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A Schatzkin

Publications and source records attributed to A Schatzkin.

At least 19 recordsLinked to original sources

Relation of age and self-reported chronic medical condition status with dietary nutrient intake in the US population.

OBJECTIVE: To examine the association of nutrient intake with age and self-reported chronic medical condition status in a large, nationally representative sample. METHODS: We used data from the Continuing Survey of Food Intakes by Individuals, 1989-1991. The analytic sample included subjects aged > or =25 years with 3 days of dietary data, and medical condition information (n=7,207). A positive response to having been informed by a doctor of having diabetes, heart disease, high blood pressure, cancer, osteoporosis, and stroke indicated the presence of chronic medical condition(s) (n=2,368). Sex-specific linear and logistic regression analyses adjusted for multiple covariates were used to examine the relation of age and morbidity status with nutrient intake. RESULTS: In men, age was associated with an increased risk of consuming <100% of the Recommended Dietary Allowance (RDA) of vitamin E, vitamin B12, calcium, zinc, and iron (p<0.05), and self-reported morbidity was associated with an increased risk of consuming <100% of the RDA of protein. Relative to men, women were more likely to report less than the RDA of most nutrients examined; however, neither age nor chronic disease status were associated with increased likelihood of reporting <100% of the RDA of any of the nutrients examined. In women, the probability of reporting <100% of the RDA of vitamin A, vitamin B6, folate, vitamin C, and iron, and in men, the probability of reporting <100% of the RDA of vitamin C, declined with age (p<0.05). No adverse effect of age and chronic disease interaction on intake of most nutrients was noted in men or women. CONCLUSIONS: Chronologic age and morbidity were associated with an increased risk of inadequate intake of several nutrients in free-living, independent men but not in women.

Adult

Is colonoscopy needed for the nonadvanced adenoma found on sigmoidoscopy? The Polyp Prevention Trial.

BACKGROUND & AIMS: The need for colonoscopy when small tubular adenomas with low-grade dysplasia are found on sigmoidoscopy is uncertain. The aim of this study was to examine the prevalence and characteristics of proximal adenomas in patients with distal adenomas. METHODS: We studied 981 subjects with distal adenomas found on the index colonoscopy before randomization in the Polyp Prevention Trial. RESULTS: Four hundred sixty patients (46.9%) had >/=1 distal adenoma that was pathologically advanced (villous component, high-grade dysplasia, or >/=1 cm); 21.5% (211 of 981) had any proximal adenoma; and 4.3% (42 of 981) (95% confidence interval [CI], 3.0-5.5) had an advanced proximal adenoma. A greater percentage of patients with an advanced distal adenoma (5.9%) (95% CI, 3.7-8.0) had an advanced proximal adenoma compared with those with a nonadvanced distal adenoma (2.9%) (95% CI, 1.4-4.3) (OR, 2.1; 95% CI, 1.1-4.3; P = 0.03). Not performing a colonoscopy in patients with a nonadvanced distal adenoma would have missed 36% (15 of 42) of the advanced proximal adenomas. CONCLUSIONS: Patients with an advanced distal adenoma are twice as likely to have an advanced proximal adenoma as patients with a nonadvanced distal adenoma. However, eschewing a colonoscopy in patients with a nonadvanced distal adenoma would result in not detecting a sizeable percentage of the prevalent advanced proximal adenomas. These data support performance of a colonoscopy in patients with a nonadvanced distal adenoma. Confirmation of these results in asymptomatic subjects undergoing screening sigmoidoscopy is advisable.

Adenoma

An evaluation of rectal mucosal proliferation measure variability sources in the polyp prevention trial: can we detect informative differences among individuals' proliferation measures amid the noise?

We assessed components of total variability of bromodeoxyuridine (BrdUrd) and proliferating cell nuclear antigen (PCNA) assays of rectal mucosal proliferation in a subset of 390 participants from the U. S. National Cancer Institute's multicenter Polyp Prevention Trial. Biopsies were blindly double-scored by two technicians. For those participants for whom at least one evaluable biopsy was obtained, a mean of 2.0 and 2.6 biopsies, and 6.2 and 8.7 crypts/biopsy were evaluated, respectively, with the BrdUrd and PCNA assays. Factors such as clinical center, scorer, and month of biopsy collection significantly affected the observed values of the labeling index (LI) and proliferative height (PH). Therefore, it is essential to control or adjust for these variables in proliferation studies. Sources of random variation for LI and PH measures remaining after the aforementioned factors include between-participant variation and several sources of within-participant variation, including variation over time, between biopsies, and between multiple measurements on the same biopsy. Both LI and PH measurements exhibited substantial variability over time, between biopsies, and from reading-to-reading of the same biopsy. When other sources of variability have been accounted for, the PCNA LI seems to have little between-participant variation. This brings into question its utility as a marker in colorectal cancer studies. The PCNA PH showed significant between-participant variability and may hold some promise as a useful marker in colorectal cancer studies. Results for BrdUrd were less conclusive. The BrdUrd LI showed marginally significant between-participant variation, whereas the corresponding variation for PH was nonsignificant.

Adult

Effect of measurement error on energy-adjustment models in nutritional epidemiology.

The use and interpretation of energy-adjustment regression models in nutritional epidemiology has been vigorously debated recently. There has been little discussion, however, regarding the effect of dietary measurement error on the performance of such models. Contrary to conventional assumptions invoked in the standard treatment of the effect of measurement error in regression analysis, reporting errors in dietary studies are usually biased, correlated with true nutrient intakes and with each other, heteroscedastic, and nonnormally distributed. Methods developed in this paper allow for this more complex error structure and are therefore more appropriate for dietary data. For practical illustration, these methods are applied to data from the Women's Health Trial Vanguard Study. The results demonstrate considerable shrinkage in the magnitude of the estimated main exposure effect in energy-adjustment models due to attenuation of the true effect and contamination from the effect of an adjusting covariate. In most cases, this shrinkage causes a sharply reduced statistical power of the corresponding significance test in comparison with measurement without error. These results emphasize the need to understand the measurement error properties of dietary instruments through validation/calibration studies and, where possible, to correct for the impact of measurement error when applying energy-adjustment models.

Aged

Intake of vitamins E, C, and A and risk of lung cancer. The NHANES I epidemiologic followup study. First National Health and Nutrition Examination Survey.

The relation between the dietary intake of vitamins E, C, and A (estimated by a 24-hour recall) and lung cancer incidence was examined in the First National Health and Nutrition Examination Survey Epidemiologic Followup Study cohort of 3,968 men and 6,100 women, aged 25-74 years. During a median follow-up period of 19 years (from 1971-1975 to 1992), 248 persons developed lung cancer. Adjusted for potential confounders using Cox proportional hazards regression methods with age as the underlying time variable, the relative risk of lung cancer for subjects in the highest quartile of vitamin C intake compared with those in the lowest quartile was 0.66 (95% confidence interval (CI) 0.45-0.96). For vitamin A intake, a protective effect was observed only for its fruit and vegetable component (carotenoids) among current smokers (relative risk = 0.49, 95% CI 0.29-0.84), but this was modified by the intensity of smoking (a statistically significant effect (relative risk = 0.33, 95% CI 0.13-0.84) was observed only for those in the lowest tertile of pack-years of smoking). The vitamin E intake-lung cancer relation was modified by the intensity of smoking with a significant protective effect confined to current smokers in the lowest tertile of pack-years of smoking (relative risk = 0.36, 95% CI 0.16-0.83). Overall, there was no additional protective effect of supplements of vitamins E, C, and A beyond that provided through dietary intake. When vitamin E, vitamin C, and carotenoid intakes were examined in combination, a strong protective effect was observed for those in the highest compared with those in the lowest quartile of all three intakes (relative risk = 0.32, 95% CI 0.14-0.74). These data provide support for a protective role of dietary vitamins E and C and of carotenoids against lung cancer risk but with a modification in effects by the intensity of cigarette exposure. While smoking avoidance is the most important behavior to reduce lung cancer risk, the daily consumption of a variety of fruits and vegetables that provides a combination of these nutrients and other potential protective factors may offer the best dietary protection against lung cancer.

Adult

Bone mass and the risk of breast cancer among postmenopausal women.

BACKGROUND: Recent studies have shown a direct relation between serum estrogen levels assessed at a single point in time and the risk of breast cancer, but no evidence links estrogen levels assessed repeatedly over an extended interval to the risk of breast cancer. Bone mass has been proposed as a marker of cumulative exposure to estrogen in women. We therefore studied the association between bone mass and the incidence of breast cancer. METHODS: Between 1967 and 1970, 1373 women who were 47 to 80 years old and had no history of breast cancer underwent posteroanterior hand radiography in the Framingham Study. We used radiogrametry to measure the cortical width of each woman's second metacarpal. Participants were followed until the end of 1993. All incident cases of breast cancer were confirmed by pathological reports. We used a Cox proportional-hazards model to examine the relation of metacarpal bone mass to the risk of postmenopausal breast cancer. RESULTS: Postmenopausal breast cancer developed in 91 subjects. Incidence rates per 1000 person-years increased from 2.0 among the women in the lowest age-specific quartile of metacarpal bone mass to 2.6, 2.7, and 7.0 among the women in the second, third, and highest quartiles, respectively. After adjustments for age and other potential confounding factors, the rate ratios for the risk of breast cancer were 1.0, 1.3, 1.3, and 3.5 from the lowest quartile to the highest (P for trend, <0.001). CONCLUSIONS: Women in the highest quartile of bone mass are at higher risk for postmenopausal breast cancer than those in the lowest quartile. The mechanisms underlying this relation are not understood, but cumulative exposure to estrogen may play a part.

Aged

A prospective study of menopausal hormones and risk of colorectal cancer (United States)

The relation of colorectal cancer and its subsites with use of menopausal hormones was evaluated in the United States among 40,464 postmenopausal women, 41 to 80 years of age, who initially volunteered for a nationwide breast-cancer screening program and were followed for an average of 7.7 years. Ever-use of menopausal hormones was not associated with risk of total colorectal cancers (relative risk [RR] = 0.99, 95 percent confidence interval [CI] = 0.79-1.2) or cancers of the colon (RR = 1.1, CI = 0.81-1.6) or rectum (RR = 1.1, CI = 0.59-1.9). Recent hormone users, however, had a small nonsignificant reduction in risk of colorectal cancer (RR = 0.78, CI = 0.55-1.1), which was most pronounced for distal colon (RR = 0.68, CI = 0.29-1.6) and rectal tumors (RR = 0.64, CI = 0.24-1.7). No effect was observed for former hormone users, and risk generally did not vary by time since last use, type of regimen, or duration of use. However, the reduced risk for recent users was stronger for users of five or more years' duration. These data show some lowering of colorectal cancer risk among recent menopausal hormone users of long duration.

Adult

Evening eating and subsequent long-term weight change in a national cohort.

OBJECTIVE: To examine the association of proportion of daily energy consumed in the evening with weight change over 10 y of follow-up. DESIGN: The data used were from the First National Health and Nutrition Examination Survey (NHANES I, 1971-75) Epidemiologic Follow-up Study (NHEFS, 1982-84). The analytic cohort included 2580 men and 4567 women aged 25-74 y at baseline (NHANES I, 1971-75). The proportion of energy consumed in the evening (after 5 pm) was estimated from a 24 h dietary recall obtained a baseline. Weight change was defined as the difference between the follow-up and baseline weights. RESULTS: Mean +/- s.e. of percent energy from evening food intake was 46 +/- 0.29 in the analytic cohort. After adjustment for multiple covariates, percent energy from evening food intake and weight change were unrelated in both men and women. CONCLUSION: Extent of evening eating was not a significant predictor of 10 y weight change in the NHEFS cohort.

Adult

Reproductive factors, oral contraceptive use, and risk of colorectal cancer.

Multiparity and use of oral contraceptives are hypothesized to reduce risk of colorectal cancer. Among 57,529 women, 31-90 years of age, who volunteered for a nationwide breast cancer screening program from 1973 to 1980, we observed 154 pathologically confirmed cases of colon cancer and 49 cases of rectal cancer in up to 10 years of follow-up (388,555 person-years). Parity was not associated with risk of colorectal cancer [age-adjusted rate ratio for > or = 4 children vs no children = 1.0; 95% confidence interval (CI) = 0.72-1.5], although decreases in proximal colon cancer and increases in distal colon cancer were observed among parous women. The effect of parity did not vary by age at diagnosis. We found no strong or consistent association for age at menarche, age at first birth, or age at natural menopause. In addition, oral contraceptive use, reflecting mainly past use, was unrelated to risk of colorectal cancer (rate ratio = 1.0; 95% CI = 0.75-1.4). These findings do not corroborate the hypothesis that reproductive events or oral contraceptives influence the development of colorectal cancer.

Adult

Serum sex hormone levels are related to breast cancer risk in postmenopausal women.

We conducted a nested case-control study to prospectively evaluate the relationship of serum estrogens and androgens to risk of breast cancer in postmenopausal women. From 1977 to 1987, 3375 postmenopausal women free of cancer and not taking replacement estrogens donated blood to the Breast Cancer Serum Bank in Columbia, Missouri. Of these, 72 were subsequently diagnosed with breast cancer. For each case, two controls matched on age and date and time of day of blood collection were selected using incidence density matching. The median age of subjects at blood collection was 62 years; the time from blood collection to diagnosis ranged from less than 1 to 9.5 years with a median of 2.9 years. Risk of breast cancer was positively and significantly associated with serum levels of estrogens and androgens. Compared to women in the lowest quartile, those in the highest quartile for non-sex hormone-binding globulin (non-SHBG) bound (bioavailable) estradiol had a relative risk of 5.2 (95% confidence interval [CI] = 1.5-18.5) and those in the highest quartile for testosterone had a relative risk of 6.2 (95% CI = 2.0-19.0). Our results lend considerable support to the hypothesis that serum concentrations of estrogens and androgens are related to the subsequent diagnosis of breast cancer in postmenopausal women.

Aged

Socioeconomic status and breast cancer mortality, 1989 through 1993: an analysis of education data from death certificates.

OBJECTIVES: This study examined whether more highly educated women were at greater risk of dying of breast cancer during 1989 through 1993. METHODS: Breast cancer mortality rates were calculated through death certificates and Current Population Survey data. RESULTS: Breast cancer mortality rates were highest among women with 12 and with 16 or more years of education. Non-Hispanic Black women had the highest mortality rates and Asian women the lowest. Positive relationships between mortality and education were found for Hispanic women as well as non-Hispanic Black and Asian women. CONCLUSIONS: The previously seen positive relationship between breast cancer mortality and education was found among US women of color but not non-Hispanic White women.

Breast Neoplasms

Using and interpreting surrogate end-points in cancer research.

Researchers have proposed a broad range of molecular, cellular and histological markers as surrogate end-points for cancer (SECs). The effect of an intervention on a 'valid' SEC is concordant with its effect on cancer incidence. The validity of a potential SEC is determined primarily by the extent to which the marker is a necessary event on the causal pathway to cancer. Colorectal adenomatous polyp formation is an example of a reasonably valid SEC because these lesions are obligate precursors of most large bowel malignancies. However, the existence of a plausible major alternative causal pathway--one bypassing the potential SEC--weakens inferences from that marker to cancer. Moreover, unless the pathway to cancer operates nearly exclusively through the SEC, an SEC that is valid for one intervention or exposure may not be valid for another. Metabolic, ecological, observational epidemiological and intervention studies may yield data that are useful in revealing these causal interrelations of intervention (exposure), SEC and cancer. Empirical studies of three questions are pertinent: (1) What is the relation of the SEC to cancer? (2) What is the relation of the intervention (exposure) to the SEC? (3) To what extent does the SEC mediate the relation between the intervention (exposure) and cancer? Data on SEC measurement error are important in ascertaining the extent to which marker results have been attenuated by such error. It is essential to carry out these studies to evaluate potential SECs (such as epithelial cell hyperproliferation) with plausible major alternative pathways to cancer. At the present time, definitive evidence on etiology and prevention will emerge only from studies with cancer end-points or SECs that are, by and large, necessary steps on the causal pathway to malignant disease.

Adenomatous Polyposis Coli

Prospective study of relative weight and risk of breast cancer: the Breast Cancer Detection Demonstration Project follow-up study, 1979 to 1987-1989.

Despite extensive research on obesity and breast cancer in recent decades, inconsistencies in the literature exist. The authors examined prospectively the relation between adult relative weight (weight (kg)/height (m)1.5) and breast cancer risk in a cohort of 54,896 women aged 31-89 years who had previously participated in the Breast Cancer Detection Demonstration Project. During a mean follow-up period of 7 years, 226 of the premenopausal women and 1,198 of the postmenopausal women developed breast cancer. Analysis was performed using Cox proportional hazards regression methods with age as the underlying time variable and adjusted for the effects of potential confounders. Among postmenopausal women, the risk of breast cancer increased with increasing relative weight (p < 0.05 for trend); relative risk for the highest compared with the lowest quintile for relative weight was 1.3 (95% confidence interval (CI) 1.1-1.6). This association was modified by age at diagnosis, with relative risks of 1.1 (95% CI 0.8-1.4), 1.2 (95% CI 0.8-1.7), and 1.8 (95% CI 1.3-2.5), respectively, for women aged < 60, 60-64, and > or = 65 years. The higher risk of breast cancer among the older and overweight women was largely confined to women whose weights were measured during the postmenopausal but not the premenopausal period. This risk pattern was observed among the naturally menopausal women, but was also apparent in the smaller group of women with bilateral oophorectomy or hysterectomy with one ovary retained. Among premenopausal women, adult relative weight was not associated with breast cancer risk. These findings suggest that the inconsistencies in the literature on obesity and breast cancer may be due in part to the differing age distributions of the populations studied. The authors conclude that prevention of obesity throughout adulthood, particularly after menopause, may help reduce breast cancer among older women.

Adult

Relation of energy, fat, and fiber intakes to plasma concentrations of estrogens and androgens in premenopausal women.

To evaluate whether diet may influence the incidence of hormone-dependent cancers through an effect on blood estrogen and androgen concentrations, we analyzed diet-blood hormone relations in a cross-sectional study. Dietary energy, fat, and fiber intakes were estimated from 7-d food records completed by 90 premenopausal women on days 14-20 of their menstrual cycles. Fasting blood specimens were collected on days 5-7, 12-15, and 21-23 of each participant's cycle and pooled to create follicular-, midcycle-, and luteal-phase samples, respectively, for analysis. Energy intake was associated inversely with plasma androstenedione and dehydroepiandrosterone sulfate (DHEAS), averaged across the three menstrual cycle phases, and directly with the probability of a luteal-phase rise in progesterone. For each additional 1 MJ (239 kcal) consumed, androstenedione decreased by 6.0% (95% CI: -8.4%, -3.6%), DHEAS decreased by 5.1% (95% CI: -9.6%, -0.4%), and the probability of a progesterone rise increased by 60% (95% CI: 5%, 145%). After energy intake was adjusted for, the ratio of polyunsaturated to saturated fat (P:S) in the diet was significantly inversely associated with plasma estradiol and estrone during the luteal phase of the menstrual cycle. For each 0.1 increment in the P:S, there was a 7.6% (95% CI: -14.3%, -0.5%) decrease in estradiol and a 6.8% (95% CI: -12.7%, -0.6%) decrease in estrone. Results of this cross-sectional study support a relation between both energy and fat ingestion and plasma sex hormone concentrations in premenopausal women.

Adult

Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study.

We conducted a controlled feeding study to evaluate the effects of fat and fiber consumption on plasma and urine sex hormones in men. The study had a crossover design and included 43 healthy men aged 19-56 y. Men were initially randomly assigned to either a low-fat, high-fiber or high-fat, low-fiber diet for 10 wk and after a 2-wk washout period crossed over to the other diet. The energy content of diets was varied to maintain constant body weight but averaged approximately 13.3 MJ (3170 kcal)/d on both diets. The low-fat diet provided 18.8% of energy from fat with a ratio of polyunsaturated to saturated fat (P:S) of 1.3, whereas the high-fat diet provided 41.0% of energy from fat with a P:S of 0.6. Total dietary fiber consumption from the low- and high-fat diets averaged 4.6 and 2.0 g.MJ-1.d-1, respectively. Mean plasma concentrations of total and sex-hormone-binding-globulin (SHBG)-bound testosterone were 13% and 15% higher, respectively, on the high-fat, low-fiber diet and the difference from the low-fat, high-fiber diet was significant for the SHBG-bound fraction (P = 0.04). Men's daily urinary excretion of testosterone also was 13% higher with the high-fat, low-fiber diet than with the low-fat, high-fiber diet (P = 0.01). Conversely, their urinary excretion of estradiol and estrone and their 2-hydroxy metabolites were 12-28% lower with the high-fat, low-fiber diet (P < or = 0.01). Results of this study suggest that diet may alter endogenous sex hormone metabolism in men.

Adult

Contribution of dieting to the inverse association between energy intake and body mass index.

OBJECTIVE: To examine the association of energy and % energy from fat with body mass index (BMI) and determine if self-reported dieting altered observed associations. DESIGN: Dietary intake data based on dietary recalls from four nonconsecutive days over a 1 year period were examined relative to BMI. The relation between energy intake and % energy from fat and BMI was examined by linear regression analysis. SUBJECTS: The sample included 1854 free-living women aged 19-50 years who participated in the 1985-6 Continuing Surveys of Food Intakes by Individuals conducted by the United States Department of Agriculture. RESULTS: Reported energy intake was inversely associated with BMI (regression coefficient (beta) = -0.001 24, standard error (s.e.) = 0.000 31). Controlling for low energy dieting alone reduced the inverse energy intake-BMI association by approximately 20% (beta = -0.001 00, s.e. = 0.000 31), compared to reductions of 16%, 13% and 10%, respectively, when health status, age and education were added individually to the energy intake-BMI linear regression. Physical activity, smoking status, % energy from fat and report of low fat dieting did not reduce the energy intake-BMI association. Controlling for nondietary factors related to BMI and potentially influencing energy intake reduced the inverse energy intake-BMI association by approximately 22% (beta = -0.000 97, s.e. = 0.00025). Further adjustment for low energy dieting on day 1 reduced the inverse energy intake-BMI association by 40% (beta = -0.000 74, s.e. = 0.000 26), suggesting that intermittent energy restriction was a significant factor in the reduced energy intake reported among overweight women. Percent energy from fat was not associated with BMI (beta = 0.049, s.e. = 0.025, P = 0.055). Exclusion of 37 women reporting poor health status further attenuated the inverse association between energy intake and BMI (beta = -0.000 64), s.e. = 0.000 26), while it strengthened the previously non-significant positive association between % energy from fat and BMI (beta = 0.062; s.e. = 0.024). CONCLUSION: Intermittent energy restriction appeared to be a significant factor in the reduced energy intake reported among overweight women in this sample. Adequate assessment of energy expenditure is required to correctly interpret the association of energy intake to body weight.

Adult

Relation of prediagnostic serum estrogen and androgen levels to breast cancer risk.

To evaluate the relation of serum sex hormones to breast cancer risk, we conducted a prospective nested case-control study using the Breast Cancer Serum Bank (Columbia, MO). This bank included serum from 3375 postmenopausal women free of cancer and not taking replacement estrogens when they donated blood between 1977 and 1987. Of these, 71 were diagnosed subsequently with breast cancer. For each case, two women alive and free of cancer at the age of the case's diagnosis and matched to the case on age and on date and time of day of blood collection were selected as controls. The median age of subjects at blood collection was 62 years, and the time from blood collection to diagnosis ranged from less than 1 to 9.5 years, with a median of 2.9 years. Postmenopausal women with elevated serum levels of total and non-sex hormone-binding globulin-bound E2 were at an increased risk of developing breast cancer. For non-sex hormone-binding globulin-bound E2, risks were elevated 4-5 fold for women in the upper three quartiles relative to those in the lowest quartile. Although breast cancer was not related to estrone or estrone sulfate concentration, the ratio of estrone sulfate to estrone was significantly inversely associated with risk, suggesting that women who develop breast cancer may be less able to metabolize estrone to its less active form. Serum testosterone was significantly positively associated with postmenopausal breast cancer; the relative risk for women in the highest versus the lowest quartile was 6.2 (95% confidence interval, 2.0-19.0). Our results support the hypothesis that prediagnostic serum estrogens and androgens are related to the subsequent diagnosis of breast cancer in postmenopausal women.

Adult