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PubMed2006

Association between coffee consumption and markers of inflammation and cardiovascular function during mental stress.

BACKGROUND: Coffee is widely consumed in the Western diet and therefore has important implications for public health. Research findings pertaining to the effects of coffee consumption on cardiovascular health are conflicting, and the role of caffeine is not clear. OBJECTIVE: To examine the relationship between coffee intake, inflammation and cardiovascular function at baseline and during mental stress, both cross-sectionally and after a 4-week period of withdrawal of coffee during which intake of caffeine was maintained. METHODS: Eighty-five healthy, non-smoking men with varying coffee-drinking habits were recruited. Blood pressure, heart rate, and markers of inflammation [C-reactive protein (CRP), von Willebrand factor antigen (vWF)], were measured at baseline and during mental stress. These measures were repeated after a 4-week period of withdrawal of coffee, during which intake of caffeine was maintained. Habitual levels of coffee and caffeine consumption were assessed from a self-reported questionnaire, and saliva samples for the analysis of caffeine concentrations were collected regularly throughout the period of withdrawal, to confirm compliance. RESULTS: Multiple linear regression analysis of pre-withdrawal data, adjusted for age, body mass index and intake of tea, red wine, fruit, vegetables, oily fish and dietary supplements revealed that coffee consumption was positively related to baseline systolic blood pressure, and increased heart rate and vWF responses to mental stress. Four weeks after withdrawal of coffee, the heightened vWF and heart rate responses to stress in habitual coffee drinkers persisted, whereas baseline systolic blood pressure had decreased. Total caffeine intake was unrelated to any measures of physiological function. CONCLUSIONS: Habitual coffee consumption is associated with heightened acute vascular inflammatory responses to mental stress, although these effects are not affected by short-term abstinence from coffee. These findings suggest that the relationship between coffee and markers of cardiovascular risk may be explained by residual or unmeasured confounding factors.

Adult↗

PubMed1983

Pharmacological characterisation of extracts of coffee dusts.

The contractile or relaxant activities or both of aqueous extracts of green and roasted coffees were assayed on isolated guinea pig tracheal spirals. Contractile and relaxant activities were compared with histamine and theophylline, respectively. Green coffee extracts induced concentration dependent contraction, but the maximal tension never exceeded 76.3% +/- 5.2 of a maximal histamine contraction (0.69 +/- 0.07 g/mm2 v 0.52 +/- 0.05 g/mm2; p (0.01). One gram of green coffee dust had a biological activity equivalent to 1.23 +/- 0.1 mg of histamine. The pD2 value of histamine was -5.17 +/- 0.05. The potency of green coffee was unaffected by mepyramine maleate (1 micrograms/ml, final bath concentration) while that of histamine was reduced 500 fold. Tissues contracted with histamine were not significantly relaxed by green coffee extracts. By contrast, roasted coffee extracts induced concentration dependent relaxation of uncontracted and histamine contracted tissues. Tissues contracted with green coffee extracts were also completely relaxed by roasted coffee extracts. The pD2 value of theophylline was -4.10 +/- 0.03. The relaxant activity of 1 g of roasted coffee was equivalent to 1.95 +/- 0.16 mg of theophylline. The potency of these extracts was significantly reduced after propranolol (1 micrograms/ml; dose ratio 1.56). Our results show that coffee dust extracts have considerable biological activity which changes from a contractile to a relaxant action as a consequence of processing. The greater incidence of adverse reactions to green coffee dust(s) in coffee workers may be related to the contractile activity present in green coffee dust.

Animals↗

PubMed2005

Relationship of coffee consumption with risk factors of atherosclerosis in rats.

AIMS: In experimental animals we investigated the relationship of coffee consumption with risk factors of atherosclerosis such as cholesterol, homocysteine, oxidative stress and inflammatory cytokines. METHODS: Forty-eight male Wistar rats were assigned to 3 treatment groups (a control diet group, 0.62% coffee diet group, and 1.36% coffee diet group), and animals were maintained on the experimental diets for 140 days. RESULTS: Coffee diets led to an increase in the caffeine concentration to 0.53 +/- 0.11 and 1.77 +/- 0.22 microg/ml, respectively, although caffeine in serum was not detected in rats fed the control diet. It also led to slightly increased total serum levels of homocysteine and cholesterol, but no significant differences were found between the control and coffee diet groups. Coffee intake did not affect the production of IL-6 and TNF-alpha induced by LPS, which contributes to the atheroma-promoting effect of recurrent bacterial infection. Regarding the biomarkers of oxidative stress, the serum level of 15-isoprostane F(2t), which was significantly increased by LPS injection, was not altered by coffee intake. In contrast, urinary 8-hydroxy-2-deoxyguanosine was significantly increased in the coffee diet groups (p < 0.05). On the other hand, serum glutathione peroxidase (GPx) activity tended to decrease in the coffee groups compared with the control group, but no significant difference was found between the control and coffee diet groups. Interestingly, a significant negative correlation was observed between GPx activity and homocysteine levels in the sera from control and coffee diet groups (r = -0.403, p < 0.05). CONCLUSIONS: This report is the first animal study on the relationship of coffee consumption with risk factors for atherosclerosis. From these results, we conclude that moderate coffee intake is not a risk factor for atherogenesis.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1997

Effects of coffee consumption on iron, zinc and copper status in nonpregnant and pregnant Sprague-Dawley rats.

To investigate the influence of coffee consumption on iron, zinc and copper status, 64 Sprague-Dawley female rats were assigned to four treatment groups: nonpregnant-given coffee, nonpregnant-given water, pregnant-given coffee and pregnant-given water. The coffee groups received a freeze-dried coffee solution (1.1% w/v) as the sole source of liquids during the 18-day study period; all groups were provided a purified diet marginal in iron ad libitum. On day 18 (of gestation in the pregnant rats), rats were intubated with 0.033 MBq59Fe after an 8 h fast and killed 4, 8, 12 or 24 h post-gavage. Fluid intake was significantly lower in the coffee groups. Coffee did not affect food consumption, weight gain, hemoglobin or hematocrit in either pregnant or nonpregnant rats. In nonpregnant rats, the percentage of 59Fe was lower in plasma and higher in the spleen and erythrocytes in the coffee group than in controls; in pregnant rats the coffee group had a higher percentage of 59Fe in the stomach (at 4 h only), blood, spleen and bone than controls. There were no significant effects of coffee on tissue concentrations of Fe, Zn or Cu in the nonpregnant group, but pregnant rats given coffee had high concentrations of Fe in the liver, bone and placenta, and low placenta Zn concentrations compared to controls. In fetuses, there were trends towards lower weight, length and percentage 59Fe, but higher liver Fe, in the coffee group than in the controls. The results suggest that coffee intake leads to (a) increased attempts at erythropoeisis, an indication of iron deficiency, in both nonpregnant and pregnant rats, and (b) impaired placental Fe transport.

Animals↗

PubMed2004

The impairment of gastroduodenal mucosal barrier by coffee.

BACKGROUND: Even though coffee is not considered to be responsible for development of peptic ulcer, it may, however, prolong its healing by increasing acidity of gastric content. In our former work we observed a profound increase in sucrose permeability (above normal values) in healthy volunteers regularly drinking coffee for years. In literature, many factors affecting sucrose permeability have been described so far. None of them, however, studied the effect of coffee. SUBJECTS, MATERIALS AND METHODS: 10 young asymptomatic habitual coffee drinkers were included in the study. The probands underwent SaLM test twice--first time without coffee restriction and second time after 48-hour coffee abstinence. The ingested SaLM solution comprised sucrose (25.0 g), lactulose (10.0 g), mannitol (2.0 g), xylose (2.0 g) and water (up to 100 ml). Urine was collected for five hours and the samples were analysed using gas chromatography. Results were compared with those of 8 young healthy volunteers not drinking coffee. Permeability for sucrose was significantly higher in the group of habitual coffee drinkers in comparison with non-coffee drinkers (p < 0.01). After 48-hour coffee abstinence sucrose excretion decreased significantly (p < 0.05) to a level not differing from that of non-coffee drinkers (p = 0.54). CONCLUSIONS: Our results indicate that coffee may damage gastroduodenal mucosa in habitual coffee drinkers. In a time period of 48 hours the gastroduodenal mucosa is capable of a significant regeneration.

Adult↗

PubMed2002

Chemical characterization of the high-molecular-weight material extracted with hot water from green and roasted robusta coffees as affected by the degree of roast.

The hot-water-soluble polymeric material from green and roasted Uganda robusta coffees submitted to different degrees of roasting was isolated and characterized, and the changes in structure and amount of galactomannans and arabinogalactans were determined and discussed in relation to the data already available for arabica coffees, obtained under the same experimental conditions. The content of arabinogalactans extracted from robusta green coffee was higher than that extracted from arabica. For roasted coffees, the amount of galactomannans extracted ranged from 0.66% to 0.92% (w/w). These values were near 50% of those obtained from the arabica coffees using the same extraction procedure. However, the amount of arabinogalactans extracted from robusta coffees (0.56-0.72%) was in the range obtained from arabica. The structures of arabinogalactans and galactomannans extracted from green and roasted coffees were not sufficiently different between robusta and arabica coffees to explain the observed differences in extraction yields for the arabinogalactans from green coffees and for the galactomannans from roasted coffees. The total polysaccharide content and the structures of the galactomannans and arabinogalactans in the two green coffee varieties investigated were also very similar. These differences in the extraction of high-molecular-weight polysaccharides between arabica and robusta roasted coffees may be related to the different susceptibility of the cell walls during the roasting process, known to result in a different porosity between arabica and robusta roasted coffees.

Chemical Fractionation↗

PubMed1993

Coffee. Facts and controversies.

In this article, we review current literature on coffee, both regular and decaffeinated, and its potential effects in humans. Moderate coffee consumption is believed to have no persistent effect on blood pressure. Large intake of coffee may increase total cholesterol levels; boiled coffee increases cholesterol levels more than filtered coffee. Consuming more than four cups per day may be associated with increased risk of acute myocardial infarction. There appears to be an association between urinary bladder cancer and coffee consumption. No association was found between ingestion of coffee and incidence of duodenal ulcer and ulcerative colitis. Increased coffee consumption by pregnant women appears to decrease fetal birth weight. Fetal heart rate, respiration, and both maternal and fetal anemia are increased with coffee consumption but coffee has not been shown to be teratogenic. Coffee consumption appears to pose no particular threat in most people if consumed in moderation. Naturally decaffeinated, filter-brewed coffee further diminishes its potential harmful effects.

Animals↗

PubMedDate not supplied

Coffee consumption and the risk of coronary heart disease and death.

OBJECTIVES: To study prospectively the relation of coffee drinking with fatal and nonfatal coronary heart disease (CHD) and all-cause mortality and to perform a cross-sectional analysis at baseline on the association between coffee drinking and CHD risk factors, diagnosed diseases, self-reported symptoms, and use of medicines. METHODS: The study cohort consisted of 20 179 randomly selected eastern Finnish men and women aged 30 to 59 years who participated in a cross-sectional risk factor survey in 1972, 1977, or 1982. Habitual coffee drinking, health behavior, major known CHD risk factors, and medical history were assessed at the baseline examination. Each subject was followed up for 10 years after the survey using the national hospital discharge and death registers. Multivariate analyses were performed by using the Cox proportional hazards model. RESULTS: In men, the risk of nonfatal myocardial infarction was not associated with coffee drinking. The age-adjusted association of coffee drinking was J shaped with CHD mortality and U shaped with all-cause mortality. The highest CHD mortality was found among those who did not drink coffee at all (multivariate adjusted). Also, in women, all-cause mortality decreased by increasing coffee drinking. The prevalence of smoking and the mean level of serum cholesterol increased with increasing coffee drinking. Non-coffee drinkers more often reported a history of various diseases and symptoms, and they also more frequently used several drugs compared with coffee drinkers. CONCLUSIONS: Coffee drinking does not increase the risk of CHD or death. In men, slightly increased mortality from CHD and all causes in heavy coffee drinkers is largely explained by the effects of smoking and a high serum cholesterol level. Arch Intern Med. 2000;160:3393-3400.

Adult↗

PubMed2003

Coffee consumption and risk of rheumatoid arthritis.

OBJECTIVE: Recent reports have suggested an association between consumption of coffee or decaffeinated coffee and the risk of rheumatoid arthritis (RA), although data are sparse and somewhat inconsistent. Furthermore, existing studies measured dietary exposures and potential confounders only at baseline and did not consider possible changes in diet or lifestyle over the followup period. We studied whether coffee, decaffeinated coffee, total coffee, tea, or overall caffeine consumption was associated with the risk of RA, using the Nurses' Health Study, a longitudinal cohort study of 121,701 women. METHODS: Information on beverage consumption was assessed with a food frequency questionnaire (FFQ) that was completed every 4 years, from baseline in 1980 through 1998. Among the 83,124 women who completed the FFQ at baseline, the diagnosis of incident RA (between 1980 and 2000) was confirmed in 480 women by a connective tissue disease screening questionnaire and medical record review for American College of Rheumatology criteria. Relationships between intake of various beverages and the risk of RA were assessed in age-adjusted models and in multivariate Cox proportional hazards models including the cumulative average intake of each beverage during the followup period, adjusted for numerous potential confounders. In addition, for direct comparisons with prior reports, multivariate analyses were repeated using only baseline beverage information. RESULTS: We did not find a significant association between decaffeinated coffee consumption of >/=4 cups/day (compared with no decaffeinated coffee consumption) and subsequent risk of incident RA, in either an adjusted multivariate model (relative risk [RR] 1.1, 95% confidence interval [95% CI] 0.5-2.2) or a multivariate model using only baseline reports of decaffeinated coffee consumption (RR 1.0, 95% CI 0.6-1.7). Similarly, there was no relationship between cumulative caffeinated coffee consumption and RA risk (RR 1.1, 95% CI 0.8-1.6 for >/=4 cups per day versus none) or between tea consumption and RA risk (RR 1.1, 95% CI 0.7-1.8 for >3 cups/day versus none). Total coffee and total caffeine consumption were also not associated with the risk of RA. CONCLUSION: In this large, prospective study, we find little evidence of an association between coffee, decaffeinated coffee, or tea consumption and the risk of RA among women.

Adult↗

PubMed1987

Coffee is highly mutagenic in the L-arabinose resistance test in Salmonella typhimurium.

The present study shows that the L-arabinose resistance test in Salmonella typhimurium detects coffee as a strong mutagen in the absence of mammalian microsomal activation. The response of the Ara forward mutation assay was 8.5 times higher than that of TA104, which is the most sensitive to coffee of the tester strains of the Ames test. Both the mutagenesis protocol (preincubation test) and the additional genetic characteristics of the bacterial tester strain (excision repair deficiency, normal lipopolysaccharide barrier, and the presence of plasmid pKM101) were critical factors in the optimal induction by coffee of forward mutations to L-arabinose resistance. All ten samples of roasted coffee analyzed with the Ara assay were highly mutagenic: one cup of coffee (150 ml) was calculated to induce 3-4 X 10(6) AraR mutants. In contrast, coffee prepared from unroasted beans (green coffee) had no mutagenic activity. Regular- and sugar-roasted coffees showed similar mutagenicities, but the specific mutagenic activity of instant coffees (1559 AraR mutants/mg) was almost 2 times that of noninstant ones (834 AraR mutants/mg). The Ara assay allowed the direct testing of coffee, although it was demonstrated that lyophilization has no effect on the mutagenicity of this beverage. Like roasted coffee, roasted barley induced a large number of AraR mutants per mg (227), though its specific mutagenic activity was approximately 4 and 7 times lower than that of noninstant and instant coffees, respectively.

Arabinose↗

PubMed2002

Effect of processing on ochratoxin A (OTA) content of coffee.

Coffee production can be roughly separated into three main steps 1) cherry processing to green coffee beans, 2) storage and transportation of green coffee to the place of consumption, and 3) green coffee processing to roasted and ground coffee and soluble coffee. The mold species which are known to produce ochratoxin A (OTA) in coffee have been identified as Aspergillus ochraceus, A. carbonarius and occasionally, A. niger. The length of time spent at a water activity > 0.80 at any moment until roasting defines the risk of mold growth and OTA production. However, the specific moment and locus of contamination have not yet been clearly identified. Since coffee husks are a significant source of OTA contamination, cleaning and grading of green coffee are effective methods for reducing OTA levels in coffee. During the process of converting green coffee to roasted and soluble coffees, up to 90% reduction in OTA levels can occur.

Coffee↗

PubMed1989

Inhibition of in vivo genotoxicity by coffee.

The possible role of coffee in modulating the in vivo genotoxicity of the well established genotoxic chemicals, mitomycin C, cyclophosphamide, procarbazine and adriamycin, was evaluated. Coffee was administered orally to mice that received the genotoxic chemicals ip. Genotoxicity was assessed in the bone-marrow micronucleus test. Doses of coffee in the range 225 to 1125 mg (dry weight)/kg body weight caused significant reductions in the in vivo genotoxicity of mitomycin C, cyclophosphamide and procarbazine but not adriamycin. The inhibitory effect was significant when the coffee was given about 2 hr before the genotoxin; there was a lesser effect when coffee was given together with the genotoxin but there was no inhibition when coffee was given 2-4 hr after the genotoxin. An experiment with mitomycin C demonstrated that the reduction in genotoxicity was dependent on the coffee dose. The inhibition of genotoxicity by coffee was observed in bone-marrow cells sampled 24, 48 or 68 hr after injecting cyclophosphamide. Freshly brewed coffee extract, standard instant coffee, decaffeinated instant coffee and freeze-dried home-brew coffee all exerted inhibitory effects.

Analysis of Variance↗

PubMed1997

Analysis of the content of the diterpenes cafestol and kahweol in coffee brews.

The diterpenes cafestol and kahweol have been implicated as the components in boiled coffee responsible for its hypercholesterolaemic effects. These particular coffee constituents have also been shown to possess anticarcinogenic effects. A simple and sensitive reverse-phase HPLC method using solid-phase extraction has been developed for the analysis of cafestol and kahweol in coffee brews. This method was used to confirm that the method of coffee brewing is a major determinant of the cup content and hence level of consumption of these diterpenes. Scandinavian-style boiled coffee and Turkish-style coffee contained the highest amounts, equivalent to 7.2 and 5.3 mg cafestol per cup and 7.2 and 5.4 mg kahweol per cup, respectively. In contrast, instant and drip-filtered coffee brews contained negligible amounts of these diterpenes, and espresso coffee contained intermediate amounts, about 1 mg cafestol and 1 mg kahweol per cup. These findings provide an explanation for the hypercholesterolaemic effect previously observed for boiled coffee and Turkish-style coffee, and the lack of effect of instant or drip-filtered coffee brews. This methodology will be of value in more correctly assessing the human exposure to these diterpenes through the consumption of coffee, and hence the potential physiological effects of different brews.

Cholesterol↗

PubMed2003

Coffee increases levels of urinary 8-hydroxydeoxyguanosine in rats.

We examined whether coffee or chlorogenic acid inhibits 8-hydroxydeoxyguanosine (8-OHdG), one of the major forms of oxidative DNA damage, in vivo and in vitro. Forty-eight male Wistar rats were assigned to three treatment groups: a control-diet group (n=16; coffee-free diet), a 0.62% coffee-diet group (n=16, dose of coffee consumed 125 mg/day), and a 1.36% coffee-diet group (n=16, dose of coffee consumed 275 mg/day) and were maintained on an experimental diet for 130 days. The coffee-diet resulted in significantly increased excretion of urinary chlorogenic acid, with the 0.62 and 1.36% coffee-diets resulting in 14.00+/-0.94 and 15.80+/-0.41 ng/mg creatinine, respectively, whereas in control rats it was not detected. Using monoclonal antibody to measure 8-OHdG, it was revealed that coffee led to a significant increase in excretion of urinary 8-OHdG on day 130 (46.62+/-13.42 ng/mg creatinine in 0.62% coffee-diet group and 64.58+/-20.15 ng/mg creatinine in 1.36% coffee-diet group, P<0.05 vs. control; control group 10.89+/-2.59 ng/mg creatinine). Furthermore, to clarify the mechanism of 8-OHdG formation by coffee, we investigated the in vitro effect of chlorogenic acid on 8-OHdG formation in human placental DNA. Chlorogenic acid alone did not lead to an increase of 8-OHdG formation, but dramatically increased it in the presence of cupric chloride and H(2)O(2). However, chlorogenic acid and cupric chloride decreased the formation of 8-OHdG in the presence of H(2)O(2). Based on these results, a possible mechanism of 8-OHdG formation in vivo by chlorogenic acid is discussed.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2003

Traits of persons who drink decaffeinated coffee.

PURPOSE: Little is known about the traits of decaffeinated coffee drinkers, who are sometimes used to ascertain whether the health effects of coffee intake are due to caffeine or some other coffee ingredient. METHODS: We studied these traits in 12,467 persons who reported type of coffee consumed at health examinations; 36% drank caffeinated only, 13% drank decaffeinated only, 27% drank both types and 24% drank no coffee. RESULTS: Odds ratios estimated from logistic regression analyses revealed that compared with regular (caffeinated) coffee drinkers or abstainers, decaffeinated coffee drinkers were less likely to be heavy coffee drinkers, smokers, alcohol drinkers, users of caffeinated soft drinks and medication and to be free of illness. Increased decaffeinated coffee drinking was associated with older age, female sex, African American ethnicity, use of special diets and cardiovascular, gastrointestinal, or neuropsychiatric symptoms. Persons on special diets were more likely to drink decaffeinated coffee whether they had heart disease or were free of any illness. CONCLUSION: These data suggest that decaffeinated coffee use is related to illness in some persons but to a healthy lifestyle in others. These potential and possibly conflicting confounding factors need to be considered when studying the health effects of coffee or caffeine.

Adult↗

PubMed2001

Effect of coffee consumption on bone metabolism.

The effects of coffee on bone metabolism are still controversial, although several studies have suggested that caffeine and/or heavy coffee consumption is associated with a significant increase in risk of fracture, osteoporosis, and periodontal disease. Therefore, we sought to clarify the relationship between coffee consumption and bone metabolism using male Wistar rats. Forty-eight male Wistar rats were assigned to three treatment groups including a control-diet group (control, n = 16, coffee-free diet), a 0.62% coffee-diet group (low caffeine, n = 16, diet supplemented with 6.2 g/kg of the control diet), and a 1.36% coffee-diet group (high caffeine, n = 16, diet supplemented with 13.6 g/kg of the control diet), and animals were maintained on an experimental diet for 140 days. Although caffeine in serum was not detected in rats fed the control diet, low-intake coffee for 140 days led to an increase in caffeine concentration to 0.53 +/- 0.11 microg/mL and high-intake coffee led to an increase of 1.77 +/- 0.22 microg/mL. No significant differences in body weight change, serum and urinary biochemical markers of bone metabolism, and bone histomorphometry were found between the coffee-diet groups and the control-diet group, except that urinary phosphorus excretion after 140 days of both coffee diets was significantly increased compared with controls (p < 0.05). In addition, the coffee diets were not associated with differences in tumor necrosis factor-alpha and interleukin-6, which have been implicated in the pathogenesis of bone loss together with interleukin-1beta. In conclusion, the present study strongly indicates that coffee does not stimulate bone loss in rats.

Amino Acids↗

PubMed2002

Antiadhesive effect of green and roasted coffee on Streptococcus mutans' adhesive properties on saliva-coated hydroxyapatite beads.

Green and roasted coffees of the two most used species, Coffea arabica and Coffea robusta, several commercial coffee samples, and known coffee components were analyzed for their ability to interfere with Streptococcus mutans' sucrose-independent adsorption to saliva-coated hydroxyapatite (HA) beads. All coffee solutions showed high antiadhesive properties. The inhibition of S. mutans' adsorption to HA beads was observed both when coffee was present in the adsorption mixture and when it was used to pretreat the beads, suggesting that coffee active molecules may adsorb to a host surface, preventing the tooth receptor from interacting with any bacterial adhesions. Among the known tested coffee components, trigonelline and nicotinic and chlorogenic acids have been shown to be very active. Dialysis separation of roasted coffee components also showed that a coffee component fraction with 1000 Da < MW < 3500 Da, commonly considered as low MW coffee melanoidins, may sensibly contribute to the roasted coffee's antiadhesive properties. The obtained results showed that all coffee solutions have antiadhesive properties, which are due to both naturally occurring and roasting-induced molecules.

Bacterial Adhesion↗

PubMed2005

Interactions between volatile and nonvolatile coffee components. 1. Screening of nonvolatile components.

This study is the first of two publications that investigate the phenomena of coffee nonvolatiles interacting with coffee volatile compounds. The purpose was to identify which coffee nonvolatile(s) are responsible for the interactions observed between nonvolatile coffee brew constituents and thiols, sulfides, pyrroles, and diketones. The overall interaction of these compounds with coffee brews prepared with green coffee beans roasted at three different roasting levels (light, medium, and dark), purified nonvolatiles, and medium roasted coffee brew fractions (1% solids after 1 or 24 h) was measured using a headspace solid-phase microextraction technique. The dark roasted coffee brew was slightly more reactive toward the selected compounds than the light roasted coffee brew. Selected pure coffee constituents, such as caffeine, trigonelline, arabinogalactans, chlorogenic acid, and caffeic acid, showed few interactions with the coffee volatiles. Upon fractionation of medium roasted coffee brew by solid-phase extraction, dialysis, size exclusion chromatography, or anion exchange chromatography, characterization of each fraction, evaluation of the interactions with the aromas, and correlation between the chemical composition of the fractions and the magnitude of the interactions, the following general conclusions were drawn. (1) Low molecular weight and positively charged melanoidins present significant interactions. (2) Strong correlations were shown between the melanoidin and protein/peptide content, on one hand, and the extent of interactions, on the other hand (R = 0.83-0.98, depending on the volatile compound). (3) Chlorogenic acids and carbohydrates play a secondary role, because only weak correlations with the interactions were found in complex matrixes.

Carbohydrates↗