Executive Summary

Clinicians have been using caffeinated analgesics to treat headache patients for decades. In recent years, however, the relationship between caffeine and headache has received attention. In the professional community, some investigators have focused on caffeine's ability to enhance analgesic efficacy, while others suggest that caffeinated analgesics may promote analgesic overuse. Reflecting the debate among professionals, conflicting reports about caffeine and its potential for abuse (either alone or in combination with analgesics) appear sporadically in the popular press. Despite the complexity of this issue, many medical and regulatory authorities, including the FDA, recognize that moderate caffeine consumption is safe. Accordingly, a basic understanding of the clinical relevance of caffeine may facilitate diagnosis of caffeine-related health issues, expand treatment options, and increase providers' ability to match therapy to the specific needs of each patient.

The series of presentations and follow-up discussions at the symposium, as well as the 2010 update, addressed important scientific findings about the relationship of caffeine and headache. Although the presentations covered a wide range of diagnostic and therapeutic issues, several clinically relevant conclusions emerged from each of the five main topics:

General
  • Taken orally, caffeine becomes pharmacologically active 6-8 minutes after ingestion and fully active within 30 minutes.
  • Caffeine has a half-life of 3-5 hours.
  • The average American consumes about 200-300 mg of caffeine daily.
  • Headache patients should be educated about the role of caffeine in managing headache.

Caffeine as an analgesic adjuvant
  • Adding caffeine to other analgesics, such as acetaminophen (APAP), aspirin (ASA), indomethacin, and prochlorperazine, enhances both their absorption and their ability to relieve tension-type headache and migraine.
  • To receive the same level of relief provided by a caffeinated analgesic, tension-type headache patients need to take 40% more of the same analgesic without caffeine.
  • In migraine clinical trials, analgesics combined with caffeine have significantly outperformed placebo, sumatriptan 50 mg, and ibuprofen 400 mg, as well as their single active ingredients.
  • By reducing the need for repeated doses, caffeinated analgesics may also reduce the risk of inappropriate use.

Medication overuse headache
  • Medication overuse headache (MOH) is an interaction between a therapeutic agent used excessively and a susceptible patient.
  • Any immediate-relief medication (nonprescription or prescription, caffeinated or non-caffeinated), when overused for the treatment of head pain, can cause MOH.
  • Patients being treated for MOH are not more likely to be taking caffeine-containing products than products without caffeine.
  • Patients with CDH are not more likely than episodic headache patients to be using or have a history of using caffeinated combinations.
  • Frequency of analgesic use appears to be more important than amount or type of agent taken per attack for the development of MOH.

Caffeine Withdrawal
  • Caffeine Withdrawal has a well-characterized constellation of symptoms that can include headache, sleepiness, and impaired concentration
  • According to the International Headache Society (IHS), patients need to consume at least 200 mg of caffeine daily for 2 weeks before a diagnosis of caffeine-withdrawal headache can be made.
  • Response to caffeine is highly individualized; withdrawal symptoms typically occur at 500 mg or more daily, but they have also been reported after chronic intake of 100 mg or less per day.
  • The frequency and severity of caffeine-withdrawal symptoms may be less common than published reports indicate, and more people may report a history of caffeine-withdrawal symptoms than experience them under double-blind conditions.

Addiction/habituation
  • The American Psychiatric Association (APA) does not recognize caffeine addiction as a classifiable disorder. Compulsive drug-seeking behavior involving caffeine has never been observed.
  • Because evidence that patients may use caffeinated analgesics to avoid caffeine-withdrawal headache is unreliable and inconsistent in experimental contexts, the phenomenon does not constitute a valid syndrome.
  • When used according to label directions, caffeine-containing analgesics pose no risk of habituation or addiction.
  • Significant caffeine abuse has not been reported by any culture in the world.
  • The symptoms of Caffeine Withdrawal are often confused with addiction, but some drugs produce adaptation and withdrawal effects if consumption suddenly ceases-without any evidence of abuse potential.