Coffee & Antioxidants

ANTIOXIDANTS IN COFFEE

Plant phenols are a large and diverse group of compounds including cinnamic acids, benzoic acids, flavonoids, proanthocyanidins, stilbenes, coumarins, lignans and lignins. It has been shown that plant phenols have strong antioxidant activity in vitro (1). As a result it has been hypothesised that plant phenols might protect cellular DNA, lipids and proteins from free radical- mediated damage in vivo. Since free radicals are believed to play a role in the development of chronic diseases such as cardiovascular disease and cancer then the consumption of plant phenols may protect against these diseases. As reviewed recently, five out of seven published observational epidemiological studies have shown that flavonols protect against cardiovascular disease but only one out of four studies showed that they protect against cancer (2). Hence the available evidence for a protective effect of flavonols against cardiovascular disease and cancer is far from conclusive and other categories of plant phenols have yet to be investigated.

Chlorogenic acids are a family of esters formed between trans-cinnamic acids and quinic acid. The commonest individual chlorogenic acid is formed between caffeic acid and quinic acid. It has been shown that both chlorogenic acid and caffeic acid are strong antioxidants in vitro (1). Coffee beans are one of the richest dietary sources of chlorogenic acid and for many consumers this will be their major dietary source (3). It has been reported that a 200 ml cup of arabica coffee contains between 70 and 200 mg chlorogenic acid whereas a cup of robusta coffee contains between 70 and 350 mg (3). It has been estimated that coffee drinkers might ingest as much as 1 g per day cinnamate esters (mostly chlorogenic acid) and 500 mg per day cinnamates (mostly caffeic acid). Coffee could supply as much as 70% of the total making it far and away the most important dietary source of this group of antioxidants (3).

The amount of chlorogenic acid or caffeic acid available to act as an antioxidant in vivo will depend on absorption from the gut which may be incomplete and any subsequent metabolism which may be extensive. It has recently been demonstrated that humans absorb about 33% of ingested chlorogenic acid and about 95% of ingested caffeic acid (4). A study of human chlorogenic acid metabolism showed that the unabsorbed chlorogenic acid which reaches the colon is hydrolysed to caffeic acid and quinic acid by the colonic microflora (5). Following dehydroxylation by the colonic microflora, absorption and further metabolism in the liver and kidney, benzoic acid is formed and conjugated to glycine to form hippuric acid. About half the ingested chlorogenic acid appears as urinary hippuric acid (5). This metabolism can be expected to considerably diminish the antioxidant activity of chlorogenic acid in vivo as hippuric acid has no antioxidant activity.

The roasting of coffee beans dramatically increases their total antioxidant activity. A roasting time of 10 minutes (medium-dark roast) was found to produce coffee with optimal oxygen scavenging and chain breaking activities in vitro (6). A study of robusta and arabica coffees from six different countries showed that robusta samples contained significantly more reducing substances than arabica samples and that protective activity measured ex vivo was significantly greater in roasted samples than in green coffee (7). Using the ABTS•+ method (the gold standard), it was confirmed that light roast or medium roast coffee has a significantly higher antioxidant activity in vitro than green coffee (8). This difference was observed despite a 19% and 45% decrease in the chlorogenic acid content of light and medium roast coffee respectively implying that other compounds make significant contributions to the total antioxidant activity of roasted coffee. Melanoidins are brown polymers formed by the Maillard reaction during the roasting of coffee beans and account for up to 25% of the dry matter. It has recently been shown by the ABTS•+ method that coffee melanoidins have significant antioxidant activity in vitro (9).

The total antioxidant activities of different plant phenol- containing beverages have been compared. Using a method based on the ex vivo oxidation of low density lipoprotein (LDL), it has been shown that coffee has significantly more total antioxidant activity than either cocoa, green tea, black tea or herbal tea (10). Using the ABTS•+ method, it has been confirmed that coffee has a significantly greater total antioxidant activity in vitro than cola, beer, a variety of fruit juices, lemon ice tea or black tea (11). A study conducted in 2004 looked at dietary sources of antioxidants and found that the single greatest contributor to total antioxidant intake was coffee (12). A further study in 2006 (13) set out to determine the content of phenolic acids in the most consumed fruits and beverages. Coffee, as wel as black and green teas were the best source among beverages with coffee containing 97mg/100 g whilst teas contained 30-36 mg/100 g

It can be concluded that coffee possesses greater in-vitro antioxidant activity than other beverages, due in part to intrinsic compounds such as chlorogenic acid, in part to compounds formed during roasting such as melanoidins and in part to as yet unidentified compounds. Authors of a study published in 2002 (14) suggested that uric acid was the main component responsible for plasma antioxidant capacity increase after tea drinking, whereas molecules other than uric acid (probably phenolic compounds) are likely to be responsible for the increase in plasma antioxidant capacity after coffee drinking. Whether the antioxidants characteristic of coffee are protective against chronic diseases such as cardiovascular disease and cancer remains to be determined. Research continues, and the conclusion of a study published in 2006 (15) consisting of a cohort of 41,836 postmenopausal women, was that 'Consumption of coffee, a major source of dietary antioxidants, may inhibit inflammation and thereby reduce the risk of cardiovascular disease and other inflammatory diseases in postmenopausal women'.
It should be noted that these results of course refer to a specific sub group and it would not, at this stage, be appropriate to extrapolate them across to the general population before further research clarifies these conclusions.

References:

1. Rice-Evans, C.A. et al. Free Radical Biology and Medicine, 20, 933-956, 1996.

2. Hollman, P.C.H. Journal of the Science of Food and Agriculture, 81, 842-852, 2001.

3. Clifford, M.N. et al. Journal of the Science of Food and Agriculture, 79, 362-372, 1999.

4. Olthof, M.R. et al. Journal of Nutrition, 131, 66-71, 2001.

5. Olthof, M.R. et al. Journal of Nutrition, 133, 1806-1814, 2003.

6. Nicoli, M.C. et al. Lebensmittel, Wissenschaft und Technologie, 30, 292-297, 1997.

7. Daglia, M. et al. Journal of Agricultural and Food Chemistry, 48, 1449-1454, 2000.

8. Del Castillo, M.D. et al. Journal of Agricultural and Food Chemistry, 50, 3698-3703, 2002.

9. Borrelli, R.C. et al. Journal of Agricultural and Food Chemistry, 50, 6527-6533, 2002.

10. Richelle, M. et al. Journal of Agricultural and Food Chemistry, 49, 3438-3442, 2001.

11. Pellegrini, N. et al. Journal of Agricultural and Food Chemistry,51, 260-264,2003.

12. Svilaas, A. et al. Journal of Nutrition, 134, 562-567, 2004.

13.Mattila P et al,

14. Natelle, F. et al. Journal of Agricultural and Food Chemistry, 50, 6211-6216, 2002.


15. Frost Andersen, L. et al. American Journal of Clinical Nutrition, 83, 2006.