Caffeine is the most widely consumed and unregulated stimulant in the world. The majority of Americans knowingly or unknowingly consume caffeine each day, usually from coffee, tea and soda, but also from chocolate, energy drinks and many over-the-counter medications. In the quantities found in most food and drinks, caffeine is very unlikely to cause toxicity; however, many drugs contain high levels of caffeine and pose a considerable risk for some users. Nerve damage can develop as a consequence of excessive caffeine intake, but it is not the most common symptom.
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Prevalence of Caffeine Toxicity
According to “Nutrition Concepts & Controversies,” 3,343 cases of caffeine poisoning were reported to the American Association of Poison Control Center in 2009. Of the 3,343 cases, 1,249 represented children younger than 6 years old, mainly because of their smaller size and lesser ability to metabolize caffeine and remove it from their blood serum. Death is not an uncommon result of caffeine toxicity, with the causes often related to heart failure, seizures and adrenal failure. There is no data to suggest that race or gender alter the biochemical effects of caffeine.
In adults, lethal toxicity from caffeine is estimated to occur between 150 and 200 mg/kg, which equates to drinking at least 80 cups of brewed coffee in a short period of time, according to the “Complete Guide to Prescription and Non-prescription Drugs” by H. Winter Griffith, M.D. In terms of lethal dosages, consumption of between 7 and 10 g of caffeine will kill most adults. Caffeine doses of 78 mg/kg can cause toxicity and serious adverse effects in young children. In 1989, the US Food and Drug Administration limited the amount of caffeine in over-the-counter drugs to a maximum of 200 mg/dose. Caffeine is commonly found in alertness-promoting drugs, menstrual aids, pain killers and diet aids.
Caffeine affects your central nervous system, heart, blood vessels, adrenal glands, thyroid gland, kidneys and a variety of neurotransmitters and hormones, but it is dose dependent. For example, at doses between 85 and 250 mg, caffeine may cause feelings of alertness, reduced fatigue and eased flow of thought, according to “Functional Biochemistry in Health and Disease." Doses between 250 and 500 mg can cause undesirable effects, such as restlessness, nervousness, insomnia, fatigue and tremors. Higher daily doses can cause severe glandular fatigue from over-production of adrenaline and other hormones, cardiovascular problems and altered brain activity that culminates in seizures. People most at risk for severe caffeine toxicity are bodybuilders and other athletes that intentionally supplement with caffeine, people addicted to drugs with caffeine, long-term energy drink addicts and epileptics, as noted by Sari Edelstein, author of “Nutrition and Public Health.”
Caffeine and Nerve Damage
Caffeine can damage nerves in a couple of ways. According to the book “Advanced Nutrition and Human Metabolism,” the main action of caffeine is to counteract the effects of the brain chemical adenosine, which results in reduced blood flow to your brain and damage to neurons. Damage to neurons in your brain is experienced as headaches, dizziness, seizures and reduced fine-motor coordination in your hands.
Further, caffeine indirectly promotes the depletion of B vitamins, some of which are needed for conductance and maintenance of nerves. As such, high consumption of caffeine can cause numbness and tingling in your arms, legs and around your head. Reducing your caffeine consumption and supplementing with a B-complex vitamin should help combat these symptoms. Long-term vitamin B-6 and B-12 deficiency often results in permanent nerve damage.
- “Nutrition Concepts & Controversies: 12th Edition”; Frances S. Sizer et al; 2011
- “Complete Guide to Prescription and Non-prescription Drugs – 2010”; H. Winter Griffith, 2009
- “Functional Biochemistry in Health and Disease”; Eric Newsholme et al; 2010
- “Nutrition and Public Health”; Sari Edelstein; 2006
- “Advanced Nutrition and Human Metabolism”; Sareen Gropper et al; 2009