饮食和前列腺癌

前列腺癌发病率在全球范围内的巨大差异提示环境因素在前列腺癌的形成和发展过程中有重要作用 ,其中饮食结构和饮食成分是主要因素之一。饮食中的热量、脂肪、各种微营养素、维生素、微量元素、异黄酮和黄酮类物质都有一定的作用。深入了解这些关系和作用机理 ,改变饮食习惯 ,将在一定程度上降低前列腺癌发生的危险性 ,降低发病率 ,改善预后。     

肠道菌群与前列腺癌进展的相关性及机制研究进展

前列腺癌是严重威胁男性健康的常见肿瘤之一,在欧美男性泌尿系肿瘤发病率中位居第1。前列腺癌的发生发展主要与遗传及代谢两大因素相关。近年来研究发现高脂饮食可导致人体肠道菌群发生改变,与前列腺癌的发生与发展联系密切,其机制可能与肠道菌群变化导致炎性因子水平以及调控表观遗传状态的酶活性改变相关。本文总结了近年来前列腺癌在肠道菌群方面的相关研究,并探讨肠道菌群与前列腺癌发生发展的关系及其可能的作用机制。     

饮食和前列腺癌

前列腺癌发病率在全球范围内的巨大差异提示环境因素在前列腺癌的形成和发展过程中有重要作用，其中饮食结构和饮食成分是主要因素之一，饮食中的热量，脂肪，各种微营养素，维生素，微量元素，异黄酮和黄酮类物质都有一定的作用，深入了解这些关系和作用机理，改变饮食习惯，将在一定程度上降低前列腺癌发生的危险性，降低发病率，改善预后。     

非编码微小核糖核酸和前列腺癌关系的研究进展

前列腺癌的发生和许多因素相关,具体的分子机制还不清楚。非编码微小核糖核酸（miRNAs）作为目前研究的热点在许多肿瘤发生、发展、浸润和转移、以及治疗靶点方面都有新的发现。然而与前列腺癌相关的miRNAs的研究还比较少,主要局限于前列腺癌中miRNAs表达谱分析、单个miRNA功能、致瘤性miRNAS和肿瘤抑制性miRNAs的研究。作者就miRNAs和前列腺癌关系研究的最新进展作简要概述。     

肝移植术后新发糖尿病危险因素研究进展

肝移植术后新发糖尿病(NODAT)是肝移植术后常见的并发症,因其发病率高、危害大,严重的影响移植物功能和受者生存质量,受到了广大学者的关注。NODAT的危险因素有许多,大致可分为不可调控性危险因素及可调控性危险因素。不可调控性危险因素主要包括年龄、性别、供肝脂肪变性、肝硬化、糖尿病家族史等;可调控性危险因素包括肥胖、钙调磷酸酶抑制剂、糖皮质激素、肝炎病毒感染、巨细胞病毒感染及移植前血糖等。笔者结合近年相关研究报道对NODAT的发生机制及危险因素进行综述。     

孟德尔随机化分析在前列腺癌病因学研究中的应用现状与展望

前列腺癌是男性泌尿生殖系统最常见的恶性肿瘤,其发病率和死亡率逐年上升,目前已成为影响男性健康的公共卫生问题。孟德尔随机化(MR)分析近年来被广泛运用于流行病学病因推断上,较一般的观察性研究避免了混杂因素干扰且因果时序清晰,其对疾病危险因素的判断更有助于疾病的早期干预和临床防治。本文综述了MR分析在前列腺癌病因学研究中的应用现状,对维生素D、端粒长度、无机盐类、睾酮水平、脂质与蛋白质、氨基酸、肠道菌群等微观暴露,以及基础疾病、药物使用、饮食因素、生活及行为习惯、青春期发育等宏观暴露与前列腺癌的因果关系进行总结,为从危险因素角度制定前列腺癌防治策略提供了依据。同时,前列腺癌领域的MR分析也具有人群分层存在偏差、数据样本量差异影响结局、纳入汇总数据时存在混杂因素、无法明确暴露影响结局的机制等不足,未来研究应当着重解决这些问题。     

前列腺癌患者围术期VTE危险因素分析及预警

目的探讨前列腺癌患者围术期发生静脉血栓栓塞症(VTE)的危险因素并制定相应预警策略,以降低术后VTE发生率。方法采用回顾性病例分析,调阅山东省某三甲医院2014年1月1日至2016年12月31日期间临床诊断匹配为前列腺癌且进行手术治疗的患者的病历资料,从中筛选出术后并发VTE患者并分析其发生VTE的危险因素。结果经单因素分析显示前列腺癌患者术后并发VTE与BMI、吸烟、高血压、纤维蛋白原含量、凝血酶原时间、活化部分凝血活酶原时间和麻醉方式相关;多因素分析显示年BMI≥24.0 kg/m^2、高血压、全麻和术后凝血酶原时间缩短是前列腺癌患者术后发生VTE的独立危险因素。结论 BMI≥24.0 kg/m^2、高血压、全麻以及术后凝血酶原时间缩短是导致前列腺癌患者围术期发生VTE的危险因素,医护人员应提高对术后VTE危险因素的认识并早期采取预防措施。     

维生素E与前列腺癌

关于硒和维生素E预防肿瘤的研究（SELECT）的最初研究没有发现补充硒或者维生素E能够减少前列腺癌的危险,却出现了与维生素E相关的前列腺癌发生的危险的增加,但是这种增加差异无统计学意义。长期的随访观察,以及更多的前列腺癌事件的发生进一步将会揭示维生素E与前列腺癌之间的关系。本文的目的就是明确在相对健康的人群中,长期使用维生素E和硒与发生前列腺癌危险之间的关系。     

胃癌风险人群筛查及危险因素分析

目的 对胃癌风险人群进行筛查，对危险因素进行分析。方法 选择本院自行设计胃癌危险因素问卷对研究对象进行调查，并对具有不同人口学特征和胃癌行为危险因素的研究对象进行分析。采用Logistic回归对胃癌的危险因素进行分析。结果 单因素分析结果指出：患者的年龄、性别、职业、婚姻状况、生活所在地、经济收入、教育水平、饮食清淡度、胃部相关疾病、饮食清淡度、腌制食品摄入、吸烟、饮酒、饮食规律度、胃癌家族史、癌症家族史与胃癌的发生相关，差异有统计学意义（P<0.05）；果蔬摄入情况与胃癌的发生无关，差异无统计学意义（P>0.05）。多因素分析结果指出年龄、性别、婚姻状况、生活所在地、经济收入、腌制食品摄入、饮食清淡度、饮食规律度、吸烟、饮酒、胃部相关疾病、胃癌家族史是胃癌的危险因素（P<0.05）。结论 年龄、性别、婚姻状况、生活所在地、经济收入、腌制食品摄入、饮食清淡度、饮食规律度、吸烟、饮酒、胃部相关疾病、胃癌家族史是胃癌的危险因素。医务人员需要结合风险人群的危险因素具体情况开展个体化指导干预，提高胃癌风险人群的认知水平，以降低发生胃癌的风险。     

内脏脂肪与胰腺癌关系的研究进展

目的 了解内脏脂肪与胰腺癌关系相关研究的进展。方法 对近年来国内外在内脏脂肪的蓄积、内脏脂肪与胰腺癌关系的潜在机制、内脏脂肪的测量以及内脏脂肪与胰腺癌预后方面相关研究的文献予以综述。结果 内脏脂肪的蓄积是多因素共同作用的结果，包括年龄、性别及性激素、内源性大麻素系统等，它分泌的多种脂肪因子在胰腺癌的发生及发展中起到了至关重要的作用，主要通过多种不同信号通路发挥促肿瘤和抗肿瘤效应。结论 临床治疗过程中，可在不影响患者病情进展的条件下，通过调整饮食、体育训练等方法降低内脏脂肪量，同时干预各种脂肪因子的作用路径，以此来改善胰腺癌患者的生活质量及生存预后。     

Diet, anthropometric measures and prostate cancer risk: a review of prospective cohort and intervention studies

We reviewed 37 prospective cohort and four intervention studies on potential dietary risk factors for prostate cancer, published between 1966 and September 2003. Some studies were limited by small size, crude measurement of dietary exposure and limited control for confounders. Intervention and prospective cohort studies support a protective role against prostate cancer for selenium, and possibly for vitamin E, pulses and tomatoes/lycopene. Overall consumption of meat, eggs, vegetables, fruit, coffee, tea, carotenoids and vitamins A, C and D was not consistently related to prostate cancer risk. Intervention studies also indicate that supplementation with beta-carotene does not lower prostate cancer risk, except possibly in men with low beta-carotene status at baseline. For specific types of meat, alcoholic drinks, dairy products, fat and anthropometric measures, most cohort studies suggest either an increased risk or no relation with prostate cancer. For calcium, two cohort studies suggest an increased risk at very high calcium intakes (>2000 mg/day). In conclusion, prospective studies are consistent with a protective role for selenium, and possibly vitamin E, pulses and tomatoes/lycopene, in the aetiology of prostate cancer. Studies are inconclusive on the role of meat, dairy products, fat, vegetables, fruits, alcohol and anthropometric measures, whereas a very high calcium intake appears to be positively associated with prostate cancer risk.     

Leptin influences cellular differentiation and progression in prostate cancer

PURPOSE: Several studies have shown a positive association of dietary fat with prostate cancer. Leptin, a peptide hormone that has a role in the regulation of body weight, currently serves as a more accurate biomarker for total body fat. We designed a study to determine whether leptin influences cellular differentiation and the progression of prostate cancer. MATERIALS AND METHODS: In this study we investigated serum leptin in 21 patients with prostate cancer, 50 with benign prostatic obstruction and 50 healthy individuals matched for sex, body mass index and age. Patients with cancer were stratified into 2 groups by the disease spread, including groups 1--organ confined and 2--advanced disease, and into 3 groups by the differentiation degree, including groups 3--Gleason sum 2 to 4 or well differentiated, 4--Gleason sum 5 to 7 or moderately differentiated and 5--Gleason sum 8 to 10 or poorly differentiated. RESULTS: We noted significant differences in serum leptin in the cancer versus control and cancer versus benign prostatic obstruction groups. In addition, in the prostate cancer group serum leptin correlated with prostate specific antigen and biopsy Gleason score. We also observed significant differences in serum leptin in groups 1 versus 2, 3 versus 5 and 4 versus 5. CONCLUSION: Leptin may have roles in the development of prostate cancer through testosterone and factors related to obesity. It influences cellular differentiation and the progression of prostate cancer.     

Dietary fat and prostate cancer progression and survival.

BACKGROUND: The association between dietary factors and the occurrence of prostate cancer has been studied extensively, but there is, as yet, no published study on the relationship between diet and disease progression among prostate cancer patients. We studied the association between dietary fat intake and prostate cancer survival. METHODS: We prospectively followed 384 men diagnosed with prostate cancer between 1990 and 1992 in the Quebec City area who participated in a case-control study of diet in relation to prostate cancer occurrence. Trained nutritionists interviewed the men on their usual diet using a diet history questionnaire. Deaths in the follow-up were documented through record linkage with the provincial mortality file and review of hospital records. The cause of death was taken as written on the death certificate. Cox proportional hazards models were used to estimate the relative risk of dying from prostate cancer associated with terciles of fat intake, expressed as percent of dietary energy, while controlling for prognostic factors and total energy. RESULTS: The median duration of follow-up was 5.2 years. During the follow-up period, 32 patients died of prostate cancer and 39 died of other causes. The 5-year disease-specific survival was 91%. After controlling for grade, clinical stage, initial treatment, age and total energy intake, we found that saturated fat consumption was significantly associated with disease-specific survival (p = 0.008). Compared to men in the lower tercile of saturated fat, those in the upper tercile had three times the risk of dying from prostate cancer (hazards ratio 3.13, 95% confidence interval 1.28-7.67). CONCLUSION: Our findings suggest that, if saturated fat is causally related to disease-specific survival, a moderate reduction of its intake below 10% of energy should reduce the risk of dying from prostate cancer. This dietary goal is already recommended for health promotion and primary prevention of heart disease and cancer.     

Estrogens and aspects of prostate disease

Estrogens have long been associated with the processes involved in prostate carcinogenesis, particularly in cancer suppression. However, the synergistic influence of low concentrations of estrogens, together with androgens, in promoting aberrant growth of the gland has also been recognized. As new insights into the complex molecular events implicated in growth regulation of the prostate are revealed, the role of the estrogens has become clearer. The present review considers this role in relation to the pathogenesis of prostate cancer and the potential cancer-repressive influence of the dietary estrogens.     

Chemoprävention des Prostatakarzinoms

Despite advances in the detection and management of prostate cancer, this disease remains a major cause of morbidity and mortality in men. Increasing attention has focused on the role of chemoprevention for prostate cancer, i.e., the administration of agents that inhibit one or more steps in the natural course of prostate carcinogenesis. We review prostate cancer chemoprevention studies in Europe.Published studies were identified in a search of MEDLINE. Information about ongoing studies was provided by author access to protocols. A variety of chemoprevention studies have focused on the role of dietary factors, vitamins, and trace elements in prostate cancer. Some of these studies have been prospective, randomized, and double-blinded, while others have used retrospective or epidemiological approaches. Large-scale randomized studies are also evaluating the role of 5alpha-reductase inhibitors, which inhibit the conversion of testosterone to the more potent androgen dihydrotestosterone.Robust evidence is lacking for the value of chemopreventive agents in prostate cancer. Current evidence does suggest that vitamin E and selenium may have a role in prostate cancer chemoprevention. Data from two studies, one examining the type 1 5alpha-reductase selective inhibitor finasteride and the other using the dual 5a-reductase inhibitor dutasteride, will determine the benefits of androgen inhibition strategies for prostate cancer chemoprevention.     

Fat reduction to prevent prostate cancer: waiting for more evidence?

Complementary medicine has become an important area of interest for patients and researchers around the world. The utilization of some of these therapies by many individuals makes it imperative to understand whether they have any role in treatment of cancer or other diseases. Some of such therapies may play a role in the prevention of prostate cancer. Clinical trials are addressing this issue, and whether these products could also improve prognosis of prostate cancer. That dietary fat reduction may help to prevent prostate cancer is supported by numerous case-control studies reported over the past several decades, but recent prospective studies suggest that the impact of fat reduction in this regard may not be great. Clinicians should be careful not to suggest such a benefit until more research provides a better picture of the situation. Breast cancer is probably the best example of why more research into dietary changes for reduction in cancer risk is needed. Once believed to play a significant role, recent prospective studies suggest that dietary fat reduction may have little effect on breast cancer prevention, although some interesting insights have been gained with regard to the method of meat preparation and the influence of genetics. Fat reduction, together with soy products or other plant estrogen foods, may have a symbiotic relationship. Numerous healthy lifestyle changes incorporated and practiced at one time (healthy diet, attainment and maintenance of normal weight, soy consumption, among others) may hold some promise in the area of cancer prevention. In the meantime any healthy lifestyle or dietary change should be encouraged, because it may reduce the risk of cardiovascular disease, which is still the number one cause of mortality. It is also an important cause of morbidity and mortality in cancer patients. Regardless, complementary medicine should probably be discussed with any patient who is initiating or undergoing conventional treatment, because of the cardiovascular benefits and overall potential impact on all-cause mortality. Whether such therapies impact on prostate carcinoma remains to be determined through additional prospective investigations.     

Insulin-like growth factors and their binding proteins in prostate cancer: Cause or consequence?☆

Insulin-like growth factors (IGFs) promote growth and survival of many types of tumor cells. Epidemiologic studies have implicated carcinogenesis with high levels of IGFs in circulation or in tissues. The levels of IGF binding proteins (IGFBPs) have been associated with reduced risk for prostate and other cancers. Experimental studies have implicated high levels of IGF-I directly and IGFBP-3 inversely in prostate cancer growth, survival, and progression. However, recent evidence suggests a much weaker association of IGF-I with prostate cancer development and a stronger antagonistic association of IGFBP-3 with prostate cancer progression. Considering the clonal heterogeneity and unpredictable progression pattern of prostate cancer, the role of any single growth factor or its regulator (IGFBP) as a single determining factor is limited. This review is a critical appraisal of the role of IGFs, IGFBP, and IGF-I receptor (the IGF axis) in both experimental and clinical prostate cancer genesis and progression.     

Inflammation and prostate carcinogenesis

Quite a few epidemiological studies including meta‐analyses indicate that prostate inflammation is associated with increased risk of prostate cancer. The cause of inflammation in the prostate is speculated to be several microorganisms that cause prostatitis or sexually transmitted infections. Other specific microorganisms, such as xenotropic murine leukemia virus‐related virus, are also reported to relate to the development of prostate cancer; however, the contribution of this microorganism to prostate cancer development needs to be carefully interpreted. Environmental factors, especially dietary factors, might also be associated with prostate cancer development. Among related dietary factors, charred meat carcinogen 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine might be a link between environmental factors and inflammation, because 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine has the potential to accelerate prostate inflammation through its estrogenic effect. In light of these findings, preventing or reducing prostate inflammation might be one strategy for chemoprevention of prostate cancer.     

Dietary fatty acids correlate with prostate cancer biopsy grade and volume in Jamaican men

PURPOSE: Jamaica has the highest incidence of prostate cancer in the world. Dietary fat is associated with prostate cancer. The Omega6 polyunsaturated fatty acids have been shown to stimulate prostate carcinogenesis and the Jamaican diet is rich in linoleic acid. We hypothesized positive correlations between Omega6 polyunsaturated fatty acid, prostate specific antigen and prostate biopsy pathology. MATERIALS AND METHODS: A total of 148 men were enrolled in Kingston, Jamaica. Serum prostate specific antigen and erythrocyte membrane polyunsaturated fatty acids were analyzed. Men with prostate specific antigen 2.6 ng/ml or greater underwent biopsy. Histopathological and statistical analyses were performed on available data. RESULTS: Of the 54 men who underwent biopsy 24 had prostate cancer, 17 had a Gleason score of 7 or greater and 11 had a tumor volume of 50% or greater. There were significant positive correlations between linoleic acid and Gleason score (p = 0.009), and the linoleic acid-to-docosahexaenoic acid (Omega3) ratio and tumor volume (p = 0.03). There was a significant negative correlation between the arachidonic acid (Omega6)-to-docosapentanoic acid (Omega3) ratio and Gleason score (p = 0.04). Statistical correlations between prostate specific antigen and polyunsaturated fatty acids were inconsistent. CONCLUSIONS: The positive correlations between linoleic acid and Gleason score, and the linoleic acid-to-docosahexaenoic acid ratio and tumor volume support studies showing that Omega6 polyunsaturated fatty acids stimulate and Omega3 polyunsaturated fatty acids inhibit prostate cancer growth. The negative correlation between the arachidonic acid-to-docosapentanoic acid ratio and Gleason score supports studies that demonstrate increased metabolism of arachidonic acid in prostate cancer to form carcinogenic metabolites, namely prostaglandin E2. Our findings support the association between dietary fatty acids and prostate cancer, and they warrant further dietary and tissue studies in high risk populations.