Coffee, despite its not-so-healthy reputation, has been quite consistently linked in the scientific literature with benefits for health including a reduced risk of cardiovascular disease, diabetes and dementia. See here, here, here, and here.
While the research regarding the effects of coffee on health is voluminous, the great majority of it comes in the form of so-called epidemiological evidence. Such studies can identify associations between things, but that’s about all. If there were 20 studies showing that coffee-drinking is associated with a reduced risk of cardiovascular disease, say, then that still would not be enough to conclude that coffee protects against cardiovascular disease. It might turn out, for instance, that coffee drinkers happen to exercise more or eat more healthily than coffee abstainers, and these are the real reasons behind the association between coffee drinking and reduced cardiovascular disease risk.
The best test of an causal link between a foodstuff and health is a randomised controlled trial – preferably placebo-controlled. In this case, this would mean randomising a group of people to drink coffee or placebo (ideally an inert coffee-tasting beverage) over a period of time. If the coffee drinking group turned out to be less likely to succumb to cardiovascular disease (assuming the two groups were essentially the same in other respects), this would be very good evidence that coffee consumption does indeed reduce disease risk.
The problem is, the chances of such a study being undertaken are virtually nil.
However, what is much more realistic is to perform clinical studies (studies in people) which monitor not disease outcomes, but so-caled ‘surrogate’ markers of disease. In the case of cardiovascular disease, traditionally scientists would focus on cholesterol levels. Personally, I am doubtful about the relevance of cholesterol levels and the benefits of cholesterol reduction. There has for some time been emerging evidence that a true key underlying process in the development of cardiovascular disease is inflammation.
I was therefore interested to read a study published in the April edition of the American Journal of Clinical Nutrition which looked at the effect of coffee-drinking on a variety of biochemical surrogate markers for disease [1]. A group of coffee drinkers were asked to abstain from drinking coffee for a month. The following month they were asked to drink four cups of coffee a day (a total of 600 mls of coffee a day). The month following this they were instructed to drink 8 cups of coffee a day.
Not surprisingly, drinking coffee was found to lead to higher blood levels of a variety of coffee-derived substances including caffeine and chlorogenic acid.
Compared to drinking no coffee, drinking 8 cups a day was associated with significantly reduced levels of inflammatory markers (interleukin-18 and 8-isoprostane), as well as significantly raised levels of adiponectin (a hormone is secreted by fat cells, and has been shown to have generally beneficial effects on the body’s physiology including an anti-inflammatory effect). These effects may be relevant not just to cardiovascular disease, but diabetes too. The authors of this study point out that inflammation is a risk factor for type 2 diabetes.
For what it’s worth, the higher coffee consumption was also associated with lower ratios of LDL to HDL cholesterol and apolipoprotein B to apolipoprotein A1. These changes in the lipid levels in the blood would generally be taken as evidence of reduced cardiovascular disease risk.
This study provides evidence that coffee-drinking can affect the body’s biochemistry in a way that could explain the know association between coffee-drinking and reduced risk of disease. It also lends some support for the idea that coffee-drinking has genuine disease-protective properties.
References:
1. Kempf K, et al. Effects of coffee consumption on subclinical inflammation and other risk factors for type 2 diabetes: a clinical trial. Am J Clin Nutr 2010;91:950-957
