Caffeine in Coffee Protects the Blood-Brain Barrier

May 15, 2008

For the first time, scientists have determined that caffeine consumption protects against the disruption of the blood-brain barrier (BBB) which "could have an important part to play in therapies against neurological disorders," according to Dr. Jonathan Geiger, chairman of the Department of Pharmacology, Physiology, and Therapeutics of the University of North Dakota's, School of Medicine and Health Sciences.

Dr. Geiger's findings were reported in the April 3, 2008 edition of the Journal of Neuroinflammation which revealed that daily caffeine protects the brain by cutting the risk of dementia because caffeine blocks the damage that cholesterol can inflict on the body by maintaining levels of proteins key in keeping the barrier strong.

The function of the BBB is to act as a filter to protect the central nervous system from carrying harmful chemicals throughout the body's bloodstream. Because people with Alzheimer's Disease (AD), strokes or other neurological diseases have BBB that work less efficiently, the stabilization of BBB is a critical element in avoiding the development of these diseases.

The study used New Zealand white rabbits one and one-half to two-years-old weighing three to four kilograms who were given 3 mg of caffeine administered in 50 ml of drinking water daily. The 3 mg dosage is the equivalent of only one cup of coffee per day for a human being. The experiment was conducted over a period of 12 weeks and involved four groups of rabbits. One was given normal food, the second was fed a normal diet plus 3 mg of caffeine per day, the third group had a 2% cholesterol enriched diet, and the fourth group had the 2% cholesterol enriched diet plus the 3 mg per day of caffeine.

At the end of the experiment, the BBB was significantly "more intact" in rabbits receiving the caffeine, Dr. Geiger said, and the "caffeine appears to block several of the disruptive effects of cholesterol that make the blood-brain barrier leaky." This "leaky" occurrence is caused by high levels of cholesterol present in fatty foods. The studies used primarily olfactory bulbs, a region of the brain "important for olfaction." AD patients experience particularly high olfactory dysfunction (loss of smell), one of the earliest symptoms of the disease.

The study also indicated that a 10-fold higher dose of the caffeine, 30 mg versus 3 mg in the rabbits, produced results virtually identical to the findings reported in the Journal. (In comparison, the average consumption of caffeine in humans is about 200 mg.)

It has been well established that the risk of developing AD has been lower in those humans with elevated levels of plasma caffeine, however, the way which cholesterol or caffeine can cause or protect against cellular damage typical in AD is not as yet understood. This study, however, points to diet-induced AD pathology which, in turn, may lead to strategies to prevent or slow the progression of this neurodegenerative disorder.

The study was supported by the US National Center for Research Resources, a component of the National Institute of Health. Other investigators and scientists participating in the study include Drs. Othman Ghribi, Xuesong Chen, Jeremy W Gawryluk, John F and Wagener.

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