.99 | 0.99-1.00 |
| a: Age, sex, and energy adjusted; b: age, sex, energy, Education, Ever sSmoking, H-pylori, and residential adjusted | ||||||
| Table 3. ORs and 95% CIs of gastric cancer for vitamins intakes for participants in different strata of H-pylori infection , body mass index, and smoking status. | ||||||||||||
| Vitamins | H-pylori infectiona | Body mass index (kg/m2)b | Smokingc | |||||||||
| Positive (n=231) | Negative (n=223) | < 25 (n=218) | >=25 (n=236) | Ever (n=166) | Never (n=288) | |||||||
| OR | 95%CI | OR | 95%CI | OR | 95%CI | OR | 95%CI | OR | 95%CI | OR | 95%CI | |
| Vitamin A (µg) | 0.99 | 0.99-1.00 | 1.00 | 0.99-1.00 | 0.99 | 0.99-1.00 | 0.99 | 0.99-1.00 | 1.00 | 0.99-1.00 | 1.00 | 0.99-1.00 |
| Carotene (µg) | 0.99 | 0.99-1.00 | 1.00 | 0.99-1.00 | 0.99 | 0.99-1.00 | 0.99 | 0.99-1.00 | 1.00 | 0.99-1.00 | 1.00 | 0.99-1.00 |
| Vitamin D (µg) | 1.17 | 0.69-1.97 | 1.99 | 1.18-3.36 | 1.81 | 1.07-3.08 | 1.12 | 0.74-1.98 | 1.31 | 0.80-2.16 | 2.08 | 1.12-3.85 |
| Vitamin E (mg) | 0.99 | 0.97-1.00 | 0.96 | 0.93-0.99 | 0.99 | 0.98-1.01 | 0.99 | 0.98-1.01 | 0.97 | 0.95-0.99 | 1.00 | 0.98-1.02 |
| Thiamin (mg) | 0.30 | 0.59-0.86 | 1.24 | 0.61-2.54 | 0.99 | 0.49-2.03 | 0.83 | 0.44-1.56 | 0.65 | 0.33-1.28 | 0.41 | 0.19-0.86 |
| Riboflavin (mg) | 0.98 | 0.79-1.22 | 1.91 | 1.37-2.66 | 0.93 | 0.72-1.20 | 1.07 | 0.83-1.38 | 1.26 | 0.98-1.61 | 1.14 | 0.87-1.47 |
| Niacin (mg) | 0.97 | 0.92-1.02 | 1.01 | 0.96-1.07 | 0.98 | 0.92-1.04 | 1.01 | 0.97-1.06 | 1.02 | 0.98-1.07 | 0.93 | 0.87-0.99 |
| Pantothenic acid (mg) | 0.92 | 0.81-1.04 | 1.34 | 1.13-1.64 | 1.01 | 0.88-1.17 | 1.03 | 0.89-1.20 | 1.06 | 0.92-1.22 | 1.02 | 0.88-1.19 |
| Pyridoxine (mg) | 0.52 | 0.31-0.85 | 1.81 | 0.93-3.50 | 1.09 | 0.66-1.80 | 1.22 | 0.69-2.14 | 0.99 | 0.58-1.67 | 0.67 | 0.36-1.25 |
| Biotin (µg) | 0.99 | 0.98-1.01 | 1.03 | 1.01-1.05 | 0.99 | 0.98-1.02 | 1.00 | 0.98-1.02 | 1.02 | 1.00-1.04 | 1.00 | 0.98-1.02 |
| Folate (µg) | 0.99 | 0.99-0.99 | 1.00 | 1.00-1.00 | 0.99 | 0.99-1.00 | 1.00 | 0.99-1.00 | 1.00 | 0.99-1.00 | 0.99 | 0.99-1.00 |
| Cobalamin (µg) | 1.17 | 0.97-1.41 | 1.36 | 1.13-1.64 | 0.86 | 0.68-1.22 | 0.97 | 0.81-1.19 | 1.24 | 1.05-1.47 | 1.33 | 1.08-1.65 |
| Ascorbic acid (mg) | 0.99 | 0.99-1.00 | 1.00 | 0.99-1.00 | 1.00 | 0.99-1.00 | 1.00 | 0.99-1.00 | 0.99 | 0.99-1.00 | 0.99 | 0.99-1.00 |
| a: Age, sex, energy, education, ever smoking, and residential adjusted; b Age, sex, energy, education, ever smoking, H-pylori, and residential adjusted; c Age, sex, energy, education, H-pylori, and residential adjusted | ||||||||||||
Discussion
This hospital based case control study figured out that GC was directly associated with riboflavin and cobalamin consumption in model A, and vitamin D and cobalamin in the model B. Thiamin, pantothenic acid, and folate intake reduced the risk of GC in model B and vitamin E was inversely associated with GC in both models. There was no significant association between vitamin A, carotene, and ascorbic acid intake with GC in the models.
Antioxidant vitamins could protect mucosa from oxidative stress associated with H-pylori, high salt consumption and nitrate and nitrite intake (Terry et al., 2000). Although the antioxidant activity of vitamin C has been well described (Padayatty et al., 2003), in the present study, there was no significant association between vitamin C intake and GC; however, some studies (Kong et al., 2014, Pakseresht et al., 2011) have reported its protective effect.
It is generally believed that, nutrients, such as folate, riboflavin, pyridoxine, and cobalamin affect DNA methylation by regulating the levels of S‐adenosyl‐L‐homocysteine and S‐adenosyl‐L-methionine (Stefanska et al., 2012). Given that the main cause of carcinogenesis is aberrations in gene expression and protein function is caused by both genetic and epigenetic modifications, it is indicated that these nutrients could protect cells from acrogenous pathways. In this study, cobalamin (B12) consumption increased the risk of GC, but thiamin (B1), pantothenic acid (B5), and folate intake decreased the risk. Dietary vitamin B12 is derived exclusively from animal food; therefore, it seems that cobalamin is a marker for consumption of animal protein in the study population. Several studies have suggested that animal protein can increase the risk of GC.
Based on the results, vitamin E intake is inversely associated with GC risk. The results are in agreement with some studies (Kong et al., 2014, Pelucchi et al., 2008) but not others (Mayne et al., 2001, Pakseresht et al., 2011). The most well-recognized function of vitamin E is preventing the cyclic propagation of lipid peroxidation (Kline et al., 2007). Alfa –tocopherol (one form of vitamin E) acts as a free radical scavenger (Yamauchi, 1997) and anticarcinogen through its ability to prevent the formation of N-nitrosamines which have been suggested to be important factors in the etiology of GC. Furthermore, this vitamin seems to play an immune modulatory role and is capable of increasing natural killer cell activity (Mergens et al., 1980).
The OR (95% CI) of Thiamin and GC risk was 0.5(0.3-0.83), which indicates that thiamin reduced the risk. The dietary intake of thiamine and cancer risk has provided conflicting results. Thiamin appears to have both cancer-promoting and anticancer properties, which vary in relation to both genomic and non-genomic factors. It has been hypothesized that excess thiamine supplementation may be a factor for increased cancer incidence in western countries compared to other countries (Boros, 2000). In contrast, Asian and African countries principally consume foods that are high in thiaminase, which may reduce thiamin exposure. Possible pathways which explain the association of thiamin with cancers include the solute carrier transporter (SLC19) gene, transketolase, transcription factor p53, and poly (ADP-ribose) polymerase-1 gene (Carraher et al., 2015). The data on the association of thiamin intake and GC are limited. It has been suggested that thiamin can reduce cancer cell proliferation (Hanberry et al., 2014).
The study results suggest that pantothenic acid consumption can reduce risk of GC. Pantethine affects cellular fatty acid metabolism; moreover, it displays anti-inflammatory properties by maintaining the asymmetric distribution of cell membrane phosphatidyl serine, resulting in the prevention of cellular response to pro-inflammatory factors (Penet et al., 2008). A large number of studies did not report any association between B5 consumption and GC risk (Mayne et al., 2001, Pakseresht et al., 2011, Ren et al., 2016).
Based on the results, vitamin D intake is associated with higher risk of GC, which is in agreement with some studies (Giovannucci et al., 2006), but some studies showed different results (La Vecchia et al., 1994, Pelucchi et al., 2008). Several studies have hypothesized that the nutritional status of vitamin D and serum levels of vitamin D may be important in risk of GC; however, the results are inconsistent (Abnet et al., 2010, Chen et al., 2007, Khayatzadeh et al., 2015). In the present study, increased consumption of dietary vitamin D was associated with a significantly higher risk of GC. In Abnet study, lower levels of serum 25(OH)D was protective against upper GI tract cancers in Asian subjects (Abnet et al., 2010). Several biologic pathways have been suggested for possible associations between higher vitamin D status and increased cancer risk. It is assumed that vitamin D could induces phase I metabolizing enzymes under certain conditions (Kutuzova and DeLuca, 2007), and it can modulate both proliferative and antiproliferative effects on preneoplastic lesions. It should be noted that UVB (Ultra Violet) generated vitamin D was not considered; therefore, serum level of vitamin D was not assessed and the estimated intake was not necessarily a perfect assessment of vitamin D status.
This hospital based case control study figured out that GC was directly associated with riboflavin and cobalamin consumption in model A, and vitamin D and cobalamin in the model B. Thiamin, pantothenic acid, and folate intake reduced the risk of GC in model B and vitamin E was inversely associated with GC in both models. There was no significant association between vitamin A, carotene, and ascorbic acid intake with GC in the models.
Antioxidant vitamins could protect mucosa from oxidative stress associated with H-pylori, high salt consumption and nitrate and nitrite intake (Terry et al., 2000). Although the antioxidant activity of vitamin C has been well described (Padayatty et al., 2003), in the present study, there was no significant association between vitamin C intake and GC; however, some studies (Kong et al., 2014, Pakseresht et al., 2011) have reported its protective effect.
It is generally believed that, nutrients, such as folate, riboflavin, pyridoxine, and cobalamin affect DNA methylation by regulating the levels of S‐adenosyl‐L‐homocysteine and S‐adenosyl‐L-methionine (Stefanska et al., 2012). Given that the main cause of carcinogenesis is aberrations in gene expression and protein function is caused by both genetic and epigenetic modifications, it is indicated that these nutrients could protect cells from acrogenous pathways. In this study, cobalamin (B12) consumption increased the risk of GC, but thiamin (B1), pantothenic acid (B5), and folate intake decreased the risk. Dietary vitamin B12 is derived exclusively from animal food; therefore, it seems that cobalamin is a marker for consumption of animal protein in the study population. Several studies have suggested that animal protein can increase the risk of GC.
Based on the results, vitamin E intake is inversely associated with GC risk. The results are in agreement with some studies (Kong et al., 2014, Pelucchi et al., 2008) but not others (Mayne et al., 2001, Pakseresht et al., 2011). The most well-recognized function of vitamin E is preventing the cyclic propagation of lipid peroxidation (Kline et al., 2007). Alfa –tocopherol (one form of vitamin E) acts as a free radical scavenger (Yamauchi, 1997) and anticarcinogen through its ability to prevent the formation of N-nitrosamines which have been suggested to be important factors in the etiology of GC. Furthermore, this vitamin seems to play an immune modulatory role and is capable of increasing natural killer cell activity (Mergens et al., 1980).
The OR (95% CI) of Thiamin and GC risk was 0.5(0.3-0.83), which indicates that thiamin reduced the risk. The dietary intake of thiamine and cancer risk has provided conflicting results. Thiamin appears to have both cancer-promoting and anticancer properties, which vary in relation to both genomic and non-genomic factors. It has been hypothesized that excess thiamine supplementation may be a factor for increased cancer incidence in western countries compared to other countries (Boros, 2000). In contrast, Asian and African countries principally consume foods that are high in thiaminase, which may reduce thiamin exposure. Possible pathways which explain the association of thiamin with cancers include the solute carrier transporter (SLC19) gene, transketolase, transcription factor p53, and poly (ADP-ribose) polymerase-1 gene (Carraher et al., 2015). The data on the association of thiamin intake and GC are limited. It has been suggested that thiamin can reduce cancer cell proliferation (Hanberry et al., 2014).
The study results suggest that pantothenic acid consumption can reduce risk of GC. Pantethine affects cellular fatty acid metabolism; moreover, it displays anti-inflammatory properties by maintaining the asymmetric distribution of cell membrane phosphatidyl serine, resulting in the prevention of cellular response to pro-inflammatory factors (Penet et al., 2008). A large number of studies did not report any association between B5 consumption and GC risk (Mayne et al., 2001, Pakseresht et al., 2011, Ren et al., 2016).
Based on the results, vitamin D intake is associated with higher risk of GC, which is in agreement with some studies (Giovannucci et al., 2006), but some studies showed different results (La Vecchia et al., 1994, Pelucchi et al., 2008). Several studies have hypothesized that the nutritional status of vitamin D and serum levels of vitamin D may be important in risk of GC; however, the results are inconsistent (Abnet et al., 2010, Chen et al., 2007, Khayatzadeh et al., 2015). In the present study, increased consumption of dietary vitamin D was associated with a significantly higher risk of GC. In Abnet study, lower levels of serum 25(OH)D was protective against upper GI tract cancers in Asian subjects (Abnet et al., 2010). Several biologic pathways have been suggested for possible associations between higher vitamin D status and increased cancer risk. It is assumed that vitamin D could induces phase I metabolizing enzymes under certain conditions (Kutuzova and DeLuca, 2007), and it can modulate both proliferative and antiproliferative effects on preneoplastic lesions. It should be noted that UVB (Ultra Violet) generated vitamin D was not considered; therefore, serum level of vitamin D was not assessed and the estimated intake was not necessarily a perfect assessment of vitamin D status.
In H-pylori positive subjects, consumption of Thiamin, Pyridoxine, and folate were inversely associated with GC. Published data suggest that infection of H-pylori can reduce the level of Thiamin, Pyridoxine, and folate (Franceschi et al., 2014, Tamura et al., 2002, Testerman et al., 2006, Uruha et al., 2011), so increased consumption can reduce the deficiency caused by H-pylori.
In H-pylori negative subjects, only vitamin E consumption was associated with lower risk and vitamin D, riboflavin, pantothenic acid, biotin, and cobalamin consumption increased the risk of GC. In this group, it is obvious that H-pylori did not exist and could not affect serum levels of vitamin D, riboflavin, pantothenic acid, biotin, and cobalamin. A new study suggest that vitamin D has a role in eradication of H-pylori (Hu, 2017), so in the absence of H-pylori, vitamin D can act as carcinogen, as mentioned in the previous section. It was mentioned that cobalamin consumption may be an indicator of animal dietary patterns; the association of vitamin D with GC could be explained in the same way.
Vitamin E was associated with lower risk of GC in ever smokers. There is evidence that cigarette smoking alters vitamin E requirements (Bruno and Traber, 2005). Increasing vitamin E consumption can replenish body stores and enhance antioxidant capacity and it could prevent carcinogenesis in this way.
Exposure to cigarette can reduce vitamin D in the blood (Brot et al., 1999), so in the ever smokers no significant association was found between vitamin D and GC. In this stratum, vitamin D consumption may retrieve body vitamin D store and in the never smokers there is no need to replenish body stores and excess vitamin D can lead to cancer.
Thiamin and niacin consumption decreased risk of GC in never smokers. Thiamin was associated with lower risk of GC in never smokers, but not in ever smokers. It could be assumed that in smokers, higher amount of vitamins is needed to decrease risk of GC. However, it should be mentioned that sample size was too small in ever smoking group which could lead to wider confidence interval and insignificant results.
This study has several relevant strengths. The first is using a validated diet history questionnaire (Toorang et al., 2019). The second strength of the study is assessing several cofounders which let us to adjust their effects on the studied associations. Nevertheless, we should mention limitation of this study. The most important weak point of the study is using a foreign food composition table. It is clear that food compositions are not the same in different regions. However, it is inevitable, since there is not any comprehensive national food composition table in Iran. The second limitation stems from the case control design of the study which is supposed to recall bias.
Conclusion
This study provided support for a possible protective effect of vitamin E, thiamin, pantothenic acid, and folate on GC risk. Vitamin D and cobalamin intake increased the risk. Further studies are suggested to assess the role of food dietary patterns in relation with GC.
Acknowledgments
This study was supported by a fund of Tehran University of Medical Sciences.
Conflict of interest
There is no potential conflict of interest.
Authors’ contributions
Toorang F and Zendehdel K designed the study. Amini N developed the non-dietary questionnaire. Sasanfar B and Hadji M supervised primary data collection and training the interviewers. Mortazavi M and Narmcheshm S did data cleaning and primary analysis. Toorang F analyzed the data and wrote the draft under the supervision of Zendehdel K. All authors reviewed the final version of the manuscript.
References
Abnet CC, et al. 2010. Circulating 25-hydroxyvitamin D and risk of esophageal and gastric cancer: Cohort Consortium Vitamin D Pooling Project of Rarer Cancers. American journal of epidemiology. 172 (1): 94-106.
Akbari M, et al. 2008. Iran cancer report. Cancer Research Center, Shahid Beheshti University of Medical Sciences.
Alireza S, et al. 2005. Cancer occurrence in Iran in 2002, an international perspective. Asian Pacific journal of cancer prevention. 6 (3): 359.
Berretta M, et al. 2012. The role of diet in gastric cancer: still an open question. Front Biosci. 17: 1640-1647.
Boros L 2000. Population thiamine status and varying cancer rates between western, Asian and African countries. Anticancer research. 20 (3B): 2245-2248.
Brot C, Jørgensen NR & Sørensen OH 1999. The influence of smoking on vitamin D status and calcium metabolism. European journal of clinical nutrition. 53 (12): 920.
Bruno RS & Traber MG 2005. Cigarette smoke alters human vitamin E requirements. Journal of nutrition. 135 (4): 671-674.
Buiatti E, et al. 1990. A case‐control study of gastric cancer and diet in Italy: II. Association with nutrients. International journal of cancer. 45 (5): 896-901.
Camara AB & Brandao IA 2019. The role of vitamin D and sunlight incidence in cancer. Anti-Cancer Agents in Medicinal Chemistry 19 (11): 1418-1436.
Carraher CE, Roner MR, Lambert RE, Arroyo L & Miller LC 2015. Synthesis of organotin polyamine ethers containing thiamine (vitamin B 1) and preliminary ability to inhibit select cancer cell lines. Journal of inorganic and organometallic polymers and materials. 25 (6): 1414-1424.
Chen W, et al. 2007. Prospective study of serum 25 (OH)-vitamin D concentration and risk of oesophageal and gastric cancers. British journal of cancer. 97 (1): 123.
Dorosti A & Tabatabaei M 2007. Food composition table.
Duell EJ, et al. 2011. Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. American journal of clinical nutrition. 94 (5): 1266-1275.
Fock K 2014. Review article: the epidemiology and prevention of gastric cancer. Alimentary pharmacology & therapeutics. 40 (3): 250-260.
Franceschi F, et al. 2014. Role of Helicobacter pylori infection on nutrition and metabolism. World journal of gastroenterology: WJG. 20 (36): 12809.
Giovannucci E, et al. 2006. Prospective study of predictors of vitamin D status and cancer incidence and mortality in men. Journal of the National Cancer Institute. 98 (7): 451-459.
Gonz CA, et al. 1994. Nutritional factors and gastric cancer in Spain. American journal of epidemiology. 139 (5): 466-473.
González CA, Sala N & Rokkas T 2013. Gastric cancer: epidemiologic aspects. Helicobacter. 18 (s1): 34-38.
Goyal H, Perisetti A, Rahman MR, Levin A & Lippi G 2019. Vitamin D and gastrointestinal cancers: a narrative review. Digestive diseases and sciences. 64 (5): 1098-1109.
Guyot F, et al. 2005. Time trends in the treatment and survival of recurrences from colorectal cancer. Annals of oncology. 16 (5): 756-761.
Hanberry BS, Berger R & Zastre JA 2014. High-dose vitamin B1 reduces proliferation in cancer cell lines analogous to dichloroacetate. Cancer chemotherapy and pharmacology. 73 (3): 585-594.
Hansson LE, et al. 1994. Nutrients and gastric cancer risk. A population‐based case‐control study in Sweden. International journal of cancer. 57 (5): 638-644.
Hu W 2017. Critical Role of Vitamin D3 in Helicobacter pylori Eradication in Stomachs. The FASEB Journal. 31 (1_supplement): 1067.1066-1067.1066.
Key TJ, et al. 2020. Diet, nutrition, and cancer risk: what do we know and what is the way forward? British medical journal. 368: 1-9.
Khayatzadeh S, Feizi A, Saneei P & Esmaillzadeh A 2015. Vitamin D intake, serum Vitamin D levels, and risk of gastric cancer: A systematic review and meta-analysis. Journal of research in medical sciences. 20 (8): 790.
Kline K, Lawson KA, Yu W & Sanders BG 2007. Vitamin E and Cancer. In Vitamins & Hormones, pp. 435-461. Academic Press.
Kong P, et al. 2014. Vitamin intake reduce the risk of gastric cancer: meta-analysis and systematic review of randomized and observational studies. PloS one. 9 (12): e116060.
Kutuzova GD & DeLuca HF 2007. 1, 25-Dihydroxyvitamin D3 regulates genes responsible for detoxification in intestine. Toxicology and applied pharmacology. 218 (1): 37-44.
La Vecchia C, Ferraroni M, D'Avanzo B, Decarli A & Franceschi S 1994. Selected micronutrient intake and the risk of gastric cancer. Cancer epidemiology, biomarkers & prevention. 3 (5): 393-398.
Lambert R, Saito H, Lucas E & Sankaranarayanan R 2012. Survival from digestive cancer in emerging countries in Asia and Africa. European journal of gastroenterology & hepatology. 24 (6): 605-612.
Lee YY & Derakhshan MH 2013. Environmental and lifestyle risk factors of gastric cancer. Archives of Iranian medicine (AIM). 16 (6).
Liu C & Russell RM 2008. Nutrition and gastric cancer risk: an update. Nutrition reviews. 66 (5): 237-249.
López‐Carrillo L, López‐Cervantes M, Ward MH, Bravo‐Alvarado J & Ramírez‐Espitia A 1999. Nutrient intake and gastric cancer in Mexico. International journal of cancer. 83 (5): 601-605.
Malekzadeh R 2013. A case-control study of the relationship between gastric cancer and meat consumption in Iran. Archives of Iranian medicine. 16 (6): 324.
Marmot M, et al. 2007. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. world cancer research.
Mayne ST, et al. 2001. Nutrient intake and risk of subtypes of esophageal and gastric cancer. Cancer epidemiology and prevention biomarkers. 10 (10): 1055-1062.
Mehrabian A, et al. 2010. Gastric cancer prevalence, according to survival data in Iran (National Study-2007). Iranian journal of public health. 39 (3): 27.
Mergens W, Chau J & Newmark H 1980. The influence of ascorbic acid and DL-alpha-tocopherol on the formation of nitrosamines in an in vitro gastrointestinal model system. IARC scientific publications.(31): 259-269.
Miranti EH, et al. 2017. Low vitamin B12 increases risk of gastric cancer: A prospective study of one‐carbon metabolism nutrients and risk of upper gastrointestinal tract cancer. International journal of cancer. 141 (6): 1120-1129.
Movahedi A & Roosta R 2000. Iranian food composition tables. National Nutrition and Food Technology Research Institute Press: Tehran.
Ono S, et al. 2009. Long-term outcomes of endoscopic submucosal dissection for superficial esophageal squamous cell neoplasms. Gastrointestinal endoscopy. 70 (5): 860-866.
Padayatty SJ, et al. 2003. Vitamin C as an antioxidant: evaluation of its role in disease prevention. Journal of the American college of nutrition. 22 (1): 18-35.
Pakseresht M, et al. 2011. Dietary habits and gastric cancer risk in north-west Iran. Cancer causes & control. 22 (5): 725-736.
Palli D, Russo A & Decarli A 2001. Dietary patterns, nutrient intake and gastric cancer in a high-risk area of Italy. Cancer causes and control. 12 (2): 163-172.
Pelucchi C, et al. 2008. Dietary intake of selected micronutrients and gastric cancer risk: an Italian case-control study. Annals of oncology. 20 (1): 160-165.
Penet MF, et al. 2008. Protection against cerebral malaria by the low-molecular-weight thiol pantethine. Proceedings of the National Academy of Sciences. 105 (4): 1321-1326.
Piazuelo MB & Correa P 2013. Gastric cancer: overview. Colombia Medica. 44 (3): 192-201.
Qiu J-L, et al. 2005. Nutritional factors and gastric cancer in Zhoushan Islands, China. World journal of gastroenterology. 11 (28): 4311.
Rawla P & Barsouk A 2019. Epidemiology of gastric cancer: global trends, risk factors and prevention. Przeglad gastroenterologiczny. 14 (1): 26.
Ren J, et al. 2016. Prospective study of serum B vitamins levels and oesophageal and gastric cancers in China. Scientific reports. 6: 35281.
Rock CL, et al. 2020. American Cancer Society guideline for diet and physical activity for cancer prevention. CA: a cancer journal for clinicians. 70 (4): 245-271.
Sasco A, Secretan M & Straif K 2004. Tobacco smoking and cancer: a brief review of recent epidemiological evidence. Lung cancer. 45: S3-S9.
Stefanska B, Karlic H, Varga F, Fabianowska‐Majewska K & Haslberger A 2012. Epigenetic mechanisms in anti‐cancer actions of bioactive food components–the implications in cancer prevention. British journal of pharmacology. 167 (2): 279-297.
Tamura A, Fujioka T & Nasu M 2002. Relation of Helicobacter pylori infection to plasma vitamin B12, folic acid, and homocysteine levels in patients who underwent diagnostic coronary arteriography. American journal of gastroenterology. 97 (4): 861-866.
Terry P, Lagergren J, Ye W, Nyrén O & Wolk A 2000. Antioxidants and cancers of the esophagus and gastric cardia. International journal of cancer. 87 (5): 750-754.
Testerman TL, Conn PB, Mobley HL & McGee DJ 2006. Nutritional requirements and antibiotic resistance patterns of Helicobacter species in chemically defined media. Journal of clinical microbiology. 44 (5): 1650-1658.
Thomson CA, LeWinn K, Newton TR, Alberts DS & Martinez ME 2003. Nutrition and diet in the development of gastrointestinal cancer. Current oncology reports. 5 (3): 192-202.
Toorang F, et al. 2019. Validation of Diet History Questionnaire in Assessing Energy and Nutrient Intakes of Iranian Population. Iranian journal of public health. 48 (6): 1074-1081.
Tramacere I, et al. 2011. A meta-analysis on alcohol drinking and gastric cancer risk. Annals of oncology. 23 (1): 23-38.
Uruha A, Shimizu T, Katoh T, Yamasaki Y & Matsubara S 2011. Wernicke's encephalopathy in a patient with peptic ulcer disease. Case reports in medicine. 2011.
Willett WC, Howe GR & Kushi LH 1997. Adjustment for total energy intake in epidemiologic studies. American journal of clinical nutrition. 65 (4): 1220S-1228S.
Xiao Q, et al. 2014. Intakes of folate, methionine, vitamin B6, and vitamin B12 with risk of esophageal and gastric cancer in a large cohort study. British journal of cancer. 110 (5): 1328-1333.
Yamauchi R 1997. Vitamin E: Mechanism of Its Antioxidant Activity.
This study was supported by a fund of Tehran University of Medical Sciences.
Conflict of interest
There is no potential conflict of interest.
Authors’ contributions
Toorang F and Zendehdel K designed the study. Amini N developed the non-dietary questionnaire. Sasanfar B and Hadji M supervised primary data collection and training the interviewers. Mortazavi M and Narmcheshm S did data cleaning and primary analysis. Toorang F analyzed the data and wrote the draft under the supervision of Zendehdel K. All authors reviewed the final version of the manuscript.
References
Abnet CC, et al. 2010. Circulating 25-hydroxyvitamin D and risk of esophageal and gastric cancer: Cohort Consortium Vitamin D Pooling Project of Rarer Cancers. American journal of epidemiology. 172 (1): 94-106.
Akbari M, et al. 2008. Iran cancer report. Cancer Research Center, Shahid Beheshti University of Medical Sciences.
Alireza S, et al. 2005. Cancer occurrence in Iran in 2002, an international perspective. Asian Pacific journal of cancer prevention. 6 (3): 359.
Berretta M, et al. 2012. The role of diet in gastric cancer: still an open question. Front Biosci. 17: 1640-1647.
Boros L 2000. Population thiamine status and varying cancer rates between western, Asian and African countries. Anticancer research. 20 (3B): 2245-2248.
Brot C, Jørgensen NR & Sørensen OH 1999. The influence of smoking on vitamin D status and calcium metabolism. European journal of clinical nutrition. 53 (12): 920.
Bruno RS & Traber MG 2005. Cigarette smoke alters human vitamin E requirements. Journal of nutrition. 135 (4): 671-674.
Buiatti E, et al. 1990. A case‐control study of gastric cancer and diet in Italy: II. Association with nutrients. International journal of cancer. 45 (5): 896-901.
Camara AB & Brandao IA 2019. The role of vitamin D and sunlight incidence in cancer. Anti-Cancer Agents in Medicinal Chemistry 19 (11): 1418-1436.
Carraher CE, Roner MR, Lambert RE, Arroyo L & Miller LC 2015. Synthesis of organotin polyamine ethers containing thiamine (vitamin B 1) and preliminary ability to inhibit select cancer cell lines. Journal of inorganic and organometallic polymers and materials. 25 (6): 1414-1424.
Chen W, et al. 2007. Prospective study of serum 25 (OH)-vitamin D concentration and risk of oesophageal and gastric cancers. British journal of cancer. 97 (1): 123.
Dorosti A & Tabatabaei M 2007. Food composition table.
Duell EJ, et al. 2011. Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. American journal of clinical nutrition. 94 (5): 1266-1275.
Fock K 2014. Review article: the epidemiology and prevention of gastric cancer. Alimentary pharmacology & therapeutics. 40 (3): 250-260.
Franceschi F, et al. 2014. Role of Helicobacter pylori infection on nutrition and metabolism. World journal of gastroenterology: WJG. 20 (36): 12809.
Giovannucci E, et al. 2006. Prospective study of predictors of vitamin D status and cancer incidence and mortality in men. Journal of the National Cancer Institute. 98 (7): 451-459.
Gonz CA, et al. 1994. Nutritional factors and gastric cancer in Spain. American journal of epidemiology. 139 (5): 466-473.
González CA, Sala N & Rokkas T 2013. Gastric cancer: epidemiologic aspects. Helicobacter. 18 (s1): 34-38.
Goyal H, Perisetti A, Rahman MR, Levin A & Lippi G 2019. Vitamin D and gastrointestinal cancers: a narrative review. Digestive diseases and sciences. 64 (5): 1098-1109.
Guyot F, et al. 2005. Time trends in the treatment and survival of recurrences from colorectal cancer. Annals of oncology. 16 (5): 756-761.
Hanberry BS, Berger R & Zastre JA 2014. High-dose vitamin B1 reduces proliferation in cancer cell lines analogous to dichloroacetate. Cancer chemotherapy and pharmacology. 73 (3): 585-594.
Hansson LE, et al. 1994. Nutrients and gastric cancer risk. A population‐based case‐control study in Sweden. International journal of cancer. 57 (5): 638-644.
Hu W 2017. Critical Role of Vitamin D3 in Helicobacter pylori Eradication in Stomachs. The FASEB Journal. 31 (1_supplement): 1067.1066-1067.1066.
Key TJ, et al. 2020. Diet, nutrition, and cancer risk: what do we know and what is the way forward? British medical journal. 368: 1-9.
Khayatzadeh S, Feizi A, Saneei P & Esmaillzadeh A 2015. Vitamin D intake, serum Vitamin D levels, and risk of gastric cancer: A systematic review and meta-analysis. Journal of research in medical sciences. 20 (8): 790.
Kline K, Lawson KA, Yu W & Sanders BG 2007. Vitamin E and Cancer. In Vitamins & Hormones, pp. 435-461. Academic Press.
Kong P, et al. 2014. Vitamin intake reduce the risk of gastric cancer: meta-analysis and systematic review of randomized and observational studies. PloS one. 9 (12): e116060.
Kutuzova GD & DeLuca HF 2007. 1, 25-Dihydroxyvitamin D3 regulates genes responsible for detoxification in intestine. Toxicology and applied pharmacology. 218 (1): 37-44.
La Vecchia C, Ferraroni M, D'Avanzo B, Decarli A & Franceschi S 1994. Selected micronutrient intake and the risk of gastric cancer. Cancer epidemiology, biomarkers & prevention. 3 (5): 393-398.
Lambert R, Saito H, Lucas E & Sankaranarayanan R 2012. Survival from digestive cancer in emerging countries in Asia and Africa. European journal of gastroenterology & hepatology. 24 (6): 605-612.
Lee YY & Derakhshan MH 2013. Environmental and lifestyle risk factors of gastric cancer. Archives of Iranian medicine (AIM). 16 (6).
Liu C & Russell RM 2008. Nutrition and gastric cancer risk: an update. Nutrition reviews. 66 (5): 237-249.
López‐Carrillo L, López‐Cervantes M, Ward MH, Bravo‐Alvarado J & Ramírez‐Espitia A 1999. Nutrient intake and gastric cancer in Mexico. International journal of cancer. 83 (5): 601-605.
Malekzadeh R 2013. A case-control study of the relationship between gastric cancer and meat consumption in Iran. Archives of Iranian medicine. 16 (6): 324.
Marmot M, et al. 2007. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. world cancer research.
Mayne ST, et al. 2001. Nutrient intake and risk of subtypes of esophageal and gastric cancer. Cancer epidemiology and prevention biomarkers. 10 (10): 1055-1062.
Mehrabian A, et al. 2010. Gastric cancer prevalence, according to survival data in Iran (National Study-2007). Iranian journal of public health. 39 (3): 27.
Mergens W, Chau J & Newmark H 1980. The influence of ascorbic acid and DL-alpha-tocopherol on the formation of nitrosamines in an in vitro gastrointestinal model system. IARC scientific publications.(31): 259-269.
Miranti EH, et al. 2017. Low vitamin B12 increases risk of gastric cancer: A prospective study of one‐carbon metabolism nutrients and risk of upper gastrointestinal tract cancer. International journal of cancer. 141 (6): 1120-1129.
Movahedi A & Roosta R 2000. Iranian food composition tables. National Nutrition and Food Technology Research Institute Press: Tehran.
Ono S, et al. 2009. Long-term outcomes of endoscopic submucosal dissection for superficial esophageal squamous cell neoplasms. Gastrointestinal endoscopy. 70 (5): 860-866.
Padayatty SJ, et al. 2003. Vitamin C as an antioxidant: evaluation of its role in disease prevention. Journal of the American college of nutrition. 22 (1): 18-35.
Pakseresht M, et al. 2011. Dietary habits and gastric cancer risk in north-west Iran. Cancer causes & control. 22 (5): 725-736.
Palli D, Russo A & Decarli A 2001. Dietary patterns, nutrient intake and gastric cancer in a high-risk area of Italy. Cancer causes and control. 12 (2): 163-172.
Pelucchi C, et al. 2008. Dietary intake of selected micronutrients and gastric cancer risk: an Italian case-control study. Annals of oncology. 20 (1): 160-165.
Penet MF, et al. 2008. Protection against cerebral malaria by the low-molecular-weight thiol pantethine. Proceedings of the National Academy of Sciences. 105 (4): 1321-1326.
Piazuelo MB & Correa P 2013. Gastric cancer: overview. Colombia Medica. 44 (3): 192-201.
Qiu J-L, et al. 2005. Nutritional factors and gastric cancer in Zhoushan Islands, China. World journal of gastroenterology. 11 (28): 4311.
Rawla P & Barsouk A 2019. Epidemiology of gastric cancer: global trends, risk factors and prevention. Przeglad gastroenterologiczny. 14 (1): 26.
Ren J, et al. 2016. Prospective study of serum B vitamins levels and oesophageal and gastric cancers in China. Scientific reports. 6: 35281.
Rock CL, et al. 2020. American Cancer Society guideline for diet and physical activity for cancer prevention. CA: a cancer journal for clinicians. 70 (4): 245-271.
Sasco A, Secretan M & Straif K 2004. Tobacco smoking and cancer: a brief review of recent epidemiological evidence. Lung cancer. 45: S3-S9.
Stefanska B, Karlic H, Varga F, Fabianowska‐Majewska K & Haslberger A 2012. Epigenetic mechanisms in anti‐cancer actions of bioactive food components–the implications in cancer prevention. British journal of pharmacology. 167 (2): 279-297.
Tamura A, Fujioka T & Nasu M 2002. Relation of Helicobacter pylori infection to plasma vitamin B12, folic acid, and homocysteine levels in patients who underwent diagnostic coronary arteriography. American journal of gastroenterology. 97 (4): 861-866.
Terry P, Lagergren J, Ye W, Nyrén O & Wolk A 2000. Antioxidants and cancers of the esophagus and gastric cardia. International journal of cancer. 87 (5): 750-754.
Testerman TL, Conn PB, Mobley HL & McGee DJ 2006. Nutritional requirements and antibiotic resistance patterns of Helicobacter species in chemically defined media. Journal of clinical microbiology. 44 (5): 1650-1658.
Thomson CA, LeWinn K, Newton TR, Alberts DS & Martinez ME 2003. Nutrition and diet in the development of gastrointestinal cancer. Current oncology reports. 5 (3): 192-202.
Toorang F, et al. 2019. Validation of Diet History Questionnaire in Assessing Energy and Nutrient Intakes of Iranian Population. Iranian journal of public health. 48 (6): 1074-1081.
Tramacere I, et al. 2011. A meta-analysis on alcohol drinking and gastric cancer risk. Annals of oncology. 23 (1): 23-38.
Uruha A, Shimizu T, Katoh T, Yamasaki Y & Matsubara S 2011. Wernicke's encephalopathy in a patient with peptic ulcer disease. Case reports in medicine. 2011.
Willett WC, Howe GR & Kushi LH 1997. Adjustment for total energy intake in epidemiologic studies. American journal of clinical nutrition. 65 (4): 1220S-1228S.
Xiao Q, et al. 2014. Intakes of folate, methionine, vitamin B6, and vitamin B12 with risk of esophageal and gastric cancer in a large cohort study. British journal of cancer. 110 (5): 1328-1333.
Yamauchi R 1997. Vitamin E: Mechanism of Its Antioxidant Activity.
Type of article: orginal article |
Subject:
public specific
Received: 2021/10/27 | Published: 2022/11/19 | ePublished: 2022/11/19
Received: 2021/10/27 | Published: 2022/11/19 | ePublished: 2022/11/19
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
