Fat distribution and cancer risk -
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This work was supported by the United States Public Health Service Grants R01CA PI: X-O Shu , R37CA PI: W Zheng and R01CA PI: G Yang. We also thank Ms Bethanie Rammer for her assistance in preparing the manuscript. Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA. You can also search for this author in PubMed Google Scholar. Correspondence to G Yang.
Reprints and permissions. Li, H. et al. Int J Obes 37 , — Download citation. Received : 02 May Revised : 09 July Accepted : 16 August Published : 18 September Issue Date : June Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article.
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Subjects Colorectal cancer Epidemiology Obesity. Abstract OBJECTIVE: The objective was to evaluate the association of body size and fat distribution with the risk of colorectal cancer CRC in Chinese men and women.
DESIGN: This was a population-based, prospective cohort study. RESULTS: A total of incident CRC cases were identified. Access through your institution. Buy or subscribe. Change institution. Learn more. References Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Google Scholar Gao Y, Lu W.
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Article CAS Google Scholar Hotamisligil GS. Article CAS Google Scholar Ullman TA, Itzkowitz SH. In addition, the amount of fat stored in different compartments, as well as the rates of most cancers, is known to differ between females and males. These facts motivated a careful sex-stratified analysis of adiposity-related cancer risk.
For their study the investigators turned to data from , participants in the UK Biobank, a cross-sectional cohort of , U. residents aged between 37 and 73, who were recruited between and and then followed for a mean time of Among the data collected from participants in the database were details about the distribution of fat in their bodies and whether they developed cancer.
They found that all cancer types, except brain, cervical, and testicular cancers are associated with at least one obesity-related trait.
In female patients, the strongest links between overall fat accumulation and cancer were in gallbladder cancer, endometrial cancer, and esophageal adenocarcinoma. In males, the strongest links between overall fat accumulation and cancer were in breast cancer, hepatocellular carcinoma, and renal cell carcinoma.
In terms of fat accumulation and distribution, there were differential effects between sexes on colorectal, esophageal, and liver cancer.
For instance, a larger proportion of fat stored in the abdomen was associated with esophageal squamous cell carcinoma in females, but not in males. Additionally, body fat accumulation was associated with a high risk for hepatocellular carcinoma in males, an effect that was not present in females.
They explained that their findings may differ from or may not be applicable to other ethnicities. They also acknowledged that because participants were older, the results are likely not directly transferable to younger populations.
In its more aggressive forms, NAFLD can drive inflammation and hepatic tissue damage by increasing endoplasmic reticulum stress, elevating production of reactive oxygen species increased oxidative stress , and higher inflammation.
Body fatness is associated with host chronic inflammation and insulin resistance and may contribute to the hepatic dysfunction underlying this relationship. Obesity is associated with increased levels of pro-inflammatory cytokines for example TNF-alpha and IL-6 and insulin, which can promote hepatocyte growth and malignant transformation through activation of the oncogenic transcription factor Signal Transducer and Activator of Transcription The resulting chronic liver injury due to chronic inflammatory processes can promote compensatory hepatocyte injury, death, tissue remodeling and regeneration, which has been shown in animal models to be a necessary factor for liver cancer development.
Animal studies also suggest that gut bacterial dysbiosis within the context of NAFLD may also propagate liver injury. Adult body fatness and colorectal cancer. Higher body fatness is associated with changes in hormonal profiles, such as increased levels of insulin, which can promote the growth of colon cancer cells and inhibit apoptosis.
Higher serum concentrations of insulin and IGF-1 have been linked to greater risk of colorectal cancer in human and experimental studies. Overall, there are convincing mechanistic data supporting a link between body fatness and colorectal cancer. Adult body fatness and post-menopausal cancer.
Body fatness directly affects levels of several circulating hormones, such as insulin and oestrogens, creating an environment that promotes carcinogenesis and suppresses apoptosis. In postmenopausal women, when the production of oestrogens from the ovaries has dramatically declined, the main source of oestrogens is from the conversion of androgens within the adipose tissue.
Consequently, overweight and obese women have higher circulating levels of oestrogens, which are well known to be associated with the development of breast cancer.
Other sex steroid hormones, including androgens and progesterone, are also likely to play a role in the relationship between obesity and breast cancer.
Elevated body fatness is also associated with hyperinsulinemia and insulin resistance, and greater circulating insulin levels have been linked to breast cancer risk. Insulin could promote breast tumour growth directly by binding to its receptor or to the IGF-I insulin-like growth factor-I receptor or indirectly by inhibiting the synthesis of sex-hormone binding globulin, which sequesters oestrogens in circulation, contributing to higher levels of bioavailable oestrogens.
Obesity is also associated with a low-grade chronic inflammatory state. Adipose tissue in obese individuals secretes pro-inflammatory cytokines and adipokines, which can promote development of breast cancer, as shown in experimental studies and more recently in epidemiological studies.
Adult body fatness and endometrial cancer. Excess body fatness increases bioavailable oestrogen levels that have been shown, when not counterbalanced by progesterone, to increase endometrial tissue mitotic activity and therefore promote endometrial carcinogenesis.
Higher insulin levels associated with excess body fatness are associated with greater risk of endometrial cancer. Insulin has been shown to enhance endometrial tumour growth either directly by binding to the insulin or to the IGF-I receptors or indirectly by inhibiting the synthesis of sex hormone binding globulin and thereby increasing oestrogen bioavailability.
Obesity-related chronic inflammation has also been specifically linked to development of endometrial cancer. Adult body fatness and kidney cancer. The vast array of epidemiological studies using diverse measures of obesity, such as weight, BMI or waist-hip ratio as well as increases in adult weight, all show similar positive associations with the risk of renal cell cancer and likely share common mechanisms.
Body fatness is a systemic process affecting host metabolism, as well as many components of the endocrine system or microenvironment, that may affect kidney carcinogenesis. For example, obesity is associated with raised levels of mitogenic and anti-apoptotic growth factors such as insulin or bioactive IGF-1 that may promote the carcinogenic process.
Higher concentrations of adiponectin, a protein secreted by adipose tissue that is inversely related to body fatness, have been associated with lower risk of kidney cancer.
In vitro experimental studies have shown that adiponectin inhibits cellular proliferation and promotes apoptosis. Obesity increases the risk of metabolic syndrome, which includes hypertension and obesity, both of which are associated with a greater risk for renal cancer.
Obesity is associated with a chronic inflammatory state that may alter susceptibility to cancer or promote carcinogenesis. Adult body fatness and cancers of the mouth, pharynx and larynx.
Specific mechanisms to support the relationship between body fatness and mouth, pharynx and larynx cancers have not been proposed to date. However, greater body fatness is associated with metabolic and endocrine abnormalities such as hyperinsulinemia and elevated levels of bioavailable oestrogen, and in other tissues, insulin and oestrogen have been shown to stimulate mitogenesis and inhibit apoptosis, leading to enhanced cellular proliferation.
Obesity has also been shown to stimulate the inflammatory response, which may also promote tumorigenesis. Further research on the mechanisms underlying the link between obesity and cancers of the mouth, pharynx and larynx is needed.
Adult body fatness and stomach cancer cardia. Being overweight and obese is also associated with higher levels of insulin, which can act as a mitogen and has anti-apoptotic properties and therefore may represent a mechanism, though there are limited data to support this hypothesis to date. Obesity has also been shown to stimulate the inflammatory response, which may promote tumorigenesis.
Adult body fatness and gallbladder cancer. The mechanisms underlying the positive association of body fatness with gallbladder cancer development are likely to be similar to those proposed for other anatomical sites, namely development of metabolic syndrome and its components, such as hyperglycemia, dyslipidemia, hyperinsulinemia and hypertension.
Chronic inflammation, production of growth factors and increased levels of pro-inflammatory cytokines are also possible cancer-promoting consequences of increased body fatness.
Interestingly, body fatness and metabolic syndrome appear to be associated with increased risk of gallstones, which has been observed as a major risk factor for gallbladder cancer development in various populations, likely through promotion of increased chronic inflammation at this site.
The stronger association of body fatness with gallbladder cancer in women than in men may in part be due to adverse effects of female sex hormones on hepatic bile secretion and gallbladder function.
Adult body fatness and ovarian cancer. Greater body fatness is associated with higher circulating levels of endogenous oestrogens and androgens, and these hormones are associated, albeit inconsistently, with higher risk of ovarian cancer.
Adipose tissue is also a source of adipokines and inflammatory cytokines that promote a low-grade inflammatory milieu, and both local and systemic pro-inflammatory factors are associated with development of ovarian cancer.
Adult body fatness and advanced prostate cancer. Greater body fatness is associated with higher risk of advanced prostate cancer.
Several biological mechanisms have been proposed that link adiposity to cancer, including dysregulated sex steroid metabolism, hyperinsulinemia and elevated levels of proinflammatory cytokines; however, the evidence linking these pathways specifically to prostate cancer is limited.
Androgens such as testosterone play critical roles in the development and function of the prostate gland. It has been hypothesised that a hypoandrogenic environment promotes the development of higher-grade prostate tumours, and at least two prospective studies have reported inverse relationships between serum testosterone levels and higher-grade prostate cancer.
Testosterone levels tend to be lower in obese males than in those of normal weight and therefore may represent a potential mediator of the body fatness-advanced prostate cancer relationship.
Hyperinsulinemia has been shown to accelerate tumour growth in prostate cancer xenograft models, and human prostate tumours commonly express the insulin receptor, suggesting that insulin may stimulate prostate cancer growth.
Background: Canncer obesity has been linked to an increased risk of colorectal cancer Muscle building exercises without weightsthe risk distribuiton with long-term status or Hypertension and migraines distribhtion body ristribution distribution has not been fully Hypertension and migraines. Tisk High waist circumference, hip circumference and waist-to-hip ratio were all associated with a higher CRC risk in men, even after adjusting for body mass index. The association was attenuated to null in women after adjusting for body mass index. This association appeared to be independent of weight change. Conclusions: Abdominal adiposity, independent of overall obesity, is associated with an increased CRC risk in men but not in women. Yang CaoBin XiaZhen ZhangAmd Hu Hypertension and migraines, Yoga poses to reduce bloating HuangJinqiu Rksk Protein sources, Fangping Hypertension and migraines Distriubtion of Body Fat Distribution and Risk of Breast Cancer rlsk Pre- and Distibution Women. Obes Facts 10 August cacer 16 4 : — Introduction: Obesity is a risk factor for both the development of and mortality from breast cancer in postmenopausal but not in premenopausal women. However, which part of the fat mass is associated with risk remains unclear, and whether the difference in the risk for breast cancer is associated with discrepancy in the distribution of fat with menstrual status requires further study. Methods: A dataset from the UK Biobank, which includedfemale participants and 5, females who developed breast cancer during a mean follow-up of 6. Body fat mass was measured according to bioelectrical impedance at baseline by trained technicians.
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