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Key Points The International Agency for Research on Cancer has determined that, based on results from epidemiological studies, people who are overweight or obese are at increased risk of developing several cancer types, including adenocarcinoma of the oesophagus, colon cancer, breast cancer (in postmenopausal women), endometrial cancer and kidney (renal-cell) cancer. Epidemiological evidence also indicates that cancers of the liver, gallbladder and pancreas are obesity related, and that obesity might also increase risk for haematopoietic cancers and for aggressive prostate cancer. No association is seen between obesity and lung cancer. Results for other cancers have been inconsistent. Insulin resistance develops as a metabolic adaptation to increased levels of circulating free fatty acids released from adipose tissue, especially intra-abdominal adipose. Insulin resistance is generally compensated by increased pancreatic insulin secretion. There is mounting epidemiological and experimental evidence to indicate that chronic hyperinsulinaemia increases risk of cancers of the colon and endometrium, and probably other tumours (for example, of the pancreas and kidney). Serum levels of insulin-like growth factor 1 (IGF1) are also associated with different forms of cancer. However, there is no simple, direct relationship between circulating levels of IGF1 and the degree of adiposity. Circulating levels of oestrogens are strongly related to adiposity. For cancers of the breast (in postmenopausal women) and endometrium, the effects of overweight and obesity on cancer risk are largely mediated by increased oestrogen levels. In 4–8% of premenopausal women, obesity and ensuing insulin resistance can either cause or aggravate syndromes of ovarian androgen excess (polycystic ovary syndrome) and chronic progesterone deficiency. There is strong evidence that such syndromes, along with reduced progesterone production, increase the risk of endometrial cancer. Successful intervention strategies for weight loss and maintenance at the individual and community level are needed to reduce cancer risk. The prevalence of obesity is rapidly increasing globally. Epidemiological studies have associated obesity with a range of cancer types, although the mechanisms by which obesity induces or promotes tumorigenesis vary by cancer site. These include insulin resistance and resultant chronic hyperinsulinaemia, increased bioavailability of steroid hormones and localized inflammation. Gaining a better understanding of the relationship between obesity and cancer can provide new insight into mechanisms of cancer pathogenesis.

Excess weight increases the risk of death from all causes and from cardiovascular disease. Some evidence suggests that adiposity also increases the risk of death from cancer. This prospective study of more than 900,000 men and women confirms that obesity is a significant risk factor for death from cancer generally and from cancer in several specific sites. This study of more than 900,000 men and women confirms that obesity is a risk factor for death from cancer. The relations between excess body weight and mortality, not only from all causes but also from cardiovascular disease, are well established. 1 – 6 Although we have known for some time that excess weight is also an important factor in death from cancer, 7 our knowledge of the magnitude of the relation, both for all cancers and for cancers at individual sites, and the public health effect of excess weight in terms of total mortality from cancer is limited. Previous studies have consistently shown associations between adiposity and increased risk of cancers of the endometrium, kidney, gallbladder (in women), breast (in postmenopausal women), . . .

Background: The assessment of air pollution exposure using only community average concentrations may lead to measurement error that lowers estimates of the health burden attributable to poor air quality. To test this hypothesis, we modeled the association between air pollution and mortality using small-area exposure measures in Los Angeles, California. Methods: Data on 22,905 subjects were extracted from the American Cancer Society cohort for the period 1982-2000 (5,856 deaths). Pollution exposures were interpolated from 23 fine particle ($\\text{PM}_{2.5}$) and 42 ozone (O₃) fixed-site monitors. Proximity to expressways was tested as a measure of traffic pollution. We assessed associations in standard and spatial multilevel Cox regression models. Results: After controlling for 44 individual covariates, all-cause mortality had a relative risk (RR) of 1.17 (95% confidence interval = 1.05-1.30) for an increase of 10 μg/m³ $\\text{PM}_{2.5}$ and a RR of 1.11 (0.99-1.25) with maximal control for both individual and contextual confounders. The RRs for mortality resulting from ischemic heart disease and lung cancer deaths were elevated, in the range of 1.24-1.6, depending on the model used. These PM results were robust to adjustments for O₃ and expressway exposure. Conclusion: Our results suggest the chronic health effects associated with within-city gradients in exposure to $\\text{PM}_{2.5}$ may be even larger than previously reported across metropolitan areas. We observed effects nearly 3 times greater than in models relying on comparisons between communities. We also found specificity in cause of death, with $\\text{PM}_{2.5}$ associated more strongly with ischemic heart disease than with cardiopulmonary or all-cause mortality.

The relation between body weight and mortality remains controversial. Important unresolved questions concern the shape of the curve relating the two variables; the optimal weight for longevity; whether the optimal weight varies according to age, race, or sex; and whether the increased death rates often observed among very lean people are causal or an artifact of leanness due to smoking or concurrent illness. Debate about the potential hazards of excessive leanness has received disproportionate attention in a culture in which obesity is far more prevalent. Much of the vast literature examining the relation between body weight and mortality 1 – 16 supports . . .

Background: Few prospective studies have examined the health risks associated with use of snuff and chewing tobacco. Methods: We studied the association between the use of spit tobacco (snuff or chewing tobacco) and mortality among men enrolled in Cancer Prevention Study I (CPS-I) in 1959 or Cancer Prevention Study II (CPS-II) in 1982. Analyses were based on men who reported exclusive use of snuff or chewing tobacco (7745 in CPS-I, 3327 in CPS-II) or no previous use of any tobacco product (69,662 in CPS-I, 111,482 in CPS-II) at baseline. Twelve-year follow-up of CPS-I, and 18-year follow-up of CPS-II identified 11,871 and 19,588 deaths, respectively. Cox proportional hazards models were used to control for age and other covariates. Results: Men who currently used snuff or chewing tobacco at baseline had higher death rates from all causes than men who did not in both CPS-I (hazard ratio [HR] = 1.17,95% CI = 1.11-1.23) and CPS-II (HR = 1.18,95% CI = 1.08-1.29). In CPS-I, current use of spit tobacco was statistically significantly associated with death from coronary heart disease (CHD), stroke, and diseases of the respiratory, digestive, and genitourinary systems, but not with death from cancer. In CPS-II, use of these products was significantly associated with death from CHD, stroke, all cancers combined, lung cancer, and cirrhosis. The associations with cardiovascular and other non-malignant endpoints were attenuated, but not eliminated, by controlling for measured covariates. Former use of spit tobacco was not associated with any endpoint in CPS-II. No clear dose response was observed with either the frequency or duration of usage for any endpoint. Conclusions: These two prospective studies provide limited evidence that current use of chewing tobacco or snuff may increase mortality from heart disease and stroke.

Much of what is known about the deleterious effects of tobacco use on health was learned from epidemiologic studies over the last half century. These studies establish unequivocally that tobacco use, particularly manufactured cigarette smoking, causes most cancers of the lung, oropharynx, larynx, and esophagus in the USA, and approximately one-third of all cancers of the pancreas, kidney, urinary bladder and uterine cervix. More recent evidence also implicates smoking with cancers of the stomach, liver and colorectum. While over half of the estimated 440 000 smoking-attributable deaths that occur annually in the USA involve non-malignant cardiovascular and respiratory conditions, smoking-attributable cancers are more recognized and feared. Geneticists increasingly study tobacco use as a model for environmental carcinogenicity. Tobacco-exposed populations provide opportunities to characterize the somatic mutations that give rise to specific cancers and to identify the inherited genetic traits that confer susceptibility or resistance. Studies to identify the genetic determinants of addiction may be particularly important. Future research to identify other susceptibility factors, such as genes that modify carcinogen metabolism or DNA repair, will need to be substantially larger and to quantify lifetime tobacco exposure with more precision than have past studies in order to distinguish gradations in risk due to exposure from those caused by genetic susceptibility. This review considers: (a) the epidemiology of tobacco use; (b) cancers presently classified as smoking-attributable by the US Surgeon General; (c) the magnitude of the epidemic of cancers and other diseases caused by tobacco use; (d) selected issues in the epidemiology of lung cancer; and (e) the interface of genetics and epidemiology in understanding, preventing, and treating tobacco-attributable disease.

BACKGROUND:Body mass index (BMI) has been linked with both increased and decreased risk of suicide attempts and deaths. METHODS:In a prospective cohort study of 1.1 million adults, participants reported their anthropometric and other characteristics in 1982. Participants were followed for cause-specific mortality through 2004. RESULTS:A total of 2231 participants died of suicide during 21.6 million person-years of follow-up. Compared with a BMI of 18.5–22.9 kg/m, adjusted hazard ratios for completed suicide were 0.99 (95% confidence interval = 0.72–1.37), 0.78 (0.69–0.88), 0.73 (0.65–0.82), 0.72 (0.62–0.83), 0.77 (0.65–0.92), and 0.55 (0.36–0.83) for BMI values <18.5, 23.0–24.9, 25.0–27.4, 27.5–29.9, 30.0–34.9, and ≥35.0 kg/m, respectively. The relationship was consistent among men and women and across geographic regions, but was limited to married individuals (test for interaction, P = 0.009). CONCLUSIONS:The risk of death from suicide is inversely related to BMI in middle-aged and older adults.

Objective: Calcium, vitamin D, and dairy product intake may reduce the risk of colorectal cancer. We therefore examined the association between these factors and risk of colorectal cancer in a large prospective cohort of United States men and women. Methods: Participants in the Cancer Prevention Study II Nutrition Cohort completed a detailed questionnaire on diet, medical history, and lifestyle in 1992-93. After excluding participants with a history of cancer or incomplete dietary information, 60,866 men and 66,883 women remained for analysis. During follow-up through 31 August 1997 we documented 421 and 262 cases of incident colorectal cancers among men and women, respectively. Multivariate-adjusted rate ratios (RR) were calculated using Cox proportional hazards models. Results: Total calcium intake (from diet and supplements) was associated with marginally lower colorectal cancer risk in men and women (RR = 0.87, 95% CI 0.67-1.12, highest vs lowest quintiles, p trend = 0.02). The association was strongest for calcium from supplements (RR = 0.69, 95% CI 0.49-0.96 for ≥500 mg/day vs none). Total vitamin D intake (from diet and multivitamins) was also inversely associated with risk of colorectal cancer, particularly among men (RR = 0.71, 95% CI 0.51-0.98, p trend = 0.02). Dairy product intake was not related to overall risk. Conclusions: Our results support the hypothesis that calcium modestly reduces risk of colorectal cancer. Vitamin D was associated with reduced risk of colorectal cancer only in men.

Large prospective studies show a significant association with obesity for several cancers, and the International Agency for Research on Cancer has classified the evidence of a causal link as ‘sufficient’ for cancers of the colon, female breast (postmenopausal), endometrium, kidney (renal cell), and esophagus (adenocarcinoma). These data, and the rising worldwide trend in obesity, suggest that overeating may be the largest avoidable cause of cancer in nonsmokers. Few obese people are successful in long-term weight reduction, and thus there is little direct evidence regarding the impact of weight reduction on cancer risk. If the correlation between obesity and cancer mortality is entirely causal, we estimate that overweight and obesity now account for one in seven of cancer deaths in men and one in five in women in the US.

Objective: Epidemiologic evidence suggests a positive association between body mass, adult height, and postmenopausal breast cancer. However, most studies have not been large enough to examine the association across a very wide range of body mass or height, and few studies have assessed the relationship between body mass or height and postmenopausal breast cancer mortality. Methods: The relation between body mass index (BMI) and height and postmenopausal breast cancer mortality was examined in the American Cancer Society's Cancer Prevention Study II (CPS-II), a large prospective mortality study of US adults enrolled in 1982. After 14 years of follow-up, 2852 breast cancer deaths were observed among 424,168 postmenopausal women who were cancer-free at interview. Cox proportional hazards modeling was used to estimate relative risks and to control for potential confounding. Results: Breast cancer mortality rates increased continually and substantially with increasing BMI (rate ratio (RR) = 3.08, 95% confidence interval (CI) = 2.09-4.51 for BMI ≥ 40.0 compared to BMI 18.5-20.49). If causal, the multivariate-adjusted RR estimates in this study correspond to approximately 30-50% of breast cancer deaths among postmenopausal women in the US population being attributable to overweight. Breast cancer mortality also increased with increasing height up to 66 inches with RR = 1.64, (95% CI = 1.23-2.18) in women 66 inches tall compared to those <60 inches. Conclusions: Postmenopausal obesity is an important and potentially avoidable predictor of fatal breast cancer in this study. These results underscore the importance of maintaining moderate weight throughout adult life.