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PubMed2004

In vitro and ex vivo antihydroxyl radical activity of green and roasted coffee.

The specific antiradical activity against the hydroxyl radical of the water soluble components in green and dark roasted Coffea arabica and Coffea robusta coffee samples, both in vitro by the chemical deoxiribose assay and ex vivo in a biological cellular system (IMR32 cells), were determined. All the tested coffee solutions showed remarkable antiradical activity. In the deoxiribose assay, all the tested solutions showed similar inhibitory activity (IA%) against the sugar degradation (IA values ranged from 45.2 to 46.9%). In the cell cultures, the survival increase (SI%) ranged from 197.0 to 394.0% with C. robusta roasted coffee being significantly more active than the other samples. The coffee solutions underwent dialysis (3500 Da cutoff membrane) to fraction their components. In both systems, the dialysates (MW < 3500 Da) either from green or roasted coffee, showed antiradical activity, while the only retentates (MW > 3500 Da) from the roasted coffee samples were active. The preparative gel-filtration chromatography of roasted coffee C. robusta dialysate gave three fractions active in the biological system, all containing chlorogenic acid derivatives. The most active fraction was found to be that containing the 5-O-caffeoilquinic acid, which shows a linear relation dose-response ranging from 0.02 to 0.10 mM. The results show that both green and roasted coffee possess antiradical activity, that their more active component is 5-O-caffeoyl-quinic acid, and moreover that roasting process induces high MW components (later Maillard reaction products, i.e., melanoidins), also possessing antiradical activity in coffee. These results could explain the neuroprotective effects found for coffee consumption in recent epidemiological studies.

Antioxidants↗
PubMed2006

Chlorogenic acids and lactones in regular and water-decaffeinated arabica coffees.

The market for decaffeinated coffees has been increasingly expanding over the years. Caffeine extraction may result in losses of other compounds such as chlorogenic acids (CGA) and, consequently, their 1,5-gamma-quinolactones (CGL) in roasted coffee. These phenolic compounds are important for flavor formation as well as the health effects of coffee; therefore, losses due to decaffeination need to be investigated. The present study evaluates the impact of decaffeination processing on CGA and CGL levels of green and roasted arabica coffees. Decaffeination produced a 16% average increase in the levels of total CGA in green coffee (dry matter), along with a 237% increase in CGL direct precursors. Different degrees of roasting showed average increments of 5.5-18% in CGL levels of decaffeinated coffee, compared to regular, a change more consistent with observed levels of total CGA than with those of CGL direct precursors in green samples. On the other hand, CGA levels in roasted coffee were 3-9% lower in decaffeinated coffee compared to regular coffee. Although differences in CGA and CGL contents of regular and decaffeinated roasted coffees appear to be relatively small, they may be enough to affect flavor characteristics as well as the biopharmacological properties of the final beverage, suggesting the need for further study.

Caffeine↗
PubMedDate not supplied

Association of coffee and caffeine intake with the risk of Parkinson disease.

CONTEXT: The projected expansion in the next several decades of the elderly population at highest risk for Parkinson disease (PD) makes identification of factors that promote or prevent the disease an important goal. OBJECTIVE: To explore the association of coffee and dietary caffeine intake with risk of PD. DESIGN, SETTING, AND PARTICIPANTS: Data were analyzed from 30 years of follow-up of 8004 Japanese-American men (aged 45-68 years) enrolled in the prospective longitudinal Honolulu Heart Program between 1965 and 1968. MAIN OUTCOME MEASURE: Incident PD, by amount of coffee intake (measured at study enrollment and 6-year follow-up) and by total dietary caffeine intake (measured at enrollment). RESULTS: During follow-up, 102 men were identified as having PD. Age-adjusted incidence of PD declined consistently with increased amounts of coffee intake, from 10.4 per 10,000 person-years in men who drank no coffee to 1.9 per 10,000 person-years in men who drank at least 28 oz/d (P<.001 for trend). Similar relationships were observed with total caffeine intake (P<.001 for trend) and caffeine from non-coffee sources (P=.03 for trend). Consumption of increasing amounts of coffee was also associated with lower risk of PD in men who were never, past, and current smokers at baseline (P=.049, P=.22, and P=.02, respectively, for trend). Other nutrients in coffee, including niacin, were unrelated to PD incidence. The relationship between caffeine and PD was unaltered by intake of milk and sugar. CONCLUSIONS: Our findings indicate that higher coffee and caffeine intake is associated with a significantly lower incidence of PD. This effect appears to be independent of smoking. The data suggest that the mechanism is related to caffeine intake and not to other nutrients contained in coffee. JAMA. 2000;283:2674-2679.

Aged↗
PubMed2006

Coffee, CYP1A2 genotype, and risk of myocardial infarction.

CONTEXT: The association between coffee intake and risk of myocardial infarction (MI) remains controversial. Coffee is a major source of caffeine, which is metabolized by the polymorphic cytochrome P450 1A2 (CYP1A2) enzyme. Individuals who are homozygous for the CYP1A2*1A allele are "rapid" caffeine metabolizers, whereas carriers of the variant CYP1A2*1F are "slow" caffeine metabolizers. OBJECTIVE: To determine whether CYP1A2 genotype modifies the association between coffee consumption and risk of acute nonfatal MI. DESIGN, SETTING, AND PARTICIPANTS: Cases (n = 2014) with a first acute nonfatal MI and population-based controls (n = 2014) living in Costa Rica between 1994 and 2004, matched for age, sex, and area of residence, were genotyped by restriction fragment-length polymorphism polymerase chain reaction. A food frequency questionnaire was used to assess the intake of caffeinated coffee. MAIN OUTCOME MEASURE: Relative risk of nonfatal MI associated with coffee intake, calculated using unconditional logistic regression. RESULTS: Fifty-five percent of cases (n = 1114) and 54% of controls (n = 1082) were carriers of the slow *1F allele. For carriers of the slow *1F allele, the multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of nonfatal MI associated with consuming less than 1, 1, 2 to 3, and 4 or more cups of coffee per day were 1.00 (reference), 0.99 (0.69-1.44), 1.36 (1.01-1.83), and 1.64 (1.14-2.34), respectively. Corresponding ORs (95% CIs) for individuals with the rapid *1A/*1A genotype were 1.00, 0.75 (0.51-1.12), 0.78 (0.56-1.09), and 0.99 (0.66-1.48) (P = .04 for gene x coffee interaction). For individuals younger than the median age of 59 years, the ORs (95% CIs) associated with consuming less than 1, 1, 2 to 3, or 4 or more cups of coffee per day were 1.00, 1.24 (0.71-2.18), 1.67 (1.08-2.60), and 2.33 (1.39-3.89), respectively, among carriers of the *1F allele. The corresponding ORs (95% CIs) for those with the *1A/*1A genotype were 1.00, 0.48 (0.26-0.87), 0.57 (0.35-0.95), and 0.83 (0.46-1.51). CONCLUSION: Intake of coffee was associated with an increased risk of nonfatal MI only among individuals with slow caffeine metabolism, suggesting that caffeine plays a role in this association.

Aged↗
PubMed1988

Comparative mutagenicity of nine brands of coffee to Salmonella typhimurium TA100, TA102, and TA104.

Nine coffee preparations, four caffeinated instant brands, three caffeinated drip coffees, and two decaffeinated coffees, one of which was an instant brand, were evaluated for mutagenicity by the Ames assay using Salmonella typhimurium TA100, TA102, and TA104. All the coffees contained direct-acting mutagens, which reverted the three strains. The inclusion of a rat microsomal enzyme preparation reduced the mutagenic response of the three strains in the presence of some of the coffee samples. Both glyoxal and methylglyoxal, 1,2-dicarbonyls found in the coffees were mutagenic. The concentration of glyoxal, methyglyoxal, diacetyl, and guiacol were measured by gas chromatography/mass spectrometry. Caffeine, furfural, and 5-methylfurfural concentrations were determined by high performance liquid chromatography. Although lower concentrations of methyglyoxal were found in the drip caffeinated coffees, the mutagenic potency of these preparations was higher than the instant coffees on a weight basis especially when TA104 was the indicator organism. Our findings agree with those of other workers who have shown that carbonyl compounds, which were present in all the brands tested, are partially responsible for the mutagenic response of coffee but that additional mutagens are also present.

Animals↗
PubMed1987

Coffee consumption and risk of pancreatic cancer.

The relationship between pancreatic cancer and coffee, decaffeinated coffee and tea drinking habits was evaluated using data from a hospital-based case-control study conducted in Northern Italy on 150 histologically confirmed cases and 605 controls with acute, non-neoplastic, other than digestive tract diseases unrelated to coffee consumption or to any of the known or potential risk factors for cancer of the pancreas. Compared with subjects who did not drink coffee, the multivariate relative risks were 1.7 for those who drank less than 2 cups per day, but only 1.4, and 1.1 respectively for drinkers of 3 or 4 and 5 or more cups. Likewise, there was no association with duration of consumption of coffee, decaffeinated coffee or tea. These findings were reviewed together with published evidence from other case-control studies (or cohort studies analyzed as case-control) of coffee and pancreatic cancer. When appropriate statistical methods were used to pool information, and the data from the first study which was the basis of the hypothesis were omitted, the relative risk of pancreatic cancer based on 1,464 cases was 1.2 for moderate coffee drinkers and 1.4 for heavy drinkers, and we suspect that at least part of this moderate residual association is confounded by cigarette smoking. Thus, although the present investigation and a general overview of published epidemiological evidence are compatible with a small effect of coffee on pancreatic carcinogenesis, interpretation of these findings is not obvious on account of the possibility of residual confounding and other sources of bias.

Adult↗
PubMed1976

Coffee consumption and mortality in a community study--Evans Co., Ga.

Total mortality showed no association with heavy coffee consumption in the four race-sex groups of Evans County. Deaths from coronary heart disease in WM, WF and BM showed no statistically significant differences between the two coffee consuming groups. Sex differences in cerebrovascular death rates, consistent in both races, suggest the possibility for a female excess of stroke deaths among coffee drinkers, and a "protective" effect of coffee drinking among males. Thus, in an area of the United States which has been designated the "Stroke Belt", neither the cardiovascular nor the cerebrovascular death rates seem strongly nor consistently related to coffee drinking habits. Although the number of deaths (339) is fairly large, representing a 13% mortality in this community over a four and one-half year observation period, the classification in four race-sex groups with further division into the groups with different coffee drinking habits limits each stratum to rather small numbers. In addition, 86 cases of CHD and CVD were diagnosed during lifetime already and, therefore, were excluded from the prospective mortality study. Confidently to refute or confirm the allegations of a detrimental influence of high coffee intake on ischemic heart disease one would need larger numbers. But in the light of our most important finding--that mortality from all causes is not increased in the high coffee consuming group--the finding of increased ischemic heart disease death rates with high coffee consumption would have to be compensated by a provocative, lower rate for other causes of death.

Black People↗
PubMed2004

4-Caffeoyl-1,5-quinide in roasted coffee inhibits [3H]naloxone binding and reverses anti-nociceptive effects of morphine in mice.

RATIONALE: Cinnamoylquinides are formed from the corresponding chlorogenic acids during coffee roasting. Instant coffee has been shown to displace binding of the mu opioid receptor antagonist, [3H]naloxone, but the putative active agent, feruloylquinide, has not been characterized. OBJECTIVES: The goal was to identify the active agent(s) in coffee by measuring the binding affinity of individual cinnamoyl-1,5-quinides to the human mu opioid receptor, and determine the effects of these compounds on morphine-induced anti-nociceptive behavior in mice. METHODS: Cinnamoyl-1,5-quinides in extracts of decaffeinated instant coffee were quantified by reverse-phase HPLC comparisons with synthetic samples of 3-coumaroyl-1,5-quinide and 4-coumaroyl-1,5-quinide, 3-caffeoyl-1,5-quinide and 4-caffeoyl-1,5-quinide (4-CQL) 3-feruloyl-1,5-quinide and 4-feruloyl-1,5-quinides and 3,4-dicaffeoyl-1,5-quinide (DICAQ). Affinities of the cinnamoyl-1,5-quinides and decaffeinated instant coffee extract were determined by displacement of [3H]naloxone binding in cultured HEK-MOR cells. Inhibition of the anti-nociceptive activity of morphine (1 mg/kg IP) was determined in C57BL/6J mice using the hot plate test at 52 degrees C. RESULTS: Extract of decaffeinated instant coffee produced a displacement K(i) of 42+/-16 mg/l, while the K(i) of a synthetic sample of 4-CQL was 4.4+/-0.4 microM. Compounds with a cinnamoyl substituent in the 4-position of the quinide, i.e. 4-CQL, DICAQ, 3,4-diferuloyl-1,5-quinide, and 3,4-dicoumaroyl-1,5-quinide, had affinities for the mu opioid receptor in the low micromolar range. In the hot plate test, coffee extract, containing 0.78% of 4-CQL, reversed the anti-nociceptive effect of morphine at 10 mg/kg IP. Two cinnamoyl-1,5-quinides found in roasted coffee, DICAQ, and 4-CQL, were active at 1 and 0.1 mg/kg IP, respectively. CONCLUSIONS: These results suggest that the previously reported anti-opioid activity of instant coffee is caused primarily by the presence of 4-CQL, and to lesser extent by other cinnamoyl-1,5-quinides.

Analgesics, Opioid↗
PubMed2006

Quality and flavour stability of coffee substitute prepared by extrusion of wheat germ and chicory roots.

A mixture of roasted chicory roots and wheat germ (1:1 w/w) was subjected to extrusion processing for preparation of coffee substitute. Comparative studies concerning sensory characteristics and headspace volatiles were carried out between genuine coffee and a freshly prepared coffee substitute. The sensory evaluation revealed similarities between the two samples. The comparative odour profile analysis showed that the sweetish/caramel-like note scored higher in our coffee substitute sample than in real coffee, whereas the other odour quality attributes showed an opposite trend. The high quality of the fresh coffee substitute was correlated to the presence of volatiles that are responsible for the fresh coffee aroma, such as: 2-methylbutanal, 3-methylbutanal, 2-methylfuran and 2,3-butanedione in high concentration. Storage of coffee substitute samples revealed a noticeable decrease in concentration of the Strecker aldehydes and diketones and a remarkable increase in phenolic compounds, whereas pyrazine and furan derivatives showed no linear changes during storage. The ratio of 2,3-butanedione/2-methylfuran (B/M) was used as an indicator for aging of coffee substitute samples. The variation in this ratio (B/M) during storage for 6 months was consistent with that of the odour profile analysis.

Asteraceae↗
PubMed1985

Circulatory effects of coffee in relation to the pharmacokinetics of caffeine.

Drinking coffee results in an increase in blood pressure (BP) after an interval of caffeine abstinence. During chronic caffeine intake this pressor response disappears and adaptation to the circulatory effects of caffeine develops. This study was designed to determine whether a pressor response to coffee occurs during chronic caffeine intake if low basal plasma caffeine levels are achieved by a period of caffeine abstinence, defined by individual plasma caffeine half-life. In 8 normotensive subjects, circulatory measurements were studied after ingestion of coffee in 2 strengths, decaffeinated coffee and hot water after a caffeine abstinence of 4.5 times individual caffeine half-life. These measurements were compared to the same protocol without intervention. Coffee of both strengths resulted in a similar increase in BP (diastolic BP +/- 15%). The coffee-induced increase in forearm blood flow and plasma epinephrine levels were less pronounced. Decaffeinated coffee induced a smaller increase of diastolic BP, and after water, no changes were observed. Additionally, a negative correlation was found between the coffee-induced BP increase and basal plasma caffeine level in a group of 30 normotensive subjects (r = -0.71, p less than 0.001). During chronic caffeine intake, subjects with short plasma caffeine half-life are exposed to a pressor response after drinking coffee, despite the phenomenon of adaptation.

Adult↗
PubMed1994

Effects of cessation of caffeinated-coffee consumption on ambulatory and resting blood pressure in men.

Coffee consumption has been weakly linked to high blood pressure (BP). The hypothesis that cessation of caffeinated-coffee consumption lowers ambulatory BP was tested in men in a randomized trial. One hundred eighty-six middle-aged, normotensive, male, habitual caffeinated-coffee consumers were recruited. Of these subjects, 150 had sufficiently complete, ambulatory BP measurements for analysis. After 2 months of standard caffeinated-coffee consumption, subjects were randomized to consume an equal amount of the same standard caffeinated coffee or a standard decaffeinated coffee, or to discontinue coffee consumption for 2 months. Diet composition, body weight and exercise did not change. Resting BP and heart rate were not different between the groups before and after intervention. In comparison with the continued caffeinated-coffee group (control), the decaffeinated-coffee group revealed significant reductions in mean ambulatory systolic BP during the morning (-4.0 +/- 11 mm Hg; p = 0.014), afternoon (-5.3 +/- 10 mm Hg; p = 0.001) and evening (-3.2 +/- 10 mm Hg; p = 0.003) hours, reductions in mean ambulatory diastolic BP during the afternoon (-1.8 +/- 10 mm Hg; p = 0.063) and evening (-1.8 +/- 10 mm Hg; p = 0.059) hours and no change in ambulatory heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The influence of roasting procedure on the formation of mutagenic compounds in coffee.

Mutagenic products can be formed during the processing of food and especially as a result of heat treatment. Direct acting mutagenic activity was found in extracts of instant coffee and roasted coffee beans using Salmonella typhimurium TA100 in vitro. The mutagenic activities of the four pure coffee varieties examined (Coffea arabica Santos, Coffea arabica Columbia, Coffee robusta Indonesia, Coffee robusta Camerun) were within the same range. Twenty milligrams per plate freeze-dried powder prepared from aqueous roast coffee extracts induced between six and ten times the number of revertants found in the negative controls. Green coffee beans had no mutagenic activity. Mutagenicity increased with roasting time up to 4 min in the Probat drum roaster and then remained constant (i.e. no further increase after 8 min, the time normally used to roast coffee). The genotoxic compounds were quickly formed at temperatures below 220 degrees C (in normally roasted coffee the beans must reach a temperature of 220 degrees C). Mutagenic activity was independent of the roasting procedure (Jetzon procedure v. Probat drum roaster).

Coffee↗
PubMed2004

Caffeinated coffee consumption and mortality after acute myocardial infarction.

BACKGROUND: Previous studies have generally suggested no effect of coffee consumption on the risk of acute myocardial infarction. The effect of coffee consumption on prognosis after acute myocardial infarction is uncertain. METHODS: In an inception cohort study, we observed 1935 patients who were hospitalized with a confirmed acute myocardial infarction between 1989 and 1994 at 45 community hospitals and tertiary care centers in the United States, as part of the Determinants of Myocardial Infarction Onset Study. Trained interviewers assessed self-reported caffeinated coffee consumption before infarction with a standardized questionnaire. We analyzed survival censored at December 31, 1995, using Cox proportional hazards regression. RESULTS: Of the 1902 patients for whom we had information on coffee intake, 315 (17%) died during a median follow-up period of 3.8 years. Coffee drinkers tended to be men, younger, and free of comorbidity, and they were more likely to be current smokers. Coffee consumption was not associated with an overall change in long-term post-infarction mortality rate. However, we did observe an unexpected and unexplained variation in the association between coffee consumption and mortality with time, with an apparent inverse association in the first 90 days after infarction. CONCLUSIONS: Self-reported coffee consumption has no overall association with post-infarction mortality. The unexpected time variation in the effect of coffee intake requires evaluation in other studies.

Aged↗
PubMed2004

Anti-genotoxicity of coffee against N-methyl-N-nitro-N-nitrosoguanidine in mouse lymphoma cells.

The main aim of this work was to test the hypothesis that instant coffee, a commonly consumed polyphenolic beverage with antioxidant activity, can protect mammalian cells against genotoxic effects in vitro. For this purpose, the L5178Y mouse lymphoma cell line was selected to assess modulatory effects of coffee on the genotoxicity of N-methyl-N-nitro-N-nitrosoguanidine (MNNG). We initiated the work with a set of preliminary experiments in which the cytokinesis-block micronucleus test was performed. Results obtained from these experiments demonstrated a dose-related decrease in genotoxicity following co-treatment of mouse lymphoma cells with three doses of caffeinated instant coffee. Both pre-treatment and co-treatment showed significant antigenotoxic effects against MNNG. Caffeinated and decaffeinated instant coffee samples inhibited genotoxicity. There was no significant change in the antigenotoxic effect of caffeinated instant coffee after filtration using a 0.2 microm filter. Similar in vitro experiments demonstrated antigenotoxic effects against MNNG when boiled coffee was used instead of instant coffee. On the basis of the findings from the above preliminary experiments, further work was carried out to evaluate the possible protective effects of caffeinated instant coffee against MNNG-induced DNA damage, mutation and chromosomal damage. Results from three or five independent experiments demonstrated significant protective effects of caffeinated instant coffee against MNNG-induced DNA damage in the comet assay, mutation at the Tk locus and chromosomal damage in the cytokinesis-block micronucleus test.

Animals↗
PubMed2006

UV light assisted decolorization of dark brown colored coffee effluent by photo-Fenton reaction.

The photochemical decolorization of coffee effluent has been examined by photo-Fenton (UV/Fe2+/H2O2) process. Effects of UV light intensity, initial coffee concentration, iron dose and H2O2 dose on the color removal of model coffee effluent have been investigated. The rate of decolorization increased with decreasing initial coffee effluent concentration. It was found that the Fe ion dose and UV light intensity enhanced the decolorization rate. The decolorization process of coffee effluent could be divided into three established phases. At the beginning of the photo-Fenton process, the instantaneous and significant increase in color of the solution was found (Phase-I). In the subsequent phase (Phase-II), the decolorization rate was initially fast and subsequently decreased. In Phase-III, the rate was accelerated and then the complete decolorization of model coffee effluent was achieved. In order to elucidate the mechanisms of coffee effluent color removal process, the concentration changes in Fe3+ and Fe2+ besides H2O2 were measured during the course of the photo-Fenton process. The rate-determining step in Phase-II was the photo-Fenton reaction or photoreduction of Fe3+. On the other hand, the decolorization process in Phase-III was highly affected by Fenton reaction or decomposition of H2O2 with Fe2+. About 93% mineralization of 250 mg L(-1) model coffee effluent was achieved after 250 min. A comparative study for TiO2, ZnO and photo-Fenton oxidation processes has been also carried out and the photo-Fenton process was found to be the most effective for color removal of coffee effluent.

Coffee↗
PubMed2003

The effects of coffee on enzymes involved in metabolism of the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in rats.

The effects of coffee on the metabolism and genotoxicity of the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were investigated. Coffee diminished the bacterial mutagenicity of PhIP in the Ames reversion assay through inhibition of cytochrome P450 1A2 (CYP1A2), a key enzyme involved in the metabolic activation of PhIP. When given as part of the diet (0, 1 or 5% w/w) to male Fischer-344 rats for 2 weeks, coffee affected the expression of hepatic enzymes involved in PhIP metabolism. Coffee increased the expression of CYP1A2 by 16-fold in the 5% coffee-treated group, and approximately half of this inductive effect was attributed to caffeine. Coffee also increased the expression of enzymes involved in the detoxication of PhIP. A 2-fold increase in expression of glutathione S-transferase alpha was observed, UDP-glucuronosyl transferase (UGTs) activities of p-nitrophenol increased 2-fold, while N(2)-and N3-glucuronidation of the genotoxic metabolite 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine (HONH-PhIP) increased by 1.3-fold in the 5% coffee-treated over the control group. The amount of PhIP (0.75 mg/kg, 24 h) eliminated in urine as the N(2)-and N3-glucuronide conjugates of HONH-PhIP increased by 1.8- and 2.5-fold, respectively, in the 5% coffee-treated group over control rats, suggesting either increased rates of N-oxidation of PhIP or N-glucuronidation of HONH-PhIP. Despite the strong induction of CYP1A2, there was no increase in PhIP-DNA adduct formation in colon and pancreas while liver adducts decreased by 50% over control animals. These data suggest that the effect of coffee on inhibition of PhIP N-oxidation and ensuing DNA damage is more important in vivo than its effect on induction of PhIP N-hydroxylation.

Animals↗
PubMed2002

Does coffee protect against liver cirrhosis?

PURPOSE: To evaluate the relation between consumption of coffee and other methylxanthine-containing beverages and liver cirrhosis. METHODS: A hospital-based case-control study of digestive tract and liver diseases was conducted in Greater Milan, Italy, including 101 cases with liver cirrhosis and 1538 controls. RESULTS: Compared with coffee non-drinkers, the multivariate odds ratio (OR) was 0.77 for one cup of coffee per day, 0.57 for two, and 0.29 for three or more. The OR for 40 years of coffee consumption or more was 0.45. Trends in risk were significant for both number of cups and duration of coffee drinking. No significant association was observed with decaffeinated coffee, tea and cola-containing beverages. The relation between coffee consumption and liver cirrhosis was not attributable to confounding and was observed across strata of tobacco, alcohol, and other major covariates of interest. In particular, an inverse relation was observed also in subjects reporting moderate alcohol drinking. CONCLUSIONS: The present study confirms, and further quantifies, the existence of an inverse association between coffee consumption and liver cirrhosis. However, the metabolism of caffeine is impaired in fasting subjects with liver cirrhosis, and the association could be due to a reduction of coffee drinking in subjects with liver cirrhosis.

Adult↗
PubMed1999

Relationship of coffee consumption with serum lipids and lipoproteins in Japanese men.

PURPOSE: To examine the relationship of instant coffee and brewed coffee with serum lipids and lipoproteins in Japanese men. METHODS: Study subjects were 4587 male self-defense officials aged 48-56 years who had a preretirement health examination at one of the three hospitals of the Self-Defense Forces from October 1986 to December 1992. A self-administered questionnaire ascertained lifestyle characteristics including consumption of a limited number of foods and beverages by all of the men. Serum concentrations of total cholesterol (TC), triglycerides (TG), and high density lipoprotein (HDL) cholesterol were measured, and low density lipoprotein (LDL) cholesterol levels were calculated from the values of TC, TG, and HDL cholesterol. RESULTS: While the consumption of brewed coffee was unrelated to any parameter of serum lipids and lipoproteins, instant coffee consumption showed a highly significant positive association with serum LDL cholesterol levels and an inverse association with serum TG levels. After adjustment for body mass index, smoking, alcohol use, green tea consumption, rank, and hospital, for each cup of instant coffee per day, LDL cholesterol levels were 0.82 mg/dl (95% confidence interval (CI) 0.29-1.35) higher, and TG levels in a natural log-scale were 0.014 mg/dl (95% CI 0.006-0.022) lower. There was also a tendency for a positive association between instant coffee intake and serum TC levels (trend p = 0.09). HDL cholesterol levels were unrelated to instant coffee consumption. These associations did not change after additional adjustment for selected foods and beverages associated with serum lipids and lipoproteins. CONCLUSIONS: The findings suggest that instant coffee, not brewed coffee, may be associated with raised levels of serum LDL cholesterol and decreased levels of serum TG.

Coffee↗