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There is a significant difference in plasma levels of the free fatty acids (FFA) in habitual coffee drinkers compared with a control group of non-coffee and decaffeinated-coffee drinkers. A significant difference in FFA levels between males and females was found under the same conditions of coffee consumption, in non-coffee drinkers and in decaffeinated-coffee drinkers.
It has been reported that rat plasma fluoride (F) concentrations are higher by up to 100% when F is administered ig in coffee or a caffeine solution compared with when it is administered in water. It was hypothesized that the consumption of caffeinated beverages has contributed to the prevalence of dental fluorosis. The present studies were done to determine the physiological mechanisms for these effects. For approximately 2 h after F was administered in coffee, plasma F concentrations were higher than when administered in water, decaffeinated coffee, or a caffeine solution (3 mg/kg), but the intergroup differences were small and generally not statistically significant. The 4-hour plasma AUC values did not differ with statistical significance. There were no differences among the groups in the renal or extrarenal (skeletal) clearances of F, which suggested that the higher plasma F concentrations in the coffee groups may have been due to a slight and transient increase in absorption rate. The possibility that caffeine per se might elevate endogenous plasma F and calcium concentrations was excluded after caffeine (25 mg/kg) ig without F was given. In addition, the renal excretion, clearance, and fractional renal clearance of calcium did not differ among the groups. The results indicated that decaffeinated coffee and caffeine had no effect on F metabolism, whereas caffeinated coffee appeared to increase the initial absorption rate but not the 4-hour bio-availability.(ABSTRACT TRUNCATED AT 250 WORDS)
Although cigarette smoking is a clear risk factor for lung cancer, the other determinants of lung cancer risk among smokers are less clear. Tea and coffee contain catechins and flavonoids, which have been shown to exhibit anticarcinogenic properties. Conversely, caffeine may elevate cancer risk through a variety of mechanisms. The current study investigated the effects of regular consumption of black tea and coffee on lung cancer risk among 993 current and former smokers with primary incident lung cancer and 986 age-, sex-, and smoking-matched hospital controls with non-neoplastic conditions. Results indicated that lung cancer risk was not different for those with the highest black tea consumption (>or=2 cups/day) compared with nondrinkers of tea [adjusted odds ratio (aOR)=0.90; 95% confidence interval (CI)=0.66-1.24]. However, elevated lung cancer risk was observed for participants who consumed 2-3 cups of regular coffee daily (aOR=1.34; 95% CI=0.99-1.82) or >or=4 cups of regular coffee daily (aOR=1.51, 95% CI=1.11-2.05). In contrast, decaffeinated coffee drinking was associated with decreased lung cancer risk for both participants who consumed or=2 cups/day (aOR=0.64; 95% CI=0.51-0.80). These results suggest that any chemoprotective effects of phytochemicals in coffee and tea may be overshadowed by the elevated risk associated with caffeine in these beverages.
OBJECTIVE: To study the association of PD with preceding smoking, alcohol, and coffee consumption using a case-control design. METHODS: The authors used the medical records linkage system of the Rochester Epidemiology Project to identify 196 subjects who developed PD in Olmsted County, MN, during the years 1976 to 1995. Each incident case was matched by age (+/-1 year) and sex to a general population control subject. The authors reviewed the complete medical records of cases and control subjects to abstract exposure information. RESULTS: For coffee consumption, the authors found an OR of 0.35 (95% CI = 0.16 to 0.78, p = 0.01), a dose-effect trend (p = 0.003), and a later age at PD onset in cases who drank coffee compared with those who never did (median 72 versus 64 years; p = 0.0002). The inverse association with coffee remained significant after adjustment for education, smoking, and alcohol drinking and was restricted to PD cases with onset at age <72 years and to men. The OR for cigarette smoking was 0.69 (95% CI = 0.45 to 1.08, p = 0.1). The authors found no association between PD and alcohol consumption. Extreme or unusual behaviors such as tobacco chewing or snuff use and a diagnosis of alcoholism were significantly more common in control subjects than cases. CONCLUSIONS: These findings suggest an inverse association between coffee drinking and PD; however, this association does not imply that coffee has a direct protective effect against PD. Alternative explanations for the association should be considered.
We examined the effect of coffee on conjugation reactions in the human colon carcinoma cell line, Caco-2. After supplementing Caco-2 cultures with both 1-naphthol (200 microM) and various concentrations of coffee, the accumulation of 1-naphthyl sulfate and glucuronide in the growth medium was determined by analytical HPLC over a 24-h period. A strong reduction in sulfo-conjugation (<50% of the control value) was observed in cells treated with coffee (IC50=4.3%), but no effect on glucuronic acid conjugation (glucuronidation) was observed. Coffee was also found to inhibit sulfotransferase (SULT) activity towards 1-naphthol in vitro to a similar extent (IC50=5.1%) as in intact Caco-2 cells, but exhibited no effect upon UDP-glucuronosyl transferase (UGT) activity in vitro. PCR analyses showed no significant changes in the expression of either SULT genes (SULT1A1 and SULT1A3) or UGT genes (UGT1A1 and UGT1A6) following treatment with coffee solutions of up to 5% in concentration. These results suggest that the consumption of coffee can modify sulfo-conjugation reactions within intestinal epithelial cells, which may possibly affect the bioavailability of therapeutic drugs and the toxicity of environmental chemicals.
BACKGROUND: The role of coffee intake as a risk factor for coronary heart disease (CHD) has been debated for decades. We examined whether the relationship between coffee intake and incidence of CHD events is dependent on the metabolism of circulating catecholamines, as determined by functional polymorphism of the catechol-O-methyltransferase (COMT) gene. METHODOLOGY/PRINCIPAL FINDINGS: In a cohort of 773 men who were 42 to 60 years old and free of symptomatic CHD at baseline in 1984-89, 78 participants experienced an acute coronary event during an average follow-up of 13 years. In logistic regression adjusting for age, smoking, family history of CHD, vitamin C deficiency, blood pressure, plasma cholesterol concentration, and diabetes, the odds ratio (90% confidence interval) comparing heavy coffee drinkers with the low activity COMT genotype with those with the high activity or heterozygotic genotypes was 3.2 (1.2-8.4). Urinary adrenaline excretion increased with increasing coffee intake, being over two-fold in heavy drinkers compared with nondrinkers (p = 0.008 for trend). CONCLUSIONS/SIGNIFICANCE: Heavy coffee consumption increases the incidence of acute coronary events in men with low but not high COMT activity. Further studies are required to determine to which extent circulating catecholamines mediate the relationship between coffee intake and CHD.
Ochratoxin A (OA)-producing fungi were identified in coffee at different stages of maturation. The toxin was quantified in coffee during terrace drying and in coffee stored in barns. By direct plating, a high level of contamination (100%) was found in the coffee beans studied, with the genus Aspergillus representing 33.2%, of which Aspergillus ochraceus and Aspergillus niger represented 10.3 and 22.9%, respectively, of the strains isolated from the coffee beans. The capacity to produce ochratoxin was determined in 155 strains of A. ochraceus and A. niger using both the agar plug method and extraction with chloroform, giving positive results for 88.1% of the A. ochraceus strains and 11.5% of the A. niger strains. Analysis for OA in the terrace and barn coffee samples showed that, independent of cultivar, year harvested, or production region, all except one of the samples analyzed showed mycotoxin levels below the limit suggested by the European Common Market (8 microg/kg), thus indicating that the problem is restricted and due to severe faults in harvesting and storage practices.
The purpose of this study was to investigate whether the renin-angiotensin-aldosterone system activity RAAA or plasma catecholamines concentrations and blood pressure are related to distinct patterns of drinking one cup of coffee in hypertensive patients with low or normal plasma renin activity. Plasma renin activity and enzyme converting angiotensin I to angiotensin II activity and serum concentration of aldosterone and catecholamines were measured by radioimmunoassay. Blood pressure was measured by ambulatory monitoring. Our data suggest that drinking one cup of coffee caused after 60 min, to 2 hours elevated systolic and after 60 min diastolic pressure, only in hypertensive patients, with low RAAA habitually drinking coffee. Hypertensive patients with normal RAAA, habitually drinking coffee, after drinking one cup of coffee had elevation only of diastolic blood pressure from 60 min to 120 min after drinking, but systolic blood pressure did not elevate. Plasma catecholamines and aldosterone concentrations, blood renin activity and enzyme converting angiotensin I to angiotensin II activity were not elevated in hypertensive patients with low or normal RAAA after drinking one cup of coffee.
Some methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms are associated with hyperhomocysteinemia. Trials have shown a plasma homocysteine raising effect of coffee. We determined the effect of a daily intake of 600 ml coffee and a supplementation of 200 microg folic acid or placebo on plasma homocysteine (tHcy) with respect to the MTHFR C677T and A1298C polymorphisms. One hundred and twenty healthy, non-smoking men (22%) and women (78%) aged 29-65 years, took part in a controlled, randomized, blinded study with two intervention periods: i) a coffee-free period of three weeks, ii) 600 ml coffee/day and a supplement of 200 microg folic acid/d or placebo for four weeks. The results showed that tHcy at baseline was significantly higher for the 677TT genotype group compared to the 677CC genotype group (p=0.0045) and that this group responded with significantly larger increase in tHcy upon coffee exposure than the 677CC and 677CT genotype groups (p=0.0045 and p=0.0041, respectively). Supplementation with 200 microg folic acid compared to placebo reduced the tHcy increasing effect of coffee in the 677TT genotype group. The A1298C polymorphism did not affect tHcy concentration significantly at any stage in the study. In conclusion, the homocysteine increasing effect of coffee is particularly seen in individuals with the homozygous 677TT genotype. Supplementation with 200 microg folic acid/d decreases this tHcy increment.
AIM: To estimate the relative risk of triggering sudden cardiac death after coffee or alcohol consumption in out-of-hospital sudden cardiac death victims. METHODS: A case-crossover design with usual frequency approach was used and the study population included persons who died out of hospital due to sudden cardiac death. By mailing 2 questionnaires, 1 to the family members of the deceased and the other to the attending physician, necessary data on the mode of cardiac death, life style, health, and several socio-demographic variables were obtained. Cases were those who died of sudden cardiac death within 1 hour after coffee consumption or within 2 hours after ingesting alcohol; but controls were those who died in the hours when they were not exposed to these stimulans. The relative risk of dying within exposed hours in comparison to non-exposed hours was parameter estimated for each risk factor. RESULTS: Among 309 sudden cardiac death victims who died in the period from January 2000 to March 2001 in Slovenia, there were 253 men and 56 women with median age at death of 57.1 and 57.7, respectively. On average, each of them had 2.8 risk factors for ischemic heart disease, and the estimated relative risk of dying during 1 hour after coffee consumption was 1.73 (95% confidence interval [CI]=1.13-2.65), and within 2 hours after alcohol consumption 3.00 (95%CI=1.61-5.68). Within both coffee drinking and alcohol consuming groups, the relative risk was different among persons with different life style habits. It ranged from 1.50 for the coffee drinkers who had been receiving medication due to risk factors of heart diseases, to 2.63 for former alcohol drinkers. Among alcohol consumers it varied from 2.66 among those who were performing less than 104 hours of physical activity of six metabolic equivalents at least, to 52.15 among those of 90 heart beats or more per minute. CONCLUSION: Our research confirmed the hypothesis that coffee or alcohol consumption is a potential trigger for sudden cardiac death in persons with risk factors for ischemic heart disease.
The main cause of allergic manifestations among workers handling green coffee beans (GCB) is sensitization to castor beans (CB), which are considered a common contaminant of the sacks used to transport coffee beans. The RAST inhibition test was used to evaluate the presence of GCB and CB allergens on the surface of the sacks coming from the major world producers of coffee and to ascertain the presence of the CB allergen in coffee beans. A significant concentration of the two allergens, i.e., GCB and CB, on the sacks was demonstrated, with the highest values found on sacks from Brazil, while the hypothesis of a significant CB contamination in coffee beans was not confirmed. We believe the presence of the CB allergen on the surface of the sacks is due to contamination occurring during stocking and transport and could easily be prevented. Appropriate measures taken during transport could effectively prevent this "undue" risk in dockers and probably also in coffee industry workers.
Reported coffee consumption during 1954 to 1958 and 1971 to 1973 was used to test for association with cardiovascular disease (CVD) incidence and lipid values in the Framingham cohort. Multivariate analysis was employed, regressing CVD on age, systolic pressure, cigarette use, body mass index, total cholesterol, and coffee intake. In pooled analyses (2648 men with 549 CVD cases and 3566 women with 462 CVD cases) coffee intake was not associated with CVD incidence in either smokers or nonsmokers, irrespective of sex. Similarly, multivariate analyses for individuals with existing cardiovascular disease showed no association between coffee intake and subsequent cardiovascular disease. In men significant negative associations between coffee and total cholesterol, and very-low-density lipoprotein cholesterol were seen, whereas in women positive associations with low-density lipoprotein cholesterol were observed. Although inconsistent effects on the lipid profile were seen, no increase in primary or secondary CVD was seen with coffee drinking.
Relationships between coffee consumption and occurrence of cancer as well as mortality were explored in a Norwegian study of 13,664 men and 2,891 women who in 1967-69 reported their coffee consumption. No statistically significant positive associations were found between coffee consumption and disease. A weak negative association was found with total cancer incidence even when the first 4 of the 11 1/2 years of follow-up were excluded, and strong negative associations with coffee drinking were noted for cancer of the kidney and nonmelanoma skin cancer. For cancer of the pancreas and bladder, no increase in incidence was found among those with a high coffee consumption. In subjects less than 65 years of age at start of follow-up, coffee drinking showed a significant inverse association with colon cancer.
The purpose of this research was to determine the effect of including fresh and ensilaged coffee pulp in rations for monogastric animals, and find the best protein and coffee pulp levels in rations for rats. Fresh coffee pulp and pulp ensilaged for 12 months were used; both kinds of pulp were sun-dried before incorporating them into the rations. The chemical analyses of the pulps revealed a lower content in caffeine, tannins, chlorogenic acid and caffeic acid in the ensilaged pulp than in fresh coffee pulp. Thirty-two experimental rations were prepared, 16 with fresh coffee pulp and 16 with the ensilaged by-product, distributed into four different protein levels (10, 15, 20 and 25%), and three levels of pulp (15, 30 and 45%) for each protein level. The rations thus prepared were fed to Wistar albino rats for a six-week period. The parameters used to measure the effect of the two types of pulp were mortality rate, food consumption, weight gain, food conversion and apparent digestibility of the rations. Ensilaged pulp had a higher nutritive value, lower toxicity and better digestibility than fresh pulp. The increase in the protein level of the ration resulted in partial protection against the negative effects of coffee pulp on the performance of animals, since this improved as the protein level of the ration increased.
A headspace gas chromatographic procedure is described for the determination of methylene chloride (MC) in decaffeinated tea and coffee. The tea or coffee sample, with added methylene bromide (MB) internal standard, is equilibrated for 1.5 h at 100 degrees C in aqueous sodium sulfate before manual headspace sampling. MC and MB are separated on a Porasil A column at 160 degrees C and detected by using a Coulson electrolytic conductivity detector. For coffee and tea samples spiked at 1.3 ppm MC, as well as commercially decaffeinated teas and coffees containing up to 8 ppm MC, coefficients of variation were 10% or less. For decaffeinated teas, problems involving sample homogeneity and loss of MC before sealing the headspace vial had to be overcome. Similar problems with decaffeinated instant and ground coffees were minimal. The headspace procedure was superior to a previously reported distillation technique. MC was readily detected at 0.05 ppm. Fourteen decaffeinated teas and 15 decaffeinated coffees were analyzed; MC was detected at levels that ranged up to 15.9 and 4.0 ppm, respectively.
We compared five graded doses of decaffeinated coffee and a widely used protein test meal (Bacto-peptone) as stimulants of acid secretion (intragastric titration) and gastrin release (radioimmunoassay) in eight healthy men. In each subject, for both acid and gastrin, the sums of the responses to all five doses were greater to decaffeinated coffee than to peptone. The mean +/- SE peak acid output in millimoles per hour was 18.5 +/- 2.9 to decaffeinated coffee and 14.7 +/- 2.7 to peptone, representing 70% and 55%, respectively, of the peak acid output to pentagastrin. The mean +/- SEM peak increment over basal rate in serum gastrin in picograms per milliliter was 84.8 +/- 4.4 to decaffeinated coffee and 44.8 +/- 2.1 to peptone. At equal concentrations, decaffeinated coffee was a more potent stimulant of acid secretion and of gastrin release than peptone. The ingredient(s) of decaffeinated coffee that accounts for its high potency in stimulating acid secretion and gastrin release has not been identified.
In a Canadian population-based case-control study of 480 males and 152 female case-control pairs, the relative risk for development of bladder cancer for ever used versus never used cigarettes was 3.9 for males and 2.4 for females, with a dose-response relationship in both sexes. A reduced risk was associated with the use of filter cigarettes compared to nonfilter cigarettes. After control for cigarette usage, a significant risk was noted for male pipe smokers. For male ex-smokers the risk after 15 years of no smoking was less than one-half that of current male smokers. Bladder cancer risk was found for workers in the chemical, rubber, photographic, petroleum, medical, and food processing industries among males and for workers occupationally exposed to dust or fumes among both sexes. Bladder cancer risk was elevated for males consuming all types of coffee, regular coffee, and instant coffee and for females consuming instant coffee, but no dose-response relationship was found. Risk was found for males consuming water from nonpublic supples but not for females. No risk was observed in males or females consuming nitrate-containing foods, beverages other than coffee, or fiddlehead greens. Hair dye usage in females and phenacetin usage in males and females carried no risk. Divergent findings by area for aspirin suggested that an overall association was not causal. Reevaluation of the data on artificial sweeteners confirmed a significant bladder cancer risk in males and a dose-response relationship. The cumulated population attributable risk for bladder cancer was 90% for males from cigarette smoking, industrial exposure, and exposure to nonpublic water supplies and 29% for females from cigarette smoking, industrial exposure, and instant coffee consumption.
Total mortality showed no association with coffee usage in the four race-sex groups of Evans County, Georgia. Deaths of coronary heart disease (CHD) in white men and women and black men showed no statistically significant difference between high and low coffee consumers. In an area that has been designated as the "Stroke Belt," neither CHD nor cerebrovascular death rates seem related to coffee-drinking habits. However, to refute or confirm the allegations of a detrimental influence of high coffee intake, larger samples are needed. Nevertheless, our finding that mortality from all causes is not increased in the high coffee-consuming group means that a finding of increased CHD mortality with high coffee consumption would have to be compensated by a protective lower rate for other causes of death.