Association between dietary fatty acid patterns and risk of oral cancer by principal component analysis
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摘要:
目的 探讨膳食脂肪酸模式与口腔癌发病的关联。 方法 采用病例对照研究设计,收集2013年11月14日至2019年3月21日在福建医科大学附属第一医院口腔颌面外科确诊的225例口腔癌新发病例以及同期在该医院进行健康体检的524例对照。应用主成分分析确定人群的膳食脂肪酸模式,并通过非条件Logistic回归分析模型计算膳食脂肪酸模式与口腔癌发病风险的OR值及其95% CI值。 结果 主成分分析共提取了6种膳食脂肪酸模式。以人群中占比最大的模式6(己酸、十三烷酸为主)为参照组,模式1(以长链饱和脂肪酸和单不饱和脂肪酸为主)和模式2(中链饱和脂肪酸和多不饱和脂肪酸为主)均可降低口腔癌的发病风险,其调整后的OR值及其95% CI值分别为0.47(95% CI:0.25~0.86)、0.45(95% CI:0.21~0.98),其他模式未观察到与口腔癌发病风险有关联(均有P>0.05)。 结论 相对于以己酸、十三烷酸为主的模式6,以长链饱和脂肪酸和单不饱和脂肪酸为主的模式1和以中链饱和脂肪酸和多不饱和脂肪酸为主的模式2与口腔癌的发病风险呈负相关。科学合理摄入脂肪酸,可能降低口腔癌的发病风险。 Abstract:Objective To explore the relationship between dietary fatty acid patterns and the risk of oral cancer. Methods A case-control study including 225 cases newly diagnosed as primary oral cancer was performed at the First Affiliated Hospital of Fujian Medical University from November 14 2013 to March 21 2019. At the same time, 524 controls were recruited from the same hospital. Principal component analysis was utilized to construct the main dietary fatty acid patterns of local residents. Unconditional Logistic regression analysis model was used to explore the association between dietary fatty acid patterns and oral cancer. Adjusted odds ratio (OR) and corresponding 95% confidence interval (CI) were calculated. Results Six dietary fatty acid patterns were extracted by principal component analysis. Pattern 6 (characterized by hexaoic acid and tridecanoic acid), which accounts for the largest proportion of the population, was used as the reference group. Compared with pattern 6, the adjusted OR (95% CI) values of pattern 1 (characterized by long-chain saturated fatty acids and monounsaturated fatty acids) and pattern 2 (characterized by medium-chain saturated fatty acids and polyunsaturated fatty acids) were 0.47 (95% CI: 0.25-0.86) and 0.45(95% CI: 0.21-0.98), respectively. No statistically significant associations were observed between other patterns and the risk of oral cancer (all P>0.05). Conclusions Compared with pattern 6 (characterized by hexaoic acid, tridecanoic acid and eicotrienoic acid), pattern 1 (characterized by long-chain saturated fatty acids and monounsaturated fatty acids) and pattern 2 (characterized by medium-chain saturated fatty acids and polyunsaturated fatty acids) are negatively correlated with the risk of oral cancer, which suggest some particular dietary fatty acids patterns may reduce the risk of oral cancer. -
表 1 病例组与对照组的一般人口学特征比较[n (%)]
Table 1. General characteristics of the case group and the control group [n (%)]
特征 病例组 对照组 χ2值 P值 年龄(岁) 66.50 < 0.001 < 60 108(48.00) 409(78.05) ≥60 117(52.00) 115(21.95) 性别 2.62 0.106 男 121(53.78) 248(47.33) 女 104(46.22) 276(52.67) 民族 0.330a 汉族 225(100.00) 519(99.05) 其他 0(0.00) 5(0.95) 文化程度 17.73 < 0.001 文盲 16(7.11) 41(7.82) 小学及初中 153(68.00) 272(51.91) 高中及以上 56(24.89) 211(40.27) 婚姻状况 5.82 0.016 已婚 205(91.11) 443(84.54) 未婚及其他 20(8.89) 81(15.46) BMI(kg/m2) 10.23 0.006 < 18.5 20(8.89) 40(7.63) 18.5~<24 144(64.00) 278(53.06) ≥24 61(27.11) 206(39.31) 居住地 3.59 0.058 农村 135(60.00) 275(52.48) 城市 90(40.00) 249(47.52) 吸烟 4.99 0.026 无 137(60.89) 363(69.27) 有 88(39.11) 161(30.73) 饮酒 17.22 < 0.001 无 148(65.78) 419(79.96) 有 77(34.22) 105(20.04) 饮茶 0.07 0.785 无 132(58.67) 313(59.73) 有 93(41.33) 211(40.27) 肿瘤家族史 1.33 0.249 无 191(84.89) 461(87.98) 有 34(15.11) 63(12.02) 注:a采用Fisher精确概率法;表中数据收集于福建省2013年11月14日至2019年3月21日。 表 2 32种脂肪酸与6种模式的因子载荷
Table 2. Factor loadings between 32 fatty acids and 6 patterns
膳食脂肪酸 模式1 模式2 模式3 模式4 模式5 模式6 6∶0 0.05 0.09 0.21 -0.15 0.01 0.52a 8∶0 0.20 -0.25a -0.07 0.03 0.07 0.03 10∶0 0.19 -0.26a -0.06 0.04 0.10 -0.01 11∶0 0.22 -0.22a -0.08 0.08 -0.06 -0.10 12∶0 0.23 -0.23a -0.04 0.01 0.05 0.02 13∶0 0.11 0.10 -0.13 -0.15 0.05 0.60a 14∶0 0.24a -0.21 -0.04 0.06 0.02 -0.02 15∶0 0.26a -0.15 0.00 0.03 0.10 -0.06 16∶0 0.25a -0.03 0.24 0.02 0.04 -0.03 17∶0 0.16 0.06 -0.06 0.25 -0.45a -0.06 18∶0 0.27a -0.08 0.03 -0.10 -0.02 0.01 19∶0 0.14 0.08 -0.10 -0.03 -0.47a 0.03 20∶0 0.21 0.07 -0.03 -0.32a -0.03 0.02 22∶0 0.12 0.17 0.03 -0.41a -0.01 -0.27 14∶1 0.22a -0.22 -0.06 -0.03 0.11 0.12 15∶1 0.10 0.13 0.38a 0.24 0.21 0.08 16∶1 0.25a 0.07 0.00 -0.02 0.01 0.05 17∶1 0.15 0.21 0.06 0.34a -0.14 -0.04 18∶1 0.26a 0.03 0.17 -0.05 -0.15 0.04 20∶1 0.08 0.13 0.41a 0.27 0.09 0.02 22∶1 0.09 0.21 -0.11 -0.14 -0.22a 0.02 16∶2 0.21 -0.24a -0.06 0.00 0.02 0.00 18∶2n-6 0.12 0.15 0.44a 0.00 -0.01 -0.03 18∶3n-3 0.17 0.17 0.22 -0.31a -0.04 -0.15 20∶2n-6 0.11 0.19 -0.17 0.16 -0.34a 0.12 20∶3n-3 0.09 0.10 -0.04 0.18 0.12 -0.36a 20∶4n-6 0.20a 0.17 -0.14 0.10 -0.01 -0.06 20∶5n-3 0.13 0.27a -0.22 0.10 0.22 -0.02 22∶3n-3 0.12 0.23 -0.23 0.06 0.28a 0.07 22∶4n-6 0.09 0.15 0.01 -0.36a 0.09 -0.25 22∶5n-3 0.13 0.25 -0.23 0.07 0.28a 0.05 22∶6n-3 0.13 0.26a -0.21 0.11 0.20 -0.03 注:a因子载荷≥0.2的膳食脂肪酸项;表中数据收集于福建省2013年11月14日至2019年3月21日。 表 3 膳食脂肪酸模式与口腔癌发病关联的非条件Logistic回归分析模型分析
Table 3. The unconditional Logistic regression of dietary fatty acid pattern on oral cancer
膳食脂肪酸模式 OR(95% CI)值 P值 OR(95% CI)值a P值a 模式6 1.00 1.00 模式1 0.54(0.31~0.93) 0.027 0.47(0.25~0.86) 0.015 模式2 0.37(0.18~0.76) 0.006 0.45(0.21~0.98) 0.044 模式3 1.01(0.64~1.61) 0.958 0.92(0.55~1.54) 0.754 模式4 0.80(0.51~1.25) 0.325 0.72(0.44~1.19) 0.201 模式5 0.95(0.56~1.62) 0.844 1.30(0.72~2.36) 0.386 注:a调整的混杂因素为年龄、性别、民族、文化程度、婚姻状况、BMI、居住地、吸烟、饮酒、饮茶、肿瘤家族史;表中数据收集于福建省2013年11月14日至2019年3月21日。 -
[1] 韩旻轩, 王林. Toll样受体2基因多态性与口腔癌的相关性[J]. 江苏医药, 2019, 45(10): 1017-1019, 1024. DOI: 10.19460/j.cnki.0253-3685.2019.10.012.Han MX, Wang L. Correlation between TLR2 polymorphisms and risk for oral cancer[J]. Jiangsu Med J, 2019, 45(10): 1017-1019, 1024. DOI: 10.19460/j.cnki.0253-3685.2019.10.012. [2] Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin, 2018, 68(6): 394-424. DOI: 10.3322/caac.21492. [3] Pascual G, Avgustinova A, Mejetta S, et al. Targeting metastasis-initiating cells through the fatty acid receptor CD36[J]. Nature, 2017, 541(7635): 41-45. DOI: 10.1038/nature20791. [4] Askari M, Darabi M, Zare MR, et al. Tissue fatty acid composition and secretory phospholipase-A2 activity in oral squamous cell carcinoma[J]. Clin Transl Oncol, 2015, 17(5): 378-383. DOI: 10.1007/s12094-014-1242-2. [5] Lee HC, Liang A, Lin YH, et al. Low dietary n-6/n-3 polyunsaturated fatty acid ratio prevents induced oral carcinoma in a hamster pouch model[J]. Prostaglandins Leukot Essent Fatty Acids, 2018, 136: 67-75. DOI: 10.1016/j.plefa.2017.03.003. [6] Smuts CM, Ricci C, Kruger LM, et al. Plasma phospholipid fatty acid patterns are associated with adiposity and the metabolic syndrome in black South Africans: a cross-sectional study[J]. Cardiovasc J Afr, 2019, 30(4): 228-238. DOI: 10.5830/CVJA-2019-026. [7] Dahm CC, Gorst-Rasmussen A, Crowe FL, et al. Fatty acid patterns and risk of prostate cancer in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition[J]. Am J Clin Nutr, 2012, 96(6): 1354-1361. DOI: 10.3945/ajcn.112.034157. [8] Radoï L, Paget-Bailly S, Menvielle G, et al. Tea and coffee consumption and risk of oral cavity cancer: results of a large population-based case-control study, the ICARE study[J]. Cancer Epidemiol, 2013, 37(3): 284-289. DOI: 10.1016/j.canep.2013.02.001. [9] 杨月欣. 中国食物成分表标准版[M]. 北京: 北京大学医学出版社, 2018.Yang YX. China food composition tables standard edition[M]. Beijing: Peking University Medical Press, 2018. [10] Willett WC, Howe GR, Kushi LH, et al. Adjustment for total energy intake in epidemiologic studies[J]. Am J Clin Nutr, 1997, 65(4): 1220-1228. DOI: 10.1093/ajcn/65.4.1220S. [11] 丘薇, 林菁, 罗丽, 等. 基于倾向性评分匹配法评估血清铬对口腔癌发病的影响[J]. 中华疾病控制杂志, 2020, 24(1): 20-25. DOI: 10.16462/j.cnki.zhjbkz.2020.01.005.Qiu W, Lin J, Luo L, et al. Pathogenesis effect of serum chromium on oral cancer based on propensity score matching[J]. Chin J Dis Control Prev, 2020, 24(1): 20-25. DOI: 10.16462/j.cnki.zhjbkz.2020.01.005. [12] 张荣琪, 陈青, 吴雨煊, 等. 血清叶酸与口腔癌发病关联的病例对照研究[J]. 中华疾病控制杂志, 2020, 24(6): 723-727, 736. DOI: 10.16462/j.cnki.zhjbkz.2020.06.020.Zhang RQ, Chen Q, Wu YX, et al. Relationship between serum folate and risk of oral cancer: a case-control study[J]. Chin J Dis Control Prev, 2020, 24(6): 723-727, 736. DOI: 10.16462/j.cnki.zhjbkz.2020.06.020. [13] 陈法, 蔡琳, 何保昌, 等. 饮茶与非吸烟、非饮酒人群口腔癌的关系研究[J]. 中华预防医学杂志, 2015, 49(8): 683-687. DOI: 10.3760/cma.j.issn.0253-9624.2015.08.004.Chen F, Cai L, He BC, et al. Effect of tea on oral cancer in nonsmokers and nondrinkers: a case-control study[J]. Chin J Prev Med, 2015, 49(8): 683-687. DOI: 10.3760/cma.j.issn.0253-9624.2015.08.004. [14] Mahin CA, Lobley CE, Grant CM, et al. Factors influencing beef eating quality, 2. Effects of nutritional regimen and genotype on muscle fibre characteristics[J]. Anim Sci, 2001, 72(2): 279-287. DOI: 10.1017/s1357729800055776. [15] 许仁溥. 脂肪酸的抗癌作用[J]. 粮油食品科技, 1988(3): 44. https://www.cnki.com.cn/Article/CJFDTOTAL-SSPJ198803032.htmXu RP. Anti-cancer effects of fatty acids[J]. Sci Technol Cereals, Oils Foods, 1988(3): 44. https://www.cnki.com.cn/Article/CJFDTOTAL-SSPJ198803032.htm [16] Shibasaki Y, Horikawa M, Ikegami K, et al. Stearate-to-palmitate ratio modulates endoplasmic reticulum stress and cell apoptosis in non-B non-C hepatoma cells[J]. Cancer Sci, 2018, 109(4): 1110-1120. DOI: 10.1111/cas.13529. [17] Crowe FL, Allen NE, Appleby PN, et al. Fatty acid composition of plasma phospholipids and risk of prostate cancer in a case-control analysis nested within the European Prospective Investigation into Cancer and Nutrition[J]. Am J Clin Nutr, 2008, 88(5): 1353-1363. DOI: 10.3945/ajcn.2008.26369. [18] May-Wilson S, Sud A, Law PJ, et al. Pro-inflammatory fatty acid profile and colorectal cancer risk: a Mendelian randomisation analysis[J]. Eur J Cancer, 2017, 84: 228-238. DOI: 10.1016/j.ejca.2017.07.034. [19] Moon HS, Batirel S, Mantzoros CS. Alpha linolenic acid and oleic acid additively down-regulate malignant potential and positively cross-regulate AMPK/S6 axis in OE19 and OE33 esophageal cancer cells[J]. Metabolism, 2014, 63(11): 1447-1454. DOI: 10.1016/j.metabol.2014.07.009. [20] Narayanan A, Baskaran SA, Amalaradjou MA, et al. Anticarcinogenic properties of medium chain fatty acids on human colorectal, skin and breast cancer cells in vitro[J]. Int J Mol Sci, 2015, 16(3): 5014-5027. DOI: 10.3390/ijms16035014. [21] Poonam V, Sanjukta N, Pranati N, et al. In Vitro anticancer activity of virgin coconut oil and its fractions in liver and oral cancer cells[J]. Anti-Cancer Agents Med Chem, 2019, 19(18): 2223-2230. DOI: 10.2174/1871520619666191021160752. [22] Dayrit FM. The properties of lauric acid and their significance in coconut oil[J]. J Am Oil Chem Soc, 2015, 92(1): 1-15. DOI: 10.1007/s11746-014-2562-7. [23] Lappano R, Sebastiani A, Cirillo F, et al. The lauric acid-activated signaling prompts apoptosis in cancer cells[J]. Cell Death Discovery, 2017, 3(1): 131-140. DOI: 10.1038/cddiscovery.2017.63. [24] Kim Y, Kim J. Intake or blood levels of n-3 polyunsaturated fatty acids and risk of colorectal cancer: a systematic review and meta-analysis of prospective studies[J]. Cancer Epidemiol Biomarkers Prev, 2020, 29(2): 288-299. DOI: 10.1158/1055-9965.EPI-19-0931. [25] Nana B, Lirong H, Meng M, et al. Anti-tumor mechanism of eicosapentaenoic acid (EPA) on ovarian tumor model by improving the immunomodulatory activity in F344 rats[J]. J Funct Foods, 2020, 65: 103739. DOI: 10.1016/j.jff.2019.103739. [26] Newell M, Baker K, Postovit LM, et al. A critical review on the effect of docosahexaenoic acid (DHA) on cancer cell cycle progression[J]. Int J Mol Sci, 2017, 18(8): 1784. DOI: 10.3390/ijms18081784. [27] 宋志秀, 杨立刚, 王月环, 等. 南京市中老年居民膳食脂肪酸摄入状况[J]. 中国老年学杂志, 2013, 33(23): 5957-5959. DOI: 10.3969/j.issn.1005-9202.2013.23.081.Song ZX, Yang LG, Wang YH, et al. The dietary fatty acids intakes and their food sources among the middle and elderly residents in Nanjing[J]. Chin J Gerontol, 2013, 33(23): 5957-5959. DOI: 10.3969/j.issn.1005-9202.2013.23.081.