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E Giovannucci

Publications and source records attributed to E Giovannucci.

At least 37 records · Page 2Linked to original sources
PubMed2001

A prospective study on intake of animal products and risk of prostate cancer.

OBJECTIVE: Association between animal products and prostate cancer have been observed in numerous observational studies, but it is not clear whether the high fat content of these foods or some other component accounts for these associations. We examine these associations among 51,529 men who contributed detailed dietary data. METHODS: Participants of the Health Professionals Follow-Up Study completed a semiquantitative food-frequency questionnaire in 1986, and subsequently in 1990 and 1994. Other data on potential risk factors were collected at baseline and in subsequent questionnaires during follow-up. Between 1986 and 1996, 1897 total cases of prostate cancer (excluding stage A1) and 249 metastatic cancers were identified. We used pooled logistic regression for analyses of diet and prostate cancer. RESULTS: Intakes of total meat, red meat, and dairy products were not associated with risk of total or advanced prostate cancer. An elevated risk for metastatic prostate cancer was observed with intake of red meat (relative risk (RR)= 1.6 for top vs. bottom quintile comparison, 95% confidence interval (CI) = 1.0-2.5); this association was slightly attenuated after controlling for saturated and alpha-linolenic fatty acids (RR = 1.5, 95% CI = 0.88-2.5). Processed meats, bacon and beef, pork or lamb as a main dish each contributed to an elevated risk of metastatic prostate cancer. Dairy product intake increased risk of metastatic prostate cancer (RR = 1.4, 95% CI = 0.91-2.2 for top vs. bottom quintile comparison), but no association remained after controlling for calcium and other fatty acids. A high intake in both red meat and dairy product was associated with a statistically significant two-fold elevation in risk of metastatic prostate cancer, compared to low intake of both products; however, most of the excess risk could be explained by known nutritional components of these foods. CONCLUSIONS: Intakes of red meat and dairy products appear to be related to increased risk of metastatic prostate cancer. While known nutrients, such as calcium and fatty acids, may explain most of the dairy association observed, it appears that a portion of the risk of metastatic prostate cancer associated with red meat intake remains unexplained.

Adult↗
PubMed2001

Insulin, insulin-like growth factors and colon cancer: a review of the evidence.

Insulin and insulin-like growth factor (IGF) axes are major determinants of proliferation and apoptosis and thus may influence carcinogenesis. In various animal models, modulation of insulin and IGF-1 levels through various means, including direct infusion, energy excess or restriction, genetically induced obesity, dietary quality including fatty acid and sucrose content, inhibition of normal insulin secretion and pharmacologic inhibition of IGF-1, influences colonic carcinogenesis. Human evidence also associates high levels of insulin and IGF-1 with increased risk of colon cancer. Clinical conditions associated with high levels of insulin (noninsulin-dependent diabetes mellitus and hypertriglyceridemia) and IGF-1 (acromegaly) are related to increased risk of colon cancer, and increased circulating concentrations of insulin and IGF-1 are related to a higher risk of colonic neoplasia. Determinants and markers of hyperinsulinemia (physical inactivity, high body mass index, central adiposity) and high IGF-1 levels (tall stature) are also related to higher risk. Many studies indicate that dietary patterns that stimulate insulin resistance or secretion, including high consumption of sucrose, various sources of starch, a high glycemic index and high saturated fatty acid intake, are associated with a higher risk of colon cancer. Although additional environmental and genetic factors affect colon cancer, the incidence of this malignancy was invariably low before the technological advances that rendered sedentary lifestyles and obesity common, and increased availability of highly processed carbohydrates and saturated fatty acids. Efforts to counter these patterns are likely to have the most potential to reduce colon cancer incidence, as well as cardiovascular disease and diabetes mellitus.

Acromegaly↗
PubMed2001

Risk of bladder cancer by geographic region in a U.S. cohort of male health professionals.

Large regional variations in bladder cancer rates have been observed for numerous decades in the United States and persist to date. We examined the incidence rates of bladder cancer by geographic region among U.S. male health professionals to determine whether diet or other lifestyle factors can account for variations observed. During 12 years of follow-up, 328 cases of bladder cancer were diagnosed in the Health Professionals Follow-up Study cohort. We inquired about diet, lifetime history of smoking, race, marital status, and other nondietary factors using mailed questionnaires. An elevated risk of bladder cancer was observed in the Northeast compared with the West [relative risk (RR) = 1.71, 95% confidence interval (CI) = 1.23-2.39], which was slightly attenuated after controlling for smoking (RR = 1.65, 95% CI = 1.18-2.30). Smoking patterns, diet, and other lifestyle factors could not account for all of the elevated bladder cancer risk in the Northeast. Bladder cancer risk was highest among men who had a long residency in the Northeast compared with a long residency in the West (RR = 1.77, 95% CI = 1.15-2.71, adjusted for smoking). Diet and other known characteristics do not appear to be responsible for the regional variations in bladder cancer rates in the United States.

Adult↗
PubMed2001

Coffee and alcohol consumption and the risk of pancreatic cancer in two prospective United States cohorts.

Although most prospective cohort studies do not support an association between coffee consumption and pancreatic cancer, the findings for alcohol are inconsistent. Recently, a large prospective cohort study of women reported statistically significant elevations in risk of pancreatic cancer for both coffee and alcoholic beverage consumption. We obtained data on coffee, alcohol, and other dietary factors using semiquantitative food frequency questionnaires administered at baseline (1986 in the Health Professionals Follow-Up Study and 1980 in the Nurses' Health Study) and in subsequent follow-up questionnaires. Data on other risk factors for pancreatic cancer, including cigarette smoking, were also available. Individuals with a history of cancer at study initiation were excluded from all of the analyses. During the 1,907,222 person-years of follow-up, 288 incident cases of pancreatic cancer were diagnosed. The data were analyzed separately for each cohort, and results were pooled to compute overall relative risks (RR). Neither coffee nor alcohol intakes were associated with an increased risk of pancreatic cancer in either cohort or after pooling the results (pooled RR, 0.62; 95% confidence interval, 0.27-1.43, for >3 cups of coffee/day versus none; and pooled RR, 1.00; 95% confidence interval, 0.57-1.76, for > or = 30 grams of alcohol/day versus none). The associations did not change with analyses examining different latency periods for coffee and alcohol. Similarly, no statistically significant associations were observed for intakes of tea, decaffeinated coffee, total caffeine, or alcoholic beverages. Data from these two large cohorts do not support any overall association between coffee intake or alcohol intake and risk of pancreatic cancer.

Adult↗
PubMed2001

An updated review of the epidemiological evidence that cigarette smoking increases risk of colorectal cancer.

Carcinogens from tobacco reach the colorectal mucosa through either the alimentary tract or the circulatory system and could possibly damage or alter expression of important cancer-related genes. Twenty-one of 22 studies found that long-term, heavy cigarette smokers have a 2-3-fold elevated risk of colorectal adenoma. Risk of large adenomas, immediate cancer precursors, was elevated in smokers in 12 of 12 studies. The studies of smoking and colorectal cancer risk conducted earlier in the twentieth century consistently did not show any association. However, 27 studies in various countries, including the vast majority of those that have been analyzed in the past several years, now show an association between tobacco use and colorectal cancer. In the United States, 15 of 16 studies conducted after 1970 in middle-age men and elderly men and, in the 1990s, in women demonstrate an association. This temporal pattern is consistent with an induction period of three to four decades between genotoxic exposure and the diagnosis of colorectal cancer and with men as a group having begun smoking several decades earlier than women. Overall, accumulating evidence, much within the past decade, strongly supports the addition of colorectal cancer to the list of tobacco-associated malignancies and the possibility that up to one in five colorectal cancers in the United States may be potentially attributable to tobacco use.

Adenoma↗
PubMed2001

The relationship between a polymorphism in CYP17 with plasma hormone levels and prostate cancer.

The A2 allele of the CYP17 gene has been thought to be associated with increased functional activity of this steroidogenic enzyme. Consequently, the A2 allele has been examined as a biomarker of individual susceptibility to hormone-related diseases among men and women. We prospectively assessed the association between the A2 allele of CYP17 and prostate cancer risk among 590 cases and 782 controls in a case-control study nested within the Physicians' Health Study cohort. We also evaluated associations between CYP17 genotype and plasma steroid hormones among controls and the potential interaction between CYP17 and SRD5A2 V89L polymorphisms in relationship with prostate cancer risk and circulating steroid hormone levels. We observed a borderline significant association between the A2 allele and prostate cancer risk (odds ratio, 1.23; 95% confidence interval, 0.99-1.54), however, we did not observe evidence of a gene-dosage effect (versus A1/A1 genotype: A1/A2 genotype; odds ratio, 1.26; 95% confidence interval, 0.99-1.59; A2/A2 genotype: odds ratio, 1.17; 95% confidence interval, 0.85-1.61). The A2 allele was not overrepresented among cases with advanced prostate cancer. Among controls, carriers of the A2 allele had steroid hormone levels similar to noncarriers. We also found no evidence of a gene-gene interaction between CYP17 and SRD5A2 V89L polymorphisms on prostate cancer risk or endogenous steroid hormone levels. These results suggest that CYP17 genotype may possibly confer a small increased susceptibility to prostate cancer but is not a strong predictor of endogenous steroid hormone levels in men.

Adult↗
PubMed2001

The impact of cancer treatment on quality of life outcomes for patients with localized prostate cancer.

PURPOSE: We evaluated the impact of localized prostate cancer treatment on general, cancer specific and symptom domains of quality of life for up to 5 years after diagnosis. MATERIALS AND METHODS: A total of 842 men from the Health Professionals Followup Study, diagnosed between 1993 and 1998, were included in cross-sectional analyses of quality of life associated with prostate cancer treatment. A subset of 146 men diagnosed after 1995 were followed prospectively. Quality of life was assessed with the Medical Outcomes Study Short-Form 36 Health Status Survey, Cancer Rehabilitation Evaluation System Short Form and University of California Los Angeles Prostate Cancer Index by mailed questionnaires. Primary treatment modality was taken from medical records and patient self-report. RESULTS: Significant treatment differences were observed in all quality of life measures, with the largest occurring in sexual, urinary and bowel symptoms. Bowel function was significantly worse in patients who received external radiation and brachytherapy compared with prostatectomy (p <0.05). Although they had better or equivalent urinary and sexual function (p <0.05), patients treated with external radiation, hormones or watchful waiting had lower generic quality of life scores in multiple domains compared with those who underwent prostatectomy. Patients who had brachytherapy had similar generic quality of life outcomes compared with prostatectomy in all domains. CONCLUSIONS: Our findings suggest that important differences in quality of life go beyond known physical symptoms associated with various prostate cancer treatment options, many of which involve making a trade-off. It is important for patients with prostate cancer and health care providers to consider these differences while making treatment decisions.

Adult↗
PubMed2000

Racial variation in prostate cancer incidence and in hormonal system markers among male health professionals.

BACKGROUND: Racial variation in prostate cancer incidence in the United States is pronounced, with African-American men having the highest rates. Whether differences in the distribution of known or suspected risk factors among racial groups explain this variation is unknown. METHODS: We evaluated prospectively the relation between prostate cancer and race among 45 410 U.S. male health professionals aged 40--75 years in 1986. We used multivariable, pooled logistic regression to adjust the rate ratio (RR) for potential dietary and lifestyle risk factors. We also measured circulating levels of steroid hormones, sex hormone-binding globulin, and vitamin D metabolites and length of the androgen receptor gene CAG repeat in a sample of African-American (n = 43), Asian (n = 52), and white (n = 55) participants and assessed variation by race in these possible prostate epithelial cell growth mediators by use of analysis of variance. Statistical tests were two-sided. RESULTS: The age-adjusted RR for prostate cancer was 1.73 (95% confidence interval [CI] = 1.23--2.45) for African-American men compared with white men. After multivariate adjustment, the RR increased to 1.81 (95% CI = 1.27--2.58). The rate of prostate cancer did not differ between Asians and whites. Steroid hormone and 1,25-dihydroxyvitamin D levels did not vary appreciably by race. However, the mean number of androgen receptor gene CAG repeats was lower among African-Americans (mean +/- standard deviation = 20.1 +/- 3.5) than among whites (22.1 +/- 3.1; P =.007) and Asians (22.1 +/- 3.9; P =.009). CONCLUSIONS: Our results confirm the elevated incidence of prostate cancer among African Americans and show that it is not explained by differences in the distribution of possible dietary and lifestyle risk factors in this cohort. Racial variation in length of the androgen receptor gene CAG repeat may explain a small part of the excess risk of prostate cancer among African-American men in this cohort.

Adult↗
PubMed2000

Prospective study of dietary supplements, macronutrients, micronutrients, and risk of bladder cancer in US men.

Data derived from laboratory investigations suggest that a number of dietary variables may contribute to bladder carcinogenesis. Although bladder cancer is the fourth leading cause of cancer in men in the United States, dietary studies are few. The authors examined the relations between intakes of macro- and micronutrients and the risk of bladder cancer among men in the prospective Health Professionals Follow-Up Study. Each participant completed a 131-item food frequency questionnaire in 1986 and in 1990, from which nutrient intakes were calculated. During 12 years of follow-up, 320 cases of bladder cancer were diagnosed. No association was observed for total caloric or macronutrient intake and bladder cancer risk. Similarly, we found no relation for dietary intake of potassium, sodium, calcium, magnesium, phosphorus, iron, or water-soluble vitamins and bladder cancer risk. Total vitamin E intake and vitamin E supplements were inversely associated with risk. In addition, a dose-response relation was observed for duration of vitamin E supplement use. A suggestive inverse association was seen with dose of vitamin C supplement use. More studies are needed to determine the role of vitamins E and C supplement intake in bladder carcinogenesis.

Adult↗
PubMed2000

Adiposity and mortality in men.

The relation between measures of adiposity and mortality has been a controversial topic. The authors examined prospectively the relation between several measures of adiposity and risks of overall and cause-specific mortality in 39,756 US men aged 40-75 years. During 10 years of follow-up (1986-1996), 1,972 deaths (747 from cancer, 423 from cardiovascular disease, and 802 from other causes) were documented. An elevated risk of death among the leanest men was partly accounted for by excess mortality during early follow-up and high mortality among those with a history of recent weight loss. After exclusion of men with substantial recent weight loss and deaths occurring during the first 4 years of follow-up, overall and cardiovascular disease mortality among men aged <65 years increased linearly with greater body mass index (BMI) (weight (kg)/height (m)2); multivariate relative risks for overall mortality were 1.0 (referent) for a BMI of <23, 1.21 for a BMI of 23-24.9, 1.19 for a BMI of 25-26.9, 1.39 for a BMI of 27-29.9, and 1.97 for a BMI of >30 (test for trend: p< 0.001). Among men aged > or =65 years, there were no significant relations between BMI and overall, cardiovascular disease, or cancer mortality risk. However, waist circumference strongly predicted risk of death from cardiovascular disease among the older men. These findings indicated that the relation between body fat and mortality was influenced by reverse causation and varied by age.

Adipose Tissue↗
PubMed2000

Proportion of colon cancer risk that might be preventable in a cohort of middle-aged US men.

OBJECTIVE: Diet and lifestyle likely play major roles in colon cancer incidence; however, the proportion of colon cancer risk that might be preventable is unknown. Thus, we estimated the proportion of colon cancer risk among men in the prospective Health Professionals Follow-up Study that might be attributable to a constellation of modifiable risk factors, and thus might be preventable. METHODS: We included 47,927 men aged 40-75 years in 1986, among whom we confirmed 411 colon cancer cases from 1986 to 1996. Risk factors considered were obesity, physical inactivity, alcohol consumption, early adulthood cigarette smoking, red meat consumption, and low intake of folic acid from supplements. We calculated a risk score that was the sum across the six risk factors of the values of 1 (better exposure) to 5 (worse exposure) corresponding to the exposure category. We entered the risk score into a logistic regression model and estimated the population attributable risk percent (PAR%) using the method of Bruzzi et al. RESULTS: After adjusting for age and family history of colorectal cancer and comparing the risk score for the combined six modifiable colon cancer risk factors at or above the approximate 20th, 10th, or 5th percentiles vs. below, the PAR% increased from 39% (95% confidence interval (CI) = 23-58%), to 48% (95% CI = 25-71%), to 55% (95% CI = 27-80%), respectively. Using a second method in which we used cut-points consistent with general-good health behaviors for each risk factor, comparing men with at least one risk factor to men without any risk factors (3.1% of the men), the PAR% was 71% (95% CI = 33-92%). CONCLUSION: The findings from this analysis suggest that, if all the members of this cohort of middle-aged US men had a modifiable exposure distribution comparable to the men with low risk scores, a large proportion of colon cancer risk might be avoidable. Additional study is required to determine whether making changes in these six risk factors now would reduce the risk of colorectal neoplasia, or whether the proportion of colon neoplasia that might be avoidable would be similar in populations with different characteristics.

Adenoma↗
PubMed2000

Diet and basal cell carcinoma of the skin in a prospective cohort of men.

BACKGROUND: Low intake of fat and high intake of specific vitamins have been hypothesized to reduce risk of basal cell carcinoma of the skin (BCC). OBJECTIVE: Our objective was to examine intakes of fat, antioxidant nutrients, retinol, folate, and vitamin D in relation to risk of BCC. DESIGN: In 1986, diet was assessed by a validated food-frequency questionnaire in 43217 male participants of the Health Professionals Follow-up Study who were 40-75 y of age and free of cancer. During 8 y of follow-up, we ascertained 3190 newly diagnosed cases of BCC. RESULTS: Total fat consumption was associated with a lower risk of BCC [relative risk (RR): 0.81; 95% CI: 0.72, 0.90 for the highest compared with the lowest quintile of intake; P for trend < 0.001). Simultaneous modeling of specific fatty acids suggested that this inverse association was limited to monounsaturated fat (RR: 0.79; 95% CI: 0.65, 0.96; P for trend = 0. 02); saturated and polyunsaturated fat were not associated with BCC risk. Folate intake was associated with a slightly higher risk of BCC (RR: 1.19; 95% CI: 1.01, 1.40; P for trend = 0.11), whereas alpha-carotene was associated with a slightly lower risk (RR: 0.88; 95% CI: 0.79, 0.99; P for trend = 0.01). Intakes of long-chain n-3 fatty acids, retinol, vitamin C, vitamin D, or vitamin E were not materially related to BCC risk. CONCLUSIONS: These findings do not support the hypothesis that diets low in fat or high in specific vitamins lower risk of BCC.

Adult↗