Effects of cafestol and kahweol from coffee grounds on serum lipids and serum liver enzymes in humans

The diterpenes cafestol and kahweol are present in unfiltered coffee in oil droplets and floating fines. They elevate serum cholesterol and alanine aminotransferase (ALT). We measured fines in coffee brews, and examined diterpene availability from spent grounds in healthy volunteers. Turkish or Scandinavian boiled coffee contained 2–5 g fines/L and French press coffee contained 1.5 g fines/L. An intake of 8 g fine grounds/d for 3 wk increased cholesterol by 0.65 mmol/L (95% CI 0.41–0.89 mmol/L) and ALT by 18 U/L (95% CI 4–32 U/L) relative to control subjects (n = 7/group). In a crossover study (n = 15), mean serum cholesterol was 4.9 mmol/L after consumption of both fine and coarse grounds for 10 d (P = 0.43). Serum ALT activities were 29 U/L on fine and 21 U/L on coarse grounds (P = 0.02). Floating fines could contribute substantially to the hyperlipidemic and ALT-elevating effect of unfiltered coffee. Diterpene measurements in coffee brews should include the contribution of fines

The cholesterol-raising diterpenes from coffee beans increase serum lipid transfer protein activity levels in humans

Cafestol and kahweol–diterpenes present in unfiltered coffee— strongly raise serum VLDL and LDL cholesterol and slightly reduce HDL cholesterol in humans. The mechanism of action is unknown. We determined whether the coffee diterpenes may affect lipoprotein metabolism via effects on lipid transfer proteins and lecithin:cholesterol acyltransferase in a randomized, double-blind cross-over study with 10 healthy male volunteers. Either cafestol (61–64 mg/day) or a mixture of cafestol (60 mg/day) and kahweol (48–54 mg/day) was given for 28 days. Serum activity levels of cholesterylester transfer protein, phospholipid transfer protein and lecithin:cholesterol acyltransferase were measured using exogenous substrate assays. Relative to baseline values, cafestol raised the mean (±S.D.) activity of cholesterylester transfer protein by 18±12% and of phospholipid transfer protein by 21±14% (both P<0.001). Relative to cafestol alone, kahweol had no significant additional effects. Lecithin:cholesterol acyltransferase activity was reduced by 11±12% by cafestol plus kahweol (P=0.02). It is concluded that the effects of coffee diterpenes on plasma lipoproteins may be connected with changes in serum activity levels of lipid transfer proteins

Health effects of unfiltered coffee : diterpenes in coffee and their effects on blood lipids and liver enzymes in man

Boiled coffee raises blood levels of cholesterol and triglycerides in man. Cafestol and kahweol are responsible. These diterpenes also raise blood levels of alanine aminotransferase (ALT). The objective of the present studies was to further specify the health effects of cafestol and kahweol.Unfiltered coffee contains up to 5 g of grounds per liter. Intake of 8 g/day of such grounds for 3 weeks raised cholesterol by 0.65 mmol/L and ALT by 18 U/L in healthy volunteers. Diterpenes in floating grounds thus contribute to the hyperlipidaemic and ALT- elevating effects of unfiltered coffee. Chemical analyses showed that boiled, cafeti6re (also called French press), and Turkish coffee are rich in diterpenes. Levels are moderate in espresso and mocha coffee, and negligible in percolated, instant, and filtered coffee.We studied the separate activities of cafestol and kahweol in a randomised, double-blind cross-over study with 10 male volunteers. Intake of 63 mg/day of cafestol for 4 weeks raised cholesterol by 17%, triglycerides by 86%, and ALT by 78%. Additional intake of 51 mg/d of kahweol only marginally raised the lipid responses, but more than doubled the ALT responses. Cafestol therefore is more hyperlipidaemic than kahweol, but both affect liver cells.To study long term effects, we gave 46 volunteers 0.9 liter/day of either filtered or cafetiere coffee for 6 months in a randomised experiment. ALT levels were still raised by 45%, and LDL by 9%, after 6 months of intake of cafetiere coffee, but most of the initial rise in triglycerides had disappeared.Lipoprotein(a) is an atherogenic particle made by the liver. We found that lipoprotein(a) levels were 65% higher in chronic drinkers of boiled coffee than in peers drinking filtered coffee. However, supplements rich in diterpenes lowered lipoprotein(a) in four experiments.In conclusion, the strong and persistent effects on total and LDL cholesterol levels are a good reason to advise patients with a high coronary risk to limit the intake of brews rich in cafestol. Effects of unfiltered coffee on triglycerides and lipoprotein(a) may be insignificant for atherogenic risk. The effects of cafestol and kahweol on liver cells may be innocuous, but coffee drinkers with raised levels of alanine aminotransferase might also do well in abstaining from unfiltered coffee

Coffee bean extracts rich and poor in kahweol both give rise to elevation of liver enzymes in healthy volunteers

BACKGROUND: Coffee oil potently raises serum cholesterol levels in humans. The diterpenes cafestol and kahweol are responsible for this elevation. Coffee oil also causes elevation of liver enzyme levels in serum. It has been suggested that cafestol is mainly responsible for the effect on serum cholesterol levels and that kahweol is mainly responsible for the effect on liver enzyme levels. The objective of this study was to investigate whether coffee oil that only contains a minute amount of kahweol indeed does not cause elevation of liver enzyme levels. METHODS: The response of serum alanine aminotransferase (ALAT) and aspartate aminotransferase (ASAT) to Robusta coffee oil (62 mg/day cafestol, 1.6 mg/day kahweol) was measured in 18 healthy volunteers. RESULTS: After nine days one subject was taken off Robusta oil treatment due to an ALAT level of 3.6 times the upper limit of normal (ULN). Another two subjects stopped treatment due to other reasons. After 16 days another two subjects were taken off Robusta oil treatment. One of those subjects had levels of 5.8 ULN for ALAT and 2.0 ULN for ASAT; the other subject had an ALAT level of 12.4 ULN and an ASAT level of 4.7 ULN. It was then decided to terminate the study. The median response of subjects to Robusta oil after 16 days was 0.27 ULN (n = 15, 25(th),75(th )percentile: 0.09;0.53) for ALAT and 0.06 ULN (25(th),75(th )percentile -0.06;0.22) for ASAT. CONCLUSIONS: We conclude that the effect on liver enzyme levels of coffee oil containing hardly any kahweol is similar to that of coffee oil containing high amounts of kahweol. Therefore it is unlikely that kahweol is the component of coffee oil that is responsible for the effect. Furthermore, we conclude that otherwise unexplained elevation of liver enzyme levels observed in patients might be caused by a switch from consumption of filtered coffee to unfiltered coffee

Reproducibility of the serum lipid response to coffee oil in healthy volunteers

BACKGROUND: Humans and animals show a certain consistency in the response of their serum lipids to fat-modified diets. This may indicate a genetic basis underlying this response. Coffee oil might be used as a model substance to investigate which genes determine differences in the serum lipid response. Before carrying out such studies our objective was to investigate to what extent the effect of coffee oil on serum lipid concentrations is reproducible within subjects. METHODS: The serum lipid response of 32 healthy volunteers was measured twice in separate five-week periods in which coffee oil was administered (69 mg cafestol / day). RESULTS: Total cholesterol levels increased by 24% in period 1 (range:0;52%) and 18% in period 2 (1;48%), LDL cholesterol by 29 % (-9;71%) and 20% (-12;57%), triglycerides by 66% (16;175%) and 58% (-13;202%), and HDL cholesterol did not change significantly: The range of the HDL response was -19;25% in period 1 and -20;33% in period 2. The correlation between the two responses was 0.20 (95%CI -0.16, 0.51) for total cholesterol, 0.16 (95%CI -0.20, 0.48) for LDL, 0.67 (95%CI 0.42, 0.83) for HDL, and 0.77 (95%CI 0.56, 0.88) for triglycerides. CONCLUSIONS: The responses of total and LDL cholesterol to coffee oil were poorly reproducible within subjects. The responses of HDL and triglycerides, however, appeared to be highly reproducible. Therefore, investigating the genetic sources of the variation in the serum-lipid response to coffee oil is more promising for HDL and triglycerides

Diterpenes from coffee beans decrease serum levels of lipoprotein(a) in humans: results from four randomized controlled trials

Objective: Unfiltered coffee raises serum LDL cholesterol in humans, owing to the presence of the diterpenes cafestol and kahweol. Norwegians with a chronic high intake of unfiltered coffee also had elevated serum levels of lipoprotein(a), an LDL-like particle which is insensitive toward dietary interventions. We now experimentally studied the influence of coffee diterpenes on lipoprotein(a) levels. Design: Four randomised controlled trials. Subjects: Healthy, normolipidemic volunteers. Interventions: Coffee, coffee oil, and pure diterpenes for 4-24 weeks. Main outcome measures: The circulating level of lipoprotein(a). Results: In 22 subjects drinking five to six strong cups of cafetiere coffee per day, the median fall in lipoprotein(a) was 1.5 mg/dL after two months (P=0.03), and 0.5 mg/dL after half a year (P>0.05), relative to 24 filter coffee drinkers. Coffee oil doses equivalent to 10-20 cups of unfiltered coffee reduced lipoprotein(a) levels by up to 5.5 mg/dL (P<0.05) in two separate trials (n=12-16 per group). A purified mixture of cafestol and kahweol, as well as cafestol alone, were also effective in reducing Lp(a) levels (n=10). Averaged over the four trials, each 10 mg/d of cafestol (plus kahweol)?the amount present in two to three cups of cafetiere coffee?decreased Lp(a) levels by 0.5 mg/dL or 4% from baseline values after four weeks (n=63). Conclusions: Coffee diterpenes are among the few dietary exceptions shown to influence serum lipoprotein(a) levels. However, the Lp(a)-reducing potency of coffee diterpenes may subside in the long run, and their adverse side effects preclude their use as lipoprotein(a)-reducing agents. Sponsorship: Supported by the Netherlands Heart Foundation through grant No. 900-562-091 of the Netherlands Organization of Scientific Research (NWO), plus supplemental funding by the Institute for Scientific Information on Coffee

Chronic consumers of boiled coffee have elevated serum levels of lipoprotein(a)

OBJECTIVES: Lipoprotein(a) consists of an LDL-particle attached to apolipoprotein(a), which is made by the liver. Diterpenes present in boiled coffee raise serum levels of LDL cholesterol and of the liver enzyme alanine aminotransferase in man. We investigated the association between intake of boiled coffee and serum levels of lipoprotein(a). DESIGN, SETTING AND SUBJECTS: Healthy Norwegians 40-42 years of age, who habitually consumed five or more cups of boiled coffee per day (n = 150) were compared with matched filter coffee consumers (n = 159) in a cross-sectional study, as part of the Norwegian National Health Screening in 1992. RESULTS: The median lipoprotein(a) level was 13.0 mg dL-1 (10th and 90th percentile: 2.5 and 75.0 mg dL-1, respectively) on boiled and 7.9 mg dL-1 (10th and 90th percentile: 1.9 and 62.5 mg dL-1, respectively) on filter coffee (P = 0.048). Means /- SE were 25.8 /- 2.4 mg dL-1 and 19.6 /- 2.0 mg dL-1, respectively (P = 0.04). Although not statistically significant, subjects consuming nine or more cups of coffee per day had higher lipoprotein(a) levels than those drinking five to eight cups per day in both coffee groups. CONCLUSION: Chronic consumers of unfiltered, boiled coffee have higher serum levels of lipoprotein(a) than filter coffee drinkers

Levels of cafestol, kahweol, and related diterpenoids in wild species of the coffee plant coffea

Abstract Specific fatty acids and sterols in food composites from seven countries were analyzed. In the 1960s, groups of 8 to 49 men from 16 cohorts, ages 40–59 years and living in the United States, Finland, the Netherlands, Italy, Greece, the former Yugoslavia, or Japan recorded their food intake. In 1987, we collected food composites representing the average food intake per cohort sample in the 1960s. The foods were transported to the Netherlands, pooled, and centrally analyzed for energy, total fat, 42 fatty acids, cholesterol, and four plant sterols. The fat content ranged from 12% of total daily energy in the Tanushimaru, Japan, cohort to 50% in the U.S. cohort sample, and the polyunsaturated to saturated fat ratio ranged from 0.17 in the east Finland cohort to 1.2 in Tanushimaru. The amount oftransfatty acids with 16 or 18 carbon atoms varied between 0.2 g/day in Corfu, Greece, and 8.6 g/day in Zutphen, Netherlands, and that of -linolenic acid between 0.8 g/day in Rome and 2.5 g/day in east Finland. The sum of eicosapentaenoic and docosahexanoic acid ranged from 0.1 (U.S. railroad) to 2.0 g/day (Ushibuka, Japan), and phytosterols from 170 (U.S. railroad) to 358 mg/day (Corfu, Greece). Thus the intake of various fatty acids and sterols with potential relevance for coronary heart disease occurrence varied 10-fold or more between cohorts. Our data can be used to generate new hypotheses about the causes of differences in incidence of diseases between countries