Like all the living cells in your body, your immune cells are studded with an array of receptors that permit them to respond to their environment and to communicate with one another. Scientists have learned that one type of receptor—the adenosine receptor—plays a vital role in regulating immune activity. When adenosine attaches to and activates these receptors, it triggers a cascade of events that eventually halt inflammation. Caffeine attaches to adenosine receptors, too, but it actually turns them off, rather than activating them. Thus, very brief exposures to caffeine may promote inflammation. However, immune cells quickly “upregulate” the receptors that are inactivated by caffeine, so long-term caffeine use (more than a few days) increases the overall number of adenosine receptors, which eventually reduces inflammation.
Studies evaluating the effects of different caffeine “vehicles” on autoimmune disorders have produced conflicting results. One 2002 Arthritis and Rheumatism study suggested that decaffeinated coffee increased a person’s risk for developing rheumatoid arthritis, while caffeinated coffee was not associated with RA onset, and green tea exerted a protective effect. Another study, published the following year in the same journal, demonstrated no link between rheumatoid arthritis risk and any of these beverages.
Still other well-designed trials have shown that caffeine—no matter the source—exerts an anti-inflammatory effect in most situations. These inconsistencies could be due to a number of factors, such as the concentrations of catechins, chlorogenic acid, and other antioxidants in the tested products or the underlying “polarity” of an autoimmune disease—that is, whether it’s driven by type 1 (Th1) or type 2 (Th2) helper cells. To further complicate this issue, caffeine may actually mediate a shift in helper-cell polarity through its actions on adenosine receptors. Clearly, more research is needed here.
Since it isn’t clear yet whether caffeine exerts any positive or negative effects on autoimmune disorders, the decision to use caffeine may just boil down to whether you feel better or worse when you consume it. If your energy levels and inflammatory symptoms seem to improve with caffeine, it’s difficult to find a compelling reason to quit. On the other hand, if caffeine aggravates your condition—or if your doctor recommends that you avoid it for other reasons—the best course is to taper your intake over several days before quitting. Trying to mitigate caffeine’s effects with dietary modifications, herbs, or special supplements is akin to taking one medication solely to deal with the undesirable side effects of another.
E Lopez-Garcia, RM van Dam, et al. Coffee consumption and markers of inflammation and endothelial dysfunction in healthy and diabetic women. The American Journal of Clinical Nutrition. 2006;84(4):888-893
EW Karlson, LA Mandl, et al. Coffee consumption and risk of rheumatoid arthritis. Arthritis and Rheumatism. 2003;48(11):3055-3060
K Varani, F Portaluppi, et al. Caffeine alters A2A adenosine receptors and their function in human platelets. Circulation. 1999;99:2499-2502
TR Mikuls, JR Cerhan, et al. Coffee, tea, and caffeine consumption and risk of rheumatoid arthritis: Results from the Iowa Women’s Health Study. Arthritis and Rheumatism. 2002;46(1):83-91
About the Author
Steve Christensen, MD – “Doom” to his close friends – was trained at the University of Utah School of Medicine. Since his premature retirement from medicine in 2003, Dr. Christensen has expanded his knowledge of alternative medicine: he is a certified herbalist; he has dabbled at the edges of Ayurvedism, shared ideas with Chinese physicians, rubbed shoulders with Native American healers and contemplated the healing powers of channeled energy.
This blog post was originally published by AutoimmuneMom.com, written by Steve Christensen, MD, and first published on Mar 31, 2012.