Herbert Stiebitz

Antioxidant‐rich coffee reduces DNA damage, elevates glutathione status and contributes to weight control: Results from an intervention study

Epidemiological and experimental evidence increasingly suggests coffee consumption to be correlated to prevention or delay of degenerative diseases connected with oxidative cellular stress. In an intervention study comprising 33 healthy volunteers, we examined DNA-protective and antioxidative effects exerted in vivo by daily ingestion of 750 mL of freshly brewed coffee rich in both green coffee bean constituents as well as roast products. The study design encompassed an initial 4 wk of wash-out, followed by 4 wk of coffee intake and 4 wk of second wash-out. At the start and after each study phase blood samples were taken to monitor biomarkers of oxidative stress response. In addition, body weight/composition and intake of energy/nutrients were recorded. In the coffee ingestion period, the primary endpoint, oxidative DNA damage as measured by the Comet assay (± FPG), was markedly reduced (p<0.001). Glutathione level (p<0.05) and GSR-activity (p<0.01) were elevated. Body weight (p<0.01)/body fat (p<0.05) and energy (p<0.001)/nutrient (p<0.001-0.05) intake were reduced. Our results allow to conclude that daily consumption of 3-4 cups of brew from a special Arabica coffee exerts health beneficial effects, as evidenced by reduced oxidative damage, body fat mass and energy/nutrient uptake.

Antioxidant effectiveness of coffee extracts and selected constituents in cell-free systems and human colon cell lines.

SCOPE Epidemiological studies suggest that coffee can reduce the risk of degenerative diseases such as diabetes type 2, cardiovascular disease and cancer. These beneficial effects have partly been attributed to the antioxidant activity of coffee. We determined composition and antioxidant potential of differentially roasted coffee extracts and investigated the impact of selected original constituents and roast products. METHODS AND RESULTS Parameters studied were direct antioxidant activity (trolox equivalent antioxidant capacity/oxygen radical absorbing capacity), cellular reactive oxygen species (ROS) level, DNA damage and protein expression of NAD(P)H: quinone oxidoreductase, γ-glutamylcysteine ligase and glutathione reductase in HT-29/Caco-2 cells at 24-h incubation. All extracts showed distinct direct antioxidant activity: medium roasts>light roast AB1 (caffeoylquinic acid (CQA)-rich Arabica Brazil extract); dark roast AB2 (N-methylpyridinium (NMP)-rich Arabica Brazil extract), and diminished t-butylhydroperoxide-induced ROS level in HT-29 cells (AB2>medium roasts>AB1). NAD(P)H:quinone oxidoreductase 1 expression and γ-glutamylcysteine ligase expression were distinctly induced by AB1 and 5-CQA, but not by AB2 and NMP. 5-CQA and caffeic acid exhibited highest trolox equivalent antioxidant capacity/oxygen radical absorbing capacity values (5-CQA: 1.3/3.5 mM and caffeic acid: 1.3/3.9 mM trolox); ROS level was distinctly diminished by 5-CQA (≥3 μM), catechol (30 μM) and trigonelline (≥30 μM), whereas menadione-induced DNA damage in Caco-2 cells was reduced by NMP compounds (1-30 μM). CONCLUSION The results emphasize that both original constituents and roast products contribute to the cellular antioxidant effectiveness of coffee.

Coffees rich in chlorogenic acid or N-methylpyridinium induce chemopreventive phase II-enzymes via the Nrf2/ARE pathway in vitro and in vivo.

Recently, the coffee constituents 5-O-caffeoylquinic acid (CGA) and N-methylpyridinium (NMP) were identified as inducers of the Nrf2/antioxidant-response element (ARE) detoxifying pathway under cell-culture condition. To study the impact of CGA and NMP on the Nrf2-activating properties of a complex coffee beverage, two different model coffees were generated by variation of the roasting conditions: a low-roast coffee rich in CGA and a heavy-roast low in CGA but containing high levels of NMP. Activation of the Nrf2/antioxidant-response element pathway was monitored in vitro and in vivo.

Dark roast coffee is more effective than light roast coffee in reducing body weight, and in restoring red blood cell vitamin E and glutathione concentrations in healthy volunteers

Recent results from prospective cohort studies have shown that moderate coffee consumption is associated with a reduced risk for diabetes mellitus type II or Alzheimers disease. Since reactive oxygen species (ROS) are believed to be involved in the pathogenesis of these diseases, antioxidants in coffee might contribute to this risk reduction. We aimed at elucidating whether a dark roast coffee beverage (CB) rich in N-methylpyridinium ions (NMP: 785 μmol/L) and low in chlorogenic acids (CGA: 523 μmol/L) has stronger antioxidant effects on human erythrocytes than a CB prepared from a light roast with opposite proportions (CGA: 4538 μmol/L; NMP: 56 μmol/L). Following a 2-wk wash out period, 500 mL of the respective CB was administered to 30 subjects daily for 4-wk. Blood and spot urine samples were collected at the beginning and at the end of each intervention. Intake of the dark roast CB most effectively improved the antioxidant status of erythrocytes: superoxide dismutase and glutathione peroxidase activity decreased by 5.8 and 15%, respectively, whereas tocopherol and total glutathione concentrations increased by 41 and 14%, respectively. Furthermore, administration of the NMP-rich CB led to a significant body weight reduction in pre-obese subjects, whereas the CGA-rich CB did not.

Quantitative Studies on Roast Kinetics for Bioactives in Coffee

Quantitative analysis of the bioactives trigonelline (1), N-methylpyridinium (2), caffeine (3), and caffeoylquinic acids (4) in a large set of roasted Arabica (total sample size n = 113) and Robusta coffees (total sample size n = 38) revealed that the concentrations of 1 and 4 significantly correlated with the roasting color (P < 0.001, two tailed), whereas that of 2 significantly correlated inversely with the color (P < 0.001, two tailed). As dark-roasted coffees were rich in N-methylpyridinium whereas light-roasted coffees were rich in trigonelline and caffeoylquinic acids, manufacturing of roast coffees rich in all four bioactives would therefore necessitate blending of two or even more coffees of different roasting colors. Additional experiments on the migration rates during coffee brewing showed that all four bioactives were nearly quantitatively extracted in the brew (>90%) when a water volume/coffee powder ratio of >16 was used.

A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blend

Coffee consumption sometimes is associated with symptoms of stomach discomfort. This work aimed to elucidate whether two coffee beverages, containing similar amounts of caffeine, but differing in their concentrations of (β) N-alkanoyl-5-hydroxytryptamides (C5HTs), chlorogenic acids (CGAs), trigonelline, and N-methylpyridinium (N-MP) have different effects on gastric acid secretion in healthy volunteers. The intragastric pH after administration of bicarbonate with/without 200 mL of a coffee beverage prepared from a market blend or dark roast blend was analyzed in nine healthy volunteers. Coffee beverages were analyzed for their contents of C5HT, N-MP, trigonelline, CGAs, and caffeine using HPLC-DAD and HPLC-MS/MS. Chemical analysis revealed higher concentrations of N-MP for the dark brown blend (87 mg/L) compared to the market blend coffee (29 mg/L), whereas concentrations of C5HT (0.012 versus 0.343 mg/L), CGAs (323 versus 1126 mg/L), and trigonelline (119 versus 343 mg/L) were lower, and caffeine concentrations were similar (607 versus 674 mg/mL). Gastric acid secretion was less effectively stimulated after administration of the dark roast blend coffee compared to the market blend. Future studies are warranted to verify whether a high ratio of N-MP to C5HT and CGAs is beneficial for reducing coffee-associated gastric acid secretion.