scholarly journals Obesity and cancer

2008 ◽  
Vol 67 (2) ◽  
pp. 128-145 ◽  
Author(s):  
Tobias Pischon ◽  
Ute Nöthlings ◽  
Heiner Boeing

The prevalence of obesity, defined as a BMI of ≥30·0 kg/m2, has increased substantially over previous decades to about 20% in industrialized countries, and a further increase is expected in the future. Epidemiological studies have shown that obesity is a risk factor for: post-menopausal breast cancer; cancers of the endometrium, colon and kidney; malignant adenomas of the oesophagus. Obese subjects have an approximately 1·5–3·5-fold increased risk of developing these cancers compared with normal-weight subjects, and it has been estimated that between 15 and 45% of these cancers can be attributed to overweight (BMI 25·0–29·9 kg/m2) and obesity in Europe. More recent studies suggest that obesity may also increase the risk of other types of cancer, including pancreatic, hepatic and gallbladder cancer. The underlying mechanisms for the increased cancer risk as a result of obesity are unclear and may vary by cancer site and also depend on the distribution of body fat. Thus, abdominal obesity as defined by waist circumference or waist:hip ratio has been shown to be more strongly related to certain cancer types than obesity as defined by BMI. Possible mechanisms that relate obesity to cancer risk include insulin resistance and resultant chronic hyperinsulinaemia, increased production of insulin-like growth factors or increased bioavailability of steroid hormones. Recent research also suggests that adipose tissue-derived hormones and cytokines (adipokines), such as leptin, adiponectin and inflammatory markers, may reflect mechanisms linked to tumourigenesis.

Author(s):  
Valentina Vicennati ◽  
Silvia Garelli ◽  
Eleonora Rinaldi ◽  
Sara Rosetti ◽  
Guido Zavatta ◽  
...  

AbstractEpidemiological studies have shown that overweight and cancer are closely related, even though obesity alone does not apparently heighten cancer risk by the same amount. Given the low overall risk of all cancers with obesity, it is unlikely that obesity alone causes cancer, but should instead be considered as a tumor promoter. There are three main hypotheses that could explain how obesity might contribute to cancer development and growth: the inflammatory cytokines from adipose tissue hypothesis, the insulin resistance and hyperinsulinemia hypothesis, and the unopposed estrogen cancer hypothesis. The link between obesity and cancer is that adipocytes constitute a major component of the tumor microenvironment for breast and abdominally metastasizing cancers, promoting tumor growth. This review will mainly focus attention on the relationship between adipose tissue, estrogens, and cancer risk.


Author(s):  
Andrea Booth ◽  
Aaron Magnuson ◽  
Josephine Fouts ◽  
Michelle Foster

AbstractAdipose tissue is a complex organ with endocrine, metabolic and immune regulatory roles. Adipose depots have been characterized to release several adipocytokines that work locally in an autocrine and paracrine fashion or peripherally in an endocrine fashion. Adipocyte hypertrophy and excessive adipose tissue accumulation, as occurs during obesity, dysregulates the microenvironment within adipose depots and systemically alters peripheral tissue metabolism. The term “adiposopathy” is used to describe this promotion of pathogenic adipocytes and associated adipose – elated disorders. Numerous epidemiological studies confirm an association between obesity and various cancer forms. Proposed mechanisms that link obesity/adiposity to high cancer risk and mortality include, but are not limited to, obesity-related insulin resistance, hyperinsulinemia, sustained hyperglycemia, glucose intolerance, oxidative stress, inflammation and/or adipocktokine production. Several epidemiological studies have demonstrated a relationship between specific circulating adipocytokines and cancer risk. The aim of this review is to define the function, in normal weight and obesity states, of well-characterized and novel adipokines including leptin, adiponectin, apelin, visfatin, resistin, chemerin, omentin, nesfatin and vaspin and summarize the data that relates their dysfunction, whether associated or direct effects, to specific cancer outcomes. Overall research suggests most adipokines promote cancer cell progression via enhancement of cell proliferation and migration, inflammation and anti-apoptosis pathways, which subsequently can prompt cancer metastasis. Further research and longitudinal studies are needed to define the specific independent and additive roles of adipokines in cancer progression and reoccurrence.


2016 ◽  
Vol 42 (5-6) ◽  
pp. 319-331 ◽  
Author(s):  
Myung Hoon Han ◽  
Jae Min Kim ◽  
Hyeong-Joong Yi ◽  
Jin Hwan Cheong ◽  
Yong Ko ◽  
...  

Background: The volume of intracerebral hemorrhage (ICH) measured at hospital admission is the strongest predictor of clinical outcomes in patients with ICH. Despite the high incidence rate of ICH in Asians, there is lack of data regarding predictors of ICH volume in this ethnic group. The purpose of this study was to determine predictors of deep ICH volume and examine their effect on short-term mortality in Asians. Methods: Hematoma volume was measured using the ABC/2 method. ICH volume was transformed to the natural log scale to normalize distributions for all analyses. We estimated the coefficients of ICH volume based on relevant predictors using multivariable linear regression. We also determined the association between body mass index (BMI) and ICH volume using a regression line and a line determined by a locally weighted scatter plot smoothing. Results: A total of 1,039 patients from 2 twin hospitals in Korea who were admitted with primary spontaneous supratentorial deep ICH over a 12-year period were enrolled in this study. The median ICH volume was 19.7 ml. The average patient age was 59.2, and 62.4% of patients were men. The mean ICH volume showed a gradual, approximately 2% decrease per 1 BMI increase in the current study, after adjusting for all relevant variables (β = -0.024; SE 0.004; p < 0.001). In addition, patients with frequent alcohol consumption showed a 10% increase in mean ICH volume (β = 0.098; SE 0.041; p = 0.016), and patients undergoing warfarin treatment showed a 30% increase in mean ICH volume after full adjustment of all relevant variables (β = 0.296; SE 0.050; p < 0.001). Relative to overweight patients, there was a 47, 11, and 18% increase in admission mean ICH volume in underweight, normal weight and obese patients, respectively. Patients in the first quartile and underweight BMI groups had 1.45-fold (hazard ratio (HR) 1.45; 95% CI 1.03-2.03; p = 0.035) and 1.77-fold (HR 1.77; 95% CI 1.10-2.84; p = 0.019) higher increased risk of death during the first 3 months after ICH, retrospectively. In addition, patients in groups with frequent alcohol consumption and warfarin use both showed a significant association with mortality 90 days after ICH. Conclusions: We demonstrated the association between various predictors and admission ICH volume with short-term mortality in Asians. Further studies are needed to account for these observations and determine their underlying mechanisms.


2021 ◽  
Vol 23 (1) ◽  
pp. 424
Author(s):  
Chiara Chiodo ◽  
Catia Morelli ◽  
Fabiola Cavaliere ◽  
Diego Sisci ◽  
Marilena Lanzino

Breast cancer prevention is a major challenge worldwide. During the last few years, efforts have been made to identify molecular breast tissue factors that could be linked to an increased risk of developing the disease in healthy women. In this concern, steroid hormones and their receptors are key players since they are deeply involved in the growth, development and lifetime changes of the mammary gland and play a crucial role in breast cancer development and progression. In particular, androgens, by binding their own receptor, seem to exert a dichotomous effect, as they reduce cell proliferation in estrogen receptor α positive (ERα+) breast cancers while promoting tumour growth in the ERα negative ones. Despite this intricate role in cancer, very little is known about the impact of androgen receptor (AR)-mediated signalling on normal breast tissue and its correlation to breast cancer risk factors. Through an accurate collection of experimental and epidemiological studies, this review aims to elucidate whether androgens might influence the susceptibility for breast cancer. Moreover, the possibility to exploit the AR as a useful marker to predict the disease will be also evaluated.


2008 ◽  
Vol 100 (08) ◽  
pp. 253-260 ◽  
Author(s):  
Jeanette Brosnan ◽  
John Bonnar ◽  
Jacqueline Conard ◽  
Cornelius Kluft ◽  
Margareta Hellgren ◽  
...  

SummaryEpidemiological studies have shown that hormone therapy (HT) increases the risk of venous thromboembolism in post menopausal women. The mechanism of this increased risk is unknown; however, activation of the haemostatic system is known to contribute to the pathogenesis of venous thromboembolism. In post-menopausal women the estrogen /progestogen composition of the HT can influence the level of haemostatic activation. It was the objective of this study to compare changes in inhibitors and activation markers of the haemostatic system in healthy post-menopausal women taking estradiol (2 mg) combined with dydrogesterone or a new progestin, trimegestone. A multicentre study of 186 women randomised to six months therapy with either estradiol (2 mg) +trimegestone (0.5 mg) or estradiol (2 mg) +dydrogesterone (10 mg) was performed. Antithrombin and protein S activity was decreased and activated protein C (APC) resistance, D-dimer and prothrombin fragment 1.2, were increased in both groups on treatment. Protein C activity was decreased and plasmin-antiplasmin complex was increased in the trimegestone group only. The increase in plasmin-antiplasmin complex and D-dimer was greater after six cycles of treatment in the trimegestone group compared with the dydro-gesterone group. In conclusion, decreased levels of inhibitors of blood coagulation and increased thrombin production were found in both groups however a greater increase in the levels of plasmin-antiplasmin complex and D-dimer was found in the tri-megestone group. This suggests an enhanced fibrinolytic response in this group. Further studies are required to determine the significance of this finding with respect to venous thrombosis risk.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mahdi Mahdavi ◽  
Atieh Amouzegar ◽  
Ladan Mehran ◽  
Elham Madreseh ◽  
Maryam Tohidi ◽  
...  

Abstract Background Due to the increasing worldwide prevalence of obesity, it is essential to determine the prevalence of obesity-related thyroid dysfunctions. The purpose of this study was to investigate the prevalence of thyroid dysfunctions, namely hypothyroidism and hyperthyroidism, and their association with BMI among adult Iranian overweight and obese individuals. Method This cross-sectional study was carried out within the framework of the Tehran Thyroid Study (TTS); 5353 participants (57.5% female) entered our study. Anthropometric measurements were performed. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and thyroid peroxidase antibody (TPOAb) were assayed. We categorized individuals into 3 BMI groups (normal-weight, overweight and obese), then calculated prevalence rate, odds ratio (OR), and 95% confidence interval (CI) for outcomes in overweight and obese groups. The normal-weight group was used as the control group. Results We found a higher prevalence of hypothyroidism (11.6% vs 8.2% Total, 4.0% vs 1.1% overt and 7.6% vs 7.1% subclinical, P < 0.001) and TPOAb positivity (17.3% vs 11.6%, P < 0.001) in obese participants compared with normal-weight participants. Hyperthyroidism’s overall prevalence was 4.2, 5.7, and 4.9% in obese, overweight, and normal-weight groups, respectively. Obesity was associated with higher odds of overt hypothyroidism (OR: 2.0, 95% CI: 1.15–3.49, P < 0.05) and TPOAb positivity (OR: 1.29, 95% CI: 1.04–1.60, P < 0.05) after adjusting for confounding variables. In contrast, no association was observed between the overweight group and the odds of hypothyroidism and TPOAb positivity in the adjusted results. Conclusions Obesity was associated with an increased risk of overt hypothyroidism and TPOAb positivity.


2008 ◽  
Vol 159 (suppl_1) ◽  
pp. S59-S66 ◽  
Author(s):  
Eve Van Cauter ◽  
Kristen L Knutson

Sleep is an important modulator of neuroendocrine function and glucose metabolism in children as well as in adults. In recent years, sleep curtailment has become a hallmark of modern society with both children and adults having shorter bedtimes than a few decades ago. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity. There is rapidly accumulating evidence from both laboratory and epidemiological studies to indicate that chronic partial sleep loss may increase the risk of obesity and weight gain. The present article reviews laboratory evidence indicating that sleep curtailment in young adults results in a constellation of metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, elevated sympathovagal balance, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. We also review cross-sectional epidemiological studies associating short sleep with increased body mass index and prospective epidemiological studies that have shown an increased risk of weight gain and obesity in children and young adults who are short sleepers. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity.


2017 ◽  
Vol 41 (S1) ◽  
pp. S585-S585
Author(s):  
R. Denman ◽  
V. Chester ◽  
J. Watson ◽  
C. Nyakunuwa ◽  
R. Alexander

BackgroundInpatient mental health settings have been described as “obesogenic” environments, due to factors including psychotropic medication, high calorie food, restricted physical activity and sedentary lifestyles. No research has investigated obesity among forensic intellectual disability inpatients, despite this populations’ increased risk. Therefore, this paper aims to evaluate the prevalence and correlates of overweight and obesity on, and during admission.MethodThe weight and body mass index data of 46 inpatients (15 women and 31 men) within a specialist intellectual disability forensic service was examined for the study.ResultsOnly six patients (13%) were a normal weight at admission, whereas 40 (87%) were overweight or obese. During their admission, 28 (61%) gained weight (average 11.8 kg), and one (2%) maintained. However, 17 patients (37%) lost weight (average 6.2 kg), though 16 remained in overweight/obese categories. There was no correlation between length of stay and weight/BMI.ConclusionsThe majority of patients were overweight or obese on admission, and approximately 60% gained weight during their admission. Women appeared at greater risk of obesity. There was no relationship between length of stay and weight. This is potentially due to the high prevalence of obesity on admission and the impact of previous admissions on weight. The results highlight the need for effective weight management interventions with this population.Disclosure of interestThe authors have not supplied their declaration of competing interest.


1998 ◽  
Vol 91 (8) ◽  
pp. 402-407 ◽  
Author(s):  
Martin Mckee ◽  
Annie Britton

Research into the effect of alcohol on cardiovascular disease has indicated protective effects from moderate consumption. These observations, made in industrialized countries, have influenced policies on alcohol in countries where the situation may be quite different—specifically, where consumption is substantially higher or patterns of drinking are different. In central and eastern Europe and the former Soviet Union, a growing body of epidemiological research indicates a positive rather than negative association between alcohol consumption and cardiovascular deaths, especially sudden cardiac deaths. By means of a systematic review of published work, we examine whether there is a physiological basis for the observed association between alcohol and heart disease seen in eastern Europe, focusing on the effects of high levels of consumption and of irregular or binge drinking. In binge drinkers, cardioprotective changes in high-density lipoproteins are not seen, and adverse changes in low-density lipoproteins are acquired. Irregular drinking is associated with an increased risk of thrombosis, occurring after cessation of drinking. It predisposes both to histological changes in the myocardium and conducting system and to a reduction in the threshold for ventricular fibrillation. Measures of frequency as well as quantity of consumption should be included in epidemiological studies. Taken with the epidemiological evidence emerging from eastern Europe, these observations have important implications for estimates of the burden of disease attributable to alcohol.


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