Tea consumption and risk of cancer of the colon and rectum.

The association between tea consumption and risk of colon and rectal cancers was investigated in a population-based case-control study conducted in Iowa (United States). Colon (n = 685) and rectal (n = 655) cancer cases age 40-85 yr were identified through the Iowa Surveillance, Epidemiology, and End Results (SEER) Cancer Registry (86% response rate); controls (n = 2,434) were frequency matched by sex and 5-yr age group (80% response rate). The usual adult consumption of tea (hot and iced), along with other information including dietary data, was self-reported using a mailed questionnaire. Total tea consumption (cups/day) was categorized as none (reference category), low (< 3.1), medium (3.1-5.0), and high (> 5.0), with cut points for tea consumers based on the 75th and 90th percentiles of use among controls. Unconditional logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals. There was no association between total tea consumption and colon cancer (ORs = 1.0, 1.1, 1.3, and 0.7) or rectal cancer (ORs = 1.0, 0.9, 1.4, and 1.0) after adjustment for age, sex, education, physical activity, smoking history, and intake of coffee, fiber, and fruits and vegetables. Results were similar when hot tea and iced tea were evaluated individually. Further adjustment for other colorectal cancer risk factors did not alter these results. There was no association with proximal or distal colon cancer. There was also no interaction between tea consumption and any of the dietary variables or total fluid on risk of colon or rectal cancer, with the exception of a suggestive positive association between an increasing frequency of tea consumption and colon cancer risk among current smokers (multivariate ORs = 1.0, 1.4, 2.0, and 1.8; P for trend = 0.1), but not among never smokers (multivariate ORs = 1.0, 1.0, 1.1, and 0.4; P for trend = 0.3). These data do not support an overall association, either positive or negative, between tea consumption and risk of colon or rectal cancer in this Mid-western US population.

Lifestyle and anthropometric risk factors for prostate cancer in a cohort of Iowa men.

PURPOSE: Several lines of evidence suggest that prostate cancer has a hormonal etiology. We evaluated factors known to modulate the endocrine system, including alcohol and tobacco use, physical activity, and obesity as risk factors for prostate cancer. METHODS: Cancer-free controls who participated in a population-based case-control study from 1986-1989 (81% response rate) were followed through 1995 for cancer incidence by linkage to the Iowa Cancer Registry; 101 incident prostate cancers were identified. RESULTS: Compared with non-users of alcohol, men who consumed <22 grams alcohol per week (relative risk [RR] = 1.1; 95% Confidence Interval [CI] 0.6-2.1), 22-96 grams alcohol per week (RR = 2.6; 95% CI 1.4-4. 6) and >96 grams alcohol per week (RR = 3.1; 95% CI 1.5-6.3) were at increased risk of prostate cancer after adjustment for age, family history of prostate cancer, body mass index, total energy, and intake of carbohydrate, linoleic acid, lycopene, retinol, and red meat (p for trend < 0.0001). The respective RRs were similar when assessing type of alcohol consumed (beer, wine or liquor) or when well-differentiated, localized tumors were excluded. Body mass index was only weakly and positively associated with prostate cancer after adjustment for age, but this association strengthened after multivariate adjustment and exclusion of well-differentiated, localized tumors. For the latter tumors, men with a BMI of 24.1-26.6 kg/m(2) and >26.6 kg/m(2) were at elevated risk compared to men with a BMI <24.1 kg/m(2). Tobacco use (cigarettes, cigar/pipe, chewing tobacco and snuff use), height, weight, and both leisure and occupational physical activity were not associated with risk of prostate cancer in this cohort. CONCLUSIONS: These data suggest that in white men obesity is a risk factor for more clinically significant prostate cancer and confirm limited previous reports showing that alcohol consumption is positively associated with prostate cancer and that this risk is not limited to any specific type of alcohol.

Tea consumption and risk of bladder and kidney cancers in a population-based case-control study.

Recent epidemiologic studies have suggested that tea may be protective against cancers of the urinary tract. The authors examined the association between usual adult tea consumption and risk of bladder and kidney cancers in a population-based case-control study that included 1,452 bladder cancer cases, 406 kidney cancer cases, and 2,434 controls. For bladder cancer, the age- and sex-adjusted odds ratios (OR) (95% confidence intervals (CI)) referent to nonusers of tea were 0.9 (0.7, 1.1) for <1.0 cup/day, 1.0 (0.8, 1.2) for 1.0-2.6 cups/day, and 0.9 (0.7, 1.1) for >2.6 cups/day (cutpoints for users based on the tertile distribution among controls). When more extreme cutpoints were used, persons who consumed >5 cups/day (>90th percentile) had a suggestive decreased risk (OR = 0.7; 95% CI 0.5, 1.0), but there was no evidence of a dose-response relation. In analyses stratified by median total beverage intake (2.6 liters/day), there was an inverse association with tea use among persons who consumed less than the median (OR = 0.5; 95% CI 0.3, 0.8) but no association for persons who consumed at or above the median. In contrast, for kidney cancer, there was no association with tea use. Adjustment for site-specific risk factors did not alter these results. This study offers only minimal support for an inverse association between tea consumption and bladder or kidney cancer risk.

Intrathecal baclofen down-regulates GABAB receptors in the rat substantia gelatinosa.

At present, it is not clear why drug tolerance develops in patients receiving intrathecal baclofen for the chronic treatment of spasticity of spinal origin. To investigate the mechanisms of tolerance to the gamma-aminobutyric acid (GABAB) agonist baclofen, rats were implanted with intrathecal catheters and continuously infused with either the drug or saline for 1, 3, or 7 days. The dose chosen, 1 microgram/hr, initially caused profound hindlimb motor weakness, but by Day 7 the rats had adapted to the drug and exhibited only minimal motor impairment. The animals were sacrificed on Day 1, 3, or 7 and quantitative autoradiography was used to determine the binding density and affinity of the GABAB receptors in the substantia gelatinosa of the lumbar spinal cord. After 1 day of drug infusion there was no change in binding parameters, but after 3 and especially after 7 days there was a significant decrease in the GABAB binding density (74% and 66%, respectively) in baclofen-treated rats as compared to saline-treated control rats. This GABAB receptor down-regulation correlated with tolerance to the motor weakness in the baclofen-treated animals and suggests that similar mechanisms contribute to drug tolerance in patients.

Spinal cord transection produces a long-term increase in GABAB binding in the rat substantia gelatinosa.

Quantitative autoradiography was used to determine changes in GABAB receptor binding in the substantia gelatinosa of the lumbar spinal cord at 4 days and at 6 weeks after a midthoracic spinal transection in rats. In the 4 day lesion animals, there was no significant change in either the density or the affinity of the GABAB binding. At 6 weeks, however, there was a 35% increase in binding density, with no significant change in affinity. The results suggest that alterations in spinal synaptic mechanisms can slowly evolve following loss of descending input to the spinal cord.