肥胖在癌症发展中的作用

IF 0.3 Q4 ONCOLOGY
Jan Goedeke, O. Muensterer
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The tendency increased gradually in all countries over a period of 25 years (1990–2015).We therefore have to expect steadily rising numbers of cancers worldwide solely due to obesity in the future. A population-based study using BMI and cancer incidence data from the GLOBOCAN project estimated that, in 2012 in the United States, about 28,000 new cases of cancer in men (3.5%) and 72,000 in women (9.5%) were due to overweight or obesity. The percentage of cases attributed to overweight or obesity varied widely for different cancer types but was as high as 54% for gallbladder cancer in women and 44% for esophageal adenocarcinoma in men. The International Agency for Research on Cancer (IARC) as part of the World Health Organization (WHO) in 2016 reported an increased risk of cancer for at least 13 cancer types [colon cancer, esophageal cancer, renal carcinoma, uterine cancer, breast cancer (during and after menopause; also in men), liver cancer, pancreatic cancer, gall bladder cancer, ovarian cancer, gastric cancer, thyroid cancer, multiple myeloma, and meningioma]. For some of these cancers, the experts even found a dose-response relationship, implying that the risk of cancer increases with BMI. Currently, there are many theories that could explain the increased incidence of cancer in obesity. The preponderance of the evidence suggests that a combination of different factors might be responsible. However, it should be reiterated that there is no direct link between obesity and the development of cancer. On the one hand, obesity seems to cause a general hormonal imbalance including hyperinsulinemia and an increase in insulinlike growth factors, as well as sex hormones. In addition, hyperplastic and hypertrophic white adipose tissue (especially visceral adipose tissue) acts as an independent active endocrine organ releasing immunologically active adipokines and other hormones. These hormonal imbalances support cell growth– promoting processes. On the other hand, obesity is associated with a state of low-grade chronic inflammation. Insulin resistance and the metabolic syndrome are associated with higher circulating concentrations of inflammation-related markers, including leptin, interleukin-6, and tumor necrosis factor, many of which have been shown to enhance tumor growth. Chronic inflammation is a well-known, obesity independent critical component of tumor development and progression. Many cancers arise from sites of infection, chronic irritation, and inflammation. Obesity is only one of many important triggers of low-grade chronic inflammation, whereas per current literature there is no study published, that clearly shows that chronic inflammation is inversely related to the development of obesity. In addition, a further mechanism that suppresses the eradication of neoplastic cells is immune paralysis, which is also due to chronic inflammation. Not least, preclinical studies showed that adipocytic progenitor cells contribute to a tumor-promoting microenvironment as well. Controlled diet and lifestyle adjustments can lower the risk of cancer. It would be naive to believe that through a healthy diet and regular physical exercise, however, cancer development were to be prevented entirely. Could losing weight reduce the risk of cancer? So far, this has not been proven, although somepreliminary study results suggest it. However, the above results should still be interpreted with caution, as the published studies were too heterogenous in their design, the populations studied and different lengths of followup, so that it is too early at the moment, to make definitive recommendations. Reducing the excess weight once acquired, however, is difficult for many people. For most patients, making sure to at least not gain further weight is the first step. Likewise, people with normal weight should at least try to maintain it. Bariatric or metabolic surgical interventions have shown some initial beneficial effect for primary prevention of cancer, although it is far too early to draw definitive conclusions. Nevertheless, weight reduction seems to provide some degree of primary prophylaxis not only concerning metabolic and cardiovascular disease, but also for developing a wide array of neoplasms. 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The International Agency for Research on Cancer (IARC) as part of the World Health Organization (WHO) in 2016 reported an increased risk of cancer for at least 13 cancer types [colon cancer, esophageal cancer, renal carcinoma, uterine cancer, breast cancer (during and after menopause; also in men), liver cancer, pancreatic cancer, gall bladder cancer, ovarian cancer, gastric cancer, thyroid cancer, multiple myeloma, and meningioma]. For some of these cancers, the experts even found a dose-response relationship, implying that the risk of cancer increases with BMI. Currently, there are many theories that could explain the increased incidence of cancer in obesity. The preponderance of the evidence suggests that a combination of different factors might be responsible. However, it should be reiterated that there is no direct link between obesity and the development of cancer. On the one hand, obesity seems to cause a general hormonal imbalance including hyperinsulinemia and an increase in insulinlike growth factors, as well as sex hormones. In addition, hyperplastic and hypertrophic white adipose tissue (especially visceral adipose tissue) acts as an independent active endocrine organ releasing immunologically active adipokines and other hormones. These hormonal imbalances support cell growth– promoting processes. On the other hand, obesity is associated with a state of low-grade chronic inflammation. Insulin resistance and the metabolic syndrome are associated with higher circulating concentrations of inflammation-related markers, including leptin, interleukin-6, and tumor necrosis factor, many of which have been shown to enhance tumor growth. Chronic inflammation is a well-known, obesity independent critical component of tumor development and progression. Many cancers arise from sites of infection, chronic irritation, and inflammation. 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引用次数: 0

摘要

长期以来,超重对健康的危害一直为人所知,科学家们早在几年前就能证明身体脂肪和癌症之间的关系。当然,并不是每个肥胖的人都会不可避免地患上癌症,但最近的科学研究表明,过多的身体脂肪对癌症的影响比以前认为的要广泛得多。这既适用于成人,也适用于儿童和青少年。2015年,经济合作与发展组织(OECD)报告称,在34个成员国中,已经有超过50%的成年人和近30%的青少年被认为超重(体重指数,BMI≥25 kg/m2体表面积),甚至肥胖(BMI≥30 kg/m2体表面积)。在25年(1990-2015年)期间,所有国家的这一趋势逐渐增加。因此,我们不得不预计,未来全球范围内仅因肥胖而患癌症的人数将稳步上升。一项基于人群的研究使用了来自GLOBOCAN项目的BMI和癌症发病率数据,估计2012年美国约有28,000例男性(3.5%)和72,000例女性(9.5%)的新癌症病例是由于超重或肥胖引起的。由于超重或肥胖导致的病例百分比在不同的癌症类型中差异很大,但在女性胆囊癌中高达54%,在男性食管癌中高达44%。作为世界卫生组织(世卫组织)的一部分,国际癌症研究机构(IARC)在2016年报告称,至少13种癌症类型(结肠癌、食道癌、肾癌、子宫癌、乳腺癌)在绝经期间和绝经后患癌症的风险增加;(也见于男性)肝癌、胰腺癌、胆囊癌、卵巢癌、胃癌、甲状腺癌、多发性骨髓瘤和脑膜瘤。对于其中一些癌症,专家们甚至发现了一种剂量-反应关系,这意味着癌症的风险随着BMI的增加而增加。目前,有许多理论可以解释肥胖导致癌症发病率增加的原因。大量证据表明,可能是多种不同因素的综合作用造成的。然而,应该重申的是,肥胖和癌症的发展之间没有直接的联系。一方面,肥胖似乎会导致普遍的激素失衡,包括高胰岛素血症和胰岛素样生长因子以及性激素的增加。此外,增殖性和肥厚性白色脂肪组织(尤其是内脏脂肪组织)作为一个独立的活跃内分泌器官,释放具有免疫活性的脂肪因子和其他激素。这些荷尔蒙失衡支持促进细胞生长的过程。另一方面,肥胖与低度慢性炎症有关。胰岛素抵抗和代谢综合征与炎症相关标志物的高循环浓度有关,包括瘦素、白细胞介素-6和肿瘤坏死因子,其中许多已被证明可促进肿瘤生长。慢性炎症是众所周知的、与肥胖无关的肿瘤发生和进展的关键组成部分。许多癌症起源于感染、慢性刺激和炎症部位。肥胖只是低度慢性炎症的众多重要触发因素之一,而根据目前的文献,还没有发表的研究清楚地表明慢性炎症与肥胖的发展呈负相关。此外,抑制肿瘤细胞根除的另一个机制是免疫麻痹,这也是由于慢性炎症。重要的是,临床前研究表明,脂肪细胞祖细胞也有助于促进肿瘤的微环境。控制饮食和调整生活方式可以降低患癌症的风险。然而,如果认为通过健康的饮食和定期的体育锻炼就可以完全预防癌症的发展,那就太天真了。减肥能降低患癌症的风险吗?到目前为止,这还没有得到证实,尽管一些初步的研究结果表明是这样的。然而,上述结果仍应谨慎解读,因为已发表的研究在设计、研究人群和随访时间上过于异质,因此现在提出明确的建议还为时过早。然而,对很多人来说,减肥是很困难的。对于大多数患者来说,确保至少不要再增加体重是第一步。同样,体重正常的人至少应该努力保持它。减肥或代谢手术干预已经显示出对初级预防癌症的一些初步有益效果,尽管得出明确的结论还为时过早。然而,减肥似乎提供了一定程度的初级预防,不仅对代谢和心血管疾病,而且对发展广泛的肿瘤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of obesity in cancer development
Being overweight has been a long-known peril to health, and scientists were able to show a relationship between body fat and cancer years ago. Of course, not every obese individual will inevitably develop cancer, but recent scientific studies show that excessive body fat has an impact on a much broader spectrum of cancers than previously thought. This applies to adults as well as children and adolescents. In 2015, the Organisation for Economic Co-operation and Development (OECD) reported that already > 50%of adults and nearly 30% of teenagers in 34 member countries were considered overweight (body mass index, BMI ≥ 25 kg/m2 body surface area), or even obese (BMI ≥30 kg/m2 body surface area). The tendency increased gradually in all countries over a period of 25 years (1990–2015).We therefore have to expect steadily rising numbers of cancers worldwide solely due to obesity in the future. A population-based study using BMI and cancer incidence data from the GLOBOCAN project estimated that, in 2012 in the United States, about 28,000 new cases of cancer in men (3.5%) and 72,000 in women (9.5%) were due to overweight or obesity. The percentage of cases attributed to overweight or obesity varied widely for different cancer types but was as high as 54% for gallbladder cancer in women and 44% for esophageal adenocarcinoma in men. The International Agency for Research on Cancer (IARC) as part of the World Health Organization (WHO) in 2016 reported an increased risk of cancer for at least 13 cancer types [colon cancer, esophageal cancer, renal carcinoma, uterine cancer, breast cancer (during and after menopause; also in men), liver cancer, pancreatic cancer, gall bladder cancer, ovarian cancer, gastric cancer, thyroid cancer, multiple myeloma, and meningioma]. For some of these cancers, the experts even found a dose-response relationship, implying that the risk of cancer increases with BMI. Currently, there are many theories that could explain the increased incidence of cancer in obesity. The preponderance of the evidence suggests that a combination of different factors might be responsible. However, it should be reiterated that there is no direct link between obesity and the development of cancer. On the one hand, obesity seems to cause a general hormonal imbalance including hyperinsulinemia and an increase in insulinlike growth factors, as well as sex hormones. In addition, hyperplastic and hypertrophic white adipose tissue (especially visceral adipose tissue) acts as an independent active endocrine organ releasing immunologically active adipokines and other hormones. These hormonal imbalances support cell growth– promoting processes. On the other hand, obesity is associated with a state of low-grade chronic inflammation. Insulin resistance and the metabolic syndrome are associated with higher circulating concentrations of inflammation-related markers, including leptin, interleukin-6, and tumor necrosis factor, many of which have been shown to enhance tumor growth. Chronic inflammation is a well-known, obesity independent critical component of tumor development and progression. Many cancers arise from sites of infection, chronic irritation, and inflammation. Obesity is only one of many important triggers of low-grade chronic inflammation, whereas per current literature there is no study published, that clearly shows that chronic inflammation is inversely related to the development of obesity. In addition, a further mechanism that suppresses the eradication of neoplastic cells is immune paralysis, which is also due to chronic inflammation. Not least, preclinical studies showed that adipocytic progenitor cells contribute to a tumor-promoting microenvironment as well. Controlled diet and lifestyle adjustments can lower the risk of cancer. It would be naive to believe that through a healthy diet and regular physical exercise, however, cancer development were to be prevented entirely. Could losing weight reduce the risk of cancer? So far, this has not been proven, although somepreliminary study results suggest it. However, the above results should still be interpreted with caution, as the published studies were too heterogenous in their design, the populations studied and different lengths of followup, so that it is too early at the moment, to make definitive recommendations. Reducing the excess weight once acquired, however, is difficult for many people. For most patients, making sure to at least not gain further weight is the first step. Likewise, people with normal weight should at least try to maintain it. Bariatric or metabolic surgical interventions have shown some initial beneficial effect for primary prevention of cancer, although it is far too early to draw definitive conclusions. Nevertheless, weight reduction seems to provide some degree of primary prophylaxis not only concerning metabolic and cardiovascular disease, but also for developing a wide array of neoplasms. Department of Pediatric Surgery, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany
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