Biomedical subjects

R S Sandler

Publications and source records attributed to R S Sandler.

At least 55 records · Page 3Linked to original sources

PubMed1998

Dietary and supplemental calcium and the recurrence of colorectal adenomas.

The association between calcium intake and the risk of colorectal neoplasia remains controversial. This analysis prospectively investigated the association between dietary and supplemental calcium intake and recurrent colorectal adenomas. Participants were part of a multicenter, randomized clinical trial of antioxidant vitamins. The study endpoints were adenomas detected between surveillance colonoscopies conducted at approximately 1 year and 4 years after study entry. Baseline intake of energy-adjusted calcium derived from a food frequency questionnaire was used as the main exposure of interest. Calcium supplement use was assessed by semiannual questionnaires. Logistic regression was used to compute odds ratios and 95% confidence limits, and Poisson regression was used to estimate rate ratios. Subjects in the fifth quintile of dietary calcium had an adjusted odds ratio of 0.72 (95% confidence interval, 0.43-1.22) compared to those in the lowest quintile. Investigation of the numbers of adenomas yielded stronger findings: the rate ratio for the fifth quintile versus the first was 0.63 (95% confidence interval, 0.39-1.02). Dietary calcium seemed to have a greater effect among individuals with a high-fat diet than among those with a low-fat diet; however, the interaction was not statistically significant. Use of calcium supplements was not related to adenoma recurrence. These results suggest that a high calcium intake may be associated with a reduction in risk of recurrent adenomas, especially among individuals on a high-fat diet.

Adenoma↗

PubMed1998

Rectal mucosal proliferation, dietary factors, and the risk of colorectal adenomas.

Colorectal cancer arises from a series of precursor stages, the so called adenoma-carcinoma sequence. Increased rectal mucosal proliferation may be an early step in this sequence. Because dietary factors are implicated in the etiology of colorectal cancer, one might predict that diet would also be associated with proliferation. We conducted this study to examine the association of diet with rectal mucosal proliferation. Rectal mucosal proliferation was measured in endoscopic biopsy specimens by proliferating cell nuclear antigen (PCNA) immunohistochemistry and whole crypt mitotic counts (WCMCs). Diet was evaluated using a validated quantitative food frequency questionnaire. The correlation between PCNA labeling index (LI) and WCMCs was determined using Kendall's tau, a nonparametric measure of correlation. Logistic regression was used to examine the effect of proliferation on adenoma status, controlling for confounders. The relationship between proliferation and dietary and demographic factors was examined using linear regression. There were 308 patients who had one or both measures of proliferation. There was no significant correlation between PCNA LI and WCMCs (Kendall's tau = 0.04; P = 0.35). Neither measure of proliferation was predictive of adenoma status, even after adjusting for potential confounders. Body mass index and calories per day were significant predictors of WCMC (P = 0.01 and P = 0.03, respectively). PCNA labeling index was not associated with any dietary variables, although its association with dietary fat nearly reached statistical significance (P = 0.09). The association between proliferation and diet were generally inconsistent. There appears to be no simple relationship between colorectal cancer risk factors, colorectal adenomas, and these two measures of rectal mucosal proliferation. We need simpler, more reliable intermediate markers for use in etiological and intervention studies.

Adenoma↗

PubMed1997

Review and analysis of the effects of olestra, a dietary fat substitute, on gastrointestinal function and symptoms.

Olestra, a dietary fat substitute, was recently made available to consumers in savory snacks in three cities. Early reports of gastrointestinal complaints attributed to olestra attracted media coverage and fostered confusion among physicians and consumers about the nature of olestra and its effects on the digestive system. We reviewed all published studies of olestra's gastrointestinal effects and all relevant unpublished studies submitted to the Food and Drug Administration. Each study was analyzed by a group of expert gastroenterologists and epidemiologists. The symptoms reported with olestra ingestion are similar to those reported with ingestion of fiber and sorbitol, although the mechanisms involved in changing stool characteristics differ among these food additives. Olestra's effects on stool habit and characteristics are due to its presence in the stool. Large amounts are more likely to induce gastrointestinal symptoms than small amounts. There is no evidence that olestra induces pathological change in bowel function: there is no increased fluid or electrolyte nor is there altered gastrointestinal motility or microflora. Olestra and triglyceride ingestion resulted in a similar frequency of symptoms in normal adults and children and in people with chronic inflammatory bowel disease in remission. Olestra traverses the digestive tract intact to become a stool additive. Some subjects develop a change in bowel habit and stool characteristics due to the presence of more olestra in the stool. These changes resemble those associated with ingestion of sorbitol and fiber.

Controlled Clinical Trials as Topic↗

PubMed1997

Intestinal effects of sulfate in drinking water on normal human subjects.

Uncontrolled observations implicate sulfate in drinking water at concentrations exceeding 500-700 mg/liter as a cause of diarrhea, but controlled studies have not been reported. We conducted a controlled study in normal adults to determine the effect of various drinking water sodium sulfate concentrations on bowel function. Ten healthy subjects were given a constant diet and fluid intake. Fluid consisted of 36 ml/kg/day of drinking water of various known sulfate concentrations and 500 ml of other fluid. In a dose-ranging study, four subjects received drinking water with sulfate concentrations of 0, 400, 600, 800, 1000, and 1200 mg/liters for six consecutive two-day periods. In a single-dose study, six other subjects received water with sulfate concentrations of 0 and 1200 mg/liter for two consecutive six-day periods. Stool mass, frequency, and consistency and mouth-to-anus appearance time of colored markers were measured. In the dose-ranging study, the only significant linear trend was decreasing mouth-to-anus appearance time with increasing sulfate concentrations. In the single-dose study, 1200 mg/liter sulfate caused a significant but clinically mild increase in mean stool mass per six-day pool from 621 g to 922 g (P = 0.03). When all 10 subjects were used to compare effects of 0 mg/liter and 1200 mg/liter sulfate, significant differences in stool consistency (P = 0.02) and transit time (P = 0.03) were observed. None of the subjects reported diarrhea or passed more than three stools per day. In 10 normal adult subjects, sulfate in drinking water at a concentration of 1200 mg/liter, which is higher than reported to occur in US municipal water sources, caused a measurable but clinically insignificant increase in stool mass and decrease in stool consistency and appearance time, but no change in stool frequency and no complaint of diarrhea.

Adult↗

PubMed1997

In vivo activation of mitogen-activated protein kinases in rat intestinal neoplasia.

BACKGROUND & AIMS: To investigate whether mitogen-activated protein kinase (MAPK) cascades might play a role in the progression of colon cancer, c-Jun N-terminal kinase (JNK) and extracellular signal regulating kinase (ERK) activity during colonic tumorigenesis were examined. METHODS: The 1,2-dimethylhydrazine (DMH)-induced colon carcinoma model was used to study the activation of these kinases during intestinal carcinogenesis. Male Sprague-Dawley rats were injected with DMH for 24 weeks. Normal-appearing intestinal mucosa from control and treated animals and DMH-induced intestinal tumors were assayed for JNK and ERK activity using solid phase in vitro kinase assays. Tumors were typed for mutations in the K-ras gene. RESULTS: There was little or no difference in JNK and ERK activity in hyperproliferative mucosa from DMH-treated animals compared with normal mucosa from control animals. However, in 16 colonic neoplasms, an average of 23-fold and 29-fold increases in JNK and ERK activities were observed, respectively, over control levels. In addition, activating protein-1 binding was strongly induced in the colonic tumors. Activation did not correlate with the presence of mutations in K-ras. CONCLUSIONS: Both the JNK and ERK MAPKs are highly activated during late progression of colorectal carcinoma. This change is dependent on the tumorigenic state rather than changes in proliferation.

1,2-Dimethylhydrazine↗

PubMed1997

Plasma selenium levels and the risk of colorectal adenomas.

Previous research has suggested that selenium may protect against the development of colorectal neoplasia. We examined the potential chemopreventive properties of selenium against colorectal adenomas while controlling for a number of dietary and life-style factors. We conducted a cross-sectional study among patients referred for colonoscopy to University of North Carolina Hospitals. Cases had one or more pathologically confirmed adenomas, and noncases had none. Plasma selenium levels were determined using graphite furnace atomic absorption spectrometry with Zeeman background correction and platform technique. Odds ratios were calculated using logistic regression analysis adjusting for potential confounders. The mean plasma selenium concentrations for cases (n = 37) and noncases (n = 36) were 107 and 120 micrograms/l, respectively (p = 0.06). Those in the fourth quartile of plasma selenium level had 0.24 times the risk (95% confidence interval = 0.06-1.04) for colorectal adenomas of those in the first quartile. The adjusted odds ratio for colorectal adenomas was 0.58 (95% confidence interval = 0.31-1.08) for a 30 microgram/l increase in plasma selenium level. Lower plasma selenium levels were associated with multiple adenomas but not with adenoma size or location. These data support a protective effect of selenium against colorectal adenomas after adjustment for possible confounders. Selenium might be a potentially useful chemopreventive agent for colorectal neoplasia.

Adenoma↗

PubMed1997

Phenolphthalein-containing laxative use in relation to adenomatous colorectal polyps in three studies.

Phenolphthalein, the active ingredient in many laxatives, was recently found to be a carcinogen in animal models. Human data suggest a laxative-colon cancer association, but few data specifically address the effects of phenolthalein-containing laxatives. We examined use of phenolphtalein-containing laxatives in relation to occurrence of adenomatous colorectal polyps in data from three case-control studies. The study conducted in Los Angeles, California (1991-1993), and the two studies conducted in North Carolina (1988-1990 and 1992-1995) altogether included 866 cases and 1,066 controls. The prevalence of using phenolphthalein-containing laxatives at least once a week in the recent past, however, was less than 5% among these subjects. The multivariate-adjusted odds ratios associated with recent use of phenolphthalein-containing laxatives once a week or more were 1.8 -95% confidence interval (CI), 0.5-6.2] in Los Angeles, 1.0 (CI, 0.4-2.2) in North Carolina (1988-1990), and 1.1 (CI, 0.2-5.7) in North Carolina (1992-1995). For use of other types of laxatives, the corresponding odds ratios were 1.3 (CI, 0.9-1.9) in Los Angeles, 1.0 (CI, 0.5-1.7) in North Carolina (1988-1990), and 0.9 (CI, 0.4-1.8) in North Carolina (1992-1995). Although the low prevalence of frequent use made for relatively wide confidence intervals, overall these data suggest that use of phenolphthalein-containing laxatives does not increase risk of adenomatous colorectal polyps.

Adenomatous Polyps↗

PubMed1997

Coffee and tea and the risk of recurrent colorectal adenomas.

Consumption of coffee has been associated with a reduction in the risk of cancer of the colon, and (less consistently) drinking tea has been associated with a reduction in the risk of rectal cancer. The effect of these beverages on the risk of colorectal adenomas, however, has not been well investigated. We used data from an adenoma prevention trial to investigate these associations. Patients with at least one recent large bowel adenoma were followed with colonoscopy 1 and 4 years after their qualifying examinations. Adenomas detected at the year 4 colonoscopy were used as end points. A food frequency questionnaire was administered at study entry and study completion; average intake over the study period was used to estimate the exposures of interest. There was no apparent association between the intake of regular coffee, decaffeinated coffee, or tea and the risk of recurrent colorectal adenomas. The relative risks and 95% confidence intervals per cup daily were 0.96 (0.87-1.05) for regular coffee, 0.97 (0.84-1.12) for decaffeinated coffee, and 1.02 (0.83-1.25) for tea. These negative findings were present both overall and for adenomas of the right and left large bowel.

Adenoma↗

PubMed1997

The relationship between gastroesophageal reflux disease and its complications with Barrett's esophagus.

BACKGROUND: Barrett's esophagus is a condition in which the stratified squamous epithelium of the esophagus is replaced by a columnar epithelium with malignant potential. Chronic gastroesophageal reflux disease (GERD) is accepted as the primary risk factor for the development of Barrett's esophagus, but only a small fraction of individuals with GERD develop Barrett's esophagus. We sought to identify factors that increase the risk of Barrett's esophagus in those with GERD. OBJECTIVE: The objective of this matched case-control study was to investigate possible clinical risk factors for Barrett's esophagus. METHODS: The study was based on 79 case patients with Barrett's esophagus and 180 control patients. Each case patient was matched to one control patient whose indication for endoscopy was GERD and one control patient who underwent endoscopy for other indications. The case and control patients were matched for age, gender, and race. All patients underwent endoscopy at Duke University Medical Center, Durham, NC, between July 1992 and August 1994. RESULTS: On average, patients with Barrett's esophagus developed reflux symptoms at an earlier age than age- and gender-matched control patients and also had a longer duration of symptoms. Complications of reflux, including esophagitis, stricture, and ulceration, were reported significantly more frequently in the group of case patients than either group of control patients. CONCLUSIONS: The results of this pilot study indicate that age of onset, duration of symptoms, and complications of GERD may be markers of increased risk of Barrett's esophagus.

Age of Onset↗

PubMed1997

Reproductive history, use of exogenous hormones, and risk of colorectal adenomas.

Evidence suggests a role for reproductive and hormonal factors in the etiology of colorectal cancer. Investigation of adenomas, the presumed precursors of cancer, and reproductive characteristics may place such associations within a particular stage of carcinogenesis. We examined parity, age at first birth, age at menopause, and age at menarche as well as contraceptive and noncontraceptive hormone use in a case-control study of 347 women (115 cases with adenomas and 232 controls) conducted in North Carolina. Using unconditional logistic regression analysis, increasing age at menopause was found to be associated with a reduction in the risk of adenomas [odds ratio (OR), 0.26; 95% confidence interval (CI), 0.10-0.68]. An increased risk for adenomas was found for women undergoing surgical menopause as compared with women undergoing natural menopause (OR, 2.10; 95% CI, 1.05-4.21). Our results suggest a reduced risk of adenomas associated with noncontraceptive hormone use that was limited to a subgroup of women with natural menopause or bilateral oophorectomy (OR, 0.39; 95% CI, 0.15-0.97). No associations were seen between other reproductive characteristics and adenomas. These results suggest protective effects for both endogenous and exogenous female hormones that operate early in the process of carcinogenesis. Alternatively, lifestyle factors or other correlates of exogenous hormone use and delayed menopause could play a role in reduced adenoma risk.

Adenoma↗

PubMed1997

Dietary iron and recurrence of colorectal adenomas.

Previous research suggests that iron acts as a prooxidant to increase the risk of colorectal neoplasia. This study examined effects of dietary intake of iron on colorectal adenoma recurrence using data from an antioxidant clinical trial. All subjects were free of polyps at study entry but had at least one adenoma removed within the 3 months before enrollment. Follow-up colonoscopies were conducted after 1 and 4 years. Patients who developed one or more adenomatous polyps between years 1 and 4 were classified as cases; all others were controls. Dietary iron intake at baseline and at the end of the study was estimated from self-administered food frequency questionnaires and averaged together for each subject, energy-adjusted, and categorized into quartiles. Odds ratios were adjusted for age, center, sex, calories, treatment group, and alcohol, fiber, folate, and fat intakes in unconditional logistic regression analysis. Dietary iron was inversely associated with adenoma risk, although risk did not decrease monotonically with increasing intake. Odds ratios comparing second, third, and fourth quartiles to the lowest quartile were 0.61 [95% confidence interval (CI), 0.37-1.02], 0.80 (95% CI, 0.45-1.44), and 0.37 (95% CI, 0.19-0.73), respectively. A limited examination showed no clear evidence that use of iron supplements affected risk of recurrence in this study population. This study provides evidence against the hypothesis that recent dietary intake of iron increases risk for colorectal adenomas. However, these results may reflect the presence of other dietary factors found in combination with iron.

Adenoma↗

PubMed1996

Micronutrients and the risk of colorectal adenomas.

Recent studies suggest that micronutrients, especially folate, calcium, iron, and antioxidant vitamins, affect the risk of colorectal neoplasia. The objective of this case-control study was to examine the association between these micronutrients and the risk of colorectal adenomas. The study was based on 236 cases with adenomatous polyps or cancer and 409 controls, all colonoscopy patients at University of North Carolina Hospitals between July 1988 and March 1991. After colonoscopy, subjects were interviewed using a semi-quantitative food frequency questionnaire, and average daily nutrient intakes were calculated. Sex-specific odds ratios relative to the lowest quartile of intake for each micronutrient were determined using unconditional logistic regression while adjusting for a number of potential confounders. In women, folate, iron, and vitamin C were inversely related to the risk of adenomas. Folate appeared to be most protective, with women in the highest quartile only 40% as likely to develop adenomas compared with women in the lowest (odds ratio = 0.39, 95% confidence interval 0.15-1.01). In men, greater vitamin E and calcium intakes were associated with reduced risk of adenomas, with vitamin E showing the strongest inverse association. Men in the highest vitamin E quartile had a risk of 0.35 (95% confidence interval 0.14-0.92) relative to those in the lowest. These study results support previous research findings that selected micronutrients protect against colorectal neoplasia.

Adenoma↗

PubMed1996

Epidemiology and risk factors for colorectal cancer.

The striking geographic differences in colorectal cancer incidence and the changes in disease risk among immigrants suggest an important environmental component to colorectal cancer risk. Table 1 lists risk factors for colorectal cancer. The categories in the table are somewhat arbitrary but are designed to provide an overall semiquantitative summary of the current epidemiologic literature. Certain of the most important risk factors (e.g., age, family history) cannot be modified. Individuals at high risk might benefit from surveillance. Dietary factors appear to be among the most important determinants of colorectal cancer risk. Diet helps to explain geographic variation in disease. A diet that is high in red meat and saturated fat appears to increase risk. Vegetables, fruits, fiber, folate, and calcium may be protective. Obesity, particularly abdominal obesity, and tall stature may be risk factors. Physical activity has been repeatedly shown to reduce the risk of colorectal cancer. Postmenopausal hormone replacement therapy may also be protective. Exciting new data suggest a significantly lower risk of colorectal cancer in regular users of aspirin and NSAIDs. It is important to recognize that the use of these drugs can have adverse as well as beneficial effects, and the appropriate dose and timing are not known. Enough information is available to make recommendations to lower the risk of colorectal cancer. Reducing red meat and fat consumption; increasing fruits, vegetables, and grains; avoiding obesity; and adopting a regular program of physical activity reduce the risk of colorectal cancer. Fortunately, these modifications also decrease the risk of cardiovascular disease, an even more important cause of mortality in Western societies.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1996

Aspirin and other nonsteroidal anti-inflammatory agents in the prevention of colorectal cancer.

Chemoprevention refers to the use of specific natural or synthetic chemical agents to reverse, suppress, or prevent the progression to invasive cancer. The ideal chemopreventive agent is safe and nontoxic over the long term. It should be easy to take and demonstrated to be effective in randomized trials in humans. Aspirin and NSAIDs meet many of the criteria for an ideal agent. The literature on aspirin and NSAIDs makes it clear that these agents can prevent colorectal cancer and precursor adenomas. That does not mean that we should make general recommendations for their use. First, we do not know the proper dose or duration. More important, these medications are accompanied by adverse effects that can be considerable. Indeed, the Medical Letter, an authoritative, unbiased publication on drugs and therapeutics, concluded that "for primary prevention in low-risk patients, more studies are required to establish whether the beneficial effect of aspirin is great enough to compensate for the possible increased risk of hemorrhagic stroke." These recommendations were directed at the use of these medications for prevention of myocardial infarction, but the same conclusions apply to colorectal cancer: although aspirin may prevent the disease, it may increase the risk of hemorrhagic strokes or cause other adverse effects. We must accurately balance the benefits and risks of these drugs, based on the results of ongoing randomized studies, before recommending aspirin for prevention of colorectal cancer. Is there anything that we can recommend to our patients for prevention of colorectal cancer? Based on observational epidemiologic studies, it is clear that individuals who consume a diet high in vegetables and natural fibers and low in fat have a reduced risk of colon cancer and polyps. Optimal nutrient intakes for the prevention of cancer might be more readily achieved via food fortification or supplementation, but this requires more research. Regular physical exercise and maintenance of normal body weight are also protective. Until the results of definitive studies of chemopreventive agents are available, we can recommend that our patients eat a sensible diet, exercise, and avoid obesity. Such an approach should protect them from cardiovascular disease, an even deadlier condition than colorectal cancer. In the future, we need randomized prevention trials that, for logistic reasons, may need to focus on the occurrence and progression of colorectal adenomas rather than carcinoma itself. Studies that test more than one compound at a time, using factorial designs, will be more efficient. We will need better information about duration and dose, adverse side effects, molecular mechanisms, and cellular sites of NSAID activity. Ultimately, we will need to know more about the biology and molecular biology of colorectal cancer and its precursors. That information will, perhaps, permit us to design agents to interrupt the pathway to cancer and to use intermediate markers more intelligently.

Adenocarcinoma↗

PubMed1996

Iron intake and the risk of colorectal cancer.

Prospectively gathered data from the National Health and Nutrition Examination Survey I and the National Health Evaluation Follow-Up Study were analyzed to evaluate the risk of colorectal cancer due to consumption of iron. Morbidity and mortality data due to colorectal cancer were available on 14,407 persons first interviewed in 1971 and followed through 1986. A total of 194 possible colorectal cancers occurred in this group over the 15-year period. Subsite analysis showed that the risk of colon cancer due to iron intake was elevated throughout the colon for both men and women, with the highest adjusted risks for the interquartile range seen in the proximal colon for females (relative risk, 1.51; 95% confidence interval, 1.41-1.60). The risk of rectal cancer was not significantly elevated for men or women. Elevated serum iron was also associated with increased risk; however, this effect was strongest in the distal (rather than proximal) colon and was significant only among females (adjusted relative risk, 1.73; 95% confidence interval, 1.03-2.92). The mean transferrin saturation was higher among cases than controls (30.7 versus 28.7%), but total iron-binding capacity did not seem to predict the occurrence of colorectal cancer. Proportional hazards models confirmed that the effects of iron and serum iron were not confounded by age, gender, energy consumption, fat intake, or other known risk factors for colorectal cancer. These data suggest that iron may confer an increased risk for colorectal cancer, and that the localization of risk may be attributable to the mode of epithelial exposure. It seems that luminal exposure to iron increases risk proximally, whereas humoral exposure increases risk distally. These differences may be due to such factors as oxidation state, binding proteins and the presence of other cofactors such as bile acids, products of bacterial metabolism.

Adult↗

PubMed1996

Correlation between biomarkers of omega-3 fatty acid consumption and questionnaire data in African American and Caucasian United States males with and without prostatic carcinoma.

Results from animal studies suggest that omega-3 fatty acids from marine sources are protective against cancer. To determine whether adipose tissue and erythrocyte membrane fatty acid composition could serve as biomarkers of essential fatty acid consumption in subjects with prostate cancer, we compared fish consumption, which was estimated using a food frequency survey, to the omega-3 fatty acid content of adipose tissue and erythrocyte membranes. The study was conducted using 127 men who had undergone a prostate biopsy. All subjects were recruited from a university hospital urology clinic. African Americans comprised 23% of the subjects, and 70% were diagnosed with prostate cancer. We found a correlation of 0.44 with 95% confidence intervals (CIs) = 0.29-0.57 between reported fish consumption and the omega-3 fatty acid eicosapentaenoic acid composition in erythrocyte membranes and 0.38 with 95% CI = 0.21-0.53 when the dietary survey was compared to eicosapentaenoic acid in adipose tissue. The survey/biomarker correlations in cases were not significantly different from the correlations in controls. The study had 90% power to detect a 0.35 difference between correlations. These results suggest that the presence of prostate cancer does not affect the adipose tissue or erythrocyte membrane biomarkers of fatty acid consumption, and that erythrocyte membranes are as useful as biomarkers as is adipose tissue. Our findings corroborate previous studies that found that tissue biomarkers can reflect past fatty acid consumption and support the use of biomarkers in case-control studies using cancer patients.

Adipose Tissue↗

PubMed1996

Biomarkers of essential fatty acid consumption and risk of prostatic carcinoma.

Animal studies have suggested that omega-6 fatty acids found in vegetable oils may promote prostate cancer. Our goal was to use erythrocyte membrane and adipose tissue fatty acid composition as biomarkers to investigate whether essential fatty acids modulated prostate cancer risk. An outpatient clinic-based study of 89 cases and 38 controls was conducted in North Carolina between July 1989 and December 1991. Cases were recruited from a university-based urology outpatient clinic. Eligible cases were more than 45 years of age and had histological confirmation of a prostate cancer diagnosis within 1 year of entry into the study. Controls were histologically confirmed free of prostate cancer. Erythrocyte membranes from venous blood and adipose tissue fatty acids from s.c. fat samples were analyzed in batches using capillary gas chromatography. Unconditional logistic regression analysis was used to calculate odds ratios for the association of each fatty acid with prostate cancer while controlling for potential confounders. Linoleic acid consumption was positively associated with prostate cancer risk. The odds ratios comparing the first and fourth quartiles of linoleic acid consumption were 3.54 (95% confidence interval, 1.0-12.53) with P trend < 0.04 for erythrocyte membranes, and 2.47 (95% confidence interval, 0.66-9.26) with P trend < 0.08 for adipose tissue. These data suggest that linoleic acid consumption may increase prostate cancer risk, which is consistent with results from animal experiments. Linoleic acid is found in vegetable oils used in cooking and in cereals, snack foods, and baked goods. Our data failed to demonstrate consistently a protective effect of marine omega-3 fatty acids on prostate cancer.

Adipose Tissue↗

PubMed1995

The risk of esophageal cancer in patients with achalasia. A population-based study.

OBJECTIVE: To determine more precise and accurate cancer risk estimates for achalasia that could be used to plan surveillance. DESIGN: Cohort. SETTING: Swedish population. PARTICIPANTS: All patients with achalasia listed in the population-based Swedish Inpatient Register from 1964 through 1989. MAIN OUTCOME MEASURES: The observed number of cancers in the cohort was compared with expected numbers of cancers (standardized incidence ratio [SIR]) for each 5-year age group and calendar year of observation, calculated using data from the Swedish Cancer Registry. RESULTS: A total of 1062 patients with achalasia accumulated 9864 years of follow-up. The mean age at entry was 57.2 years, and the mean age at cancer diagnosis was 71.0 years. Esophageal cancer occurred in 24 patients. The risk of esophageal cancer in the first year after achalasia diagnosis was extremely high (SIR, 126.3; 95% confidence interval [CI], 63.0 to 226.1) as a consequence of prevalent cancers leading to distal esophageal obstruction simulating achalasia. During years 1 to 24, the risk was increased more than 16-fold (SIR, 16.6; 95% CI, 8.8 to 28.3). Annual surveillance after the first year would require 406 endoscopic examinations in men and 2220 in women to detect one cancer. CONCLUSIONS: Patients with achalasia are at markedly increased risk of developing esophageal cancer. A substantial number of surveillance examinations might be required to screen for cancers, especially in women. It is not known whether surveillance will result in improved survival.

Adult↗