Cocaine is a highly addictive recreational drug, traditionally extracted from the coca plant grown in south America and more recently Columbia. This drug was commonly used throughout the United States during the 19th century to remove pain as an anesthetic, increase labor as a stimulant, and as a food additive until the Jones-Miller Act of 1920 and the Controlled Substances Act of 1970 restricted the capacity to manufacture, import, or possess cocaine(Das, 1993). Modern cocaine consumption skyrocketed during the 1980s and early 2000s, with North America holding the largest per capita consumption of cocaine. Furthermore a steady increase of both cocaine use and cocaine induced seizures in developing nations demonstrates a need for further research treating the effects of cocaine use, namely addiction and acute toxicity (United Nations Publications, 2013).
Cocaine gives its user a ‘high’ due to its capacity to turn off the re-uptake of ‘feel good’ molecules which regulate reward-motivation systems within the brain. Usually a neurotransmitter such as Dopamine is release from a Dopaminergic cell and interacts with its neighboring cell for a short period of time until it is either destroyed or brought back to the first cell; however, Cocaine stops the reuptake of molecules such as Dopamine causing a longer, more intense high(Schindler, 1996). Since cocaine doesn’t specifically target the dopamine pathway, neurons which use neurotransmitters such as epinephrine and norepinephrine and ion channels for controlling sodium concentrations are also effected. The heart for example is excessively stimulated causing the surrounding cardiovascular blood network to be tightened (vasoconstriction), causing an increase in heart rate and blood flow. Large amounts of cocaine can sustain this constricted state for long periods of time, causing a decrease in the oxygen supply for the heart (ischemia) resulting in a heart attack (myocardial infarction) (O’Leary and Hancox, 2008).
Cocaine usually has a short period of activity and resulting high, after which it is broken down in the liver to two non-toxic metabolites. Since cocaine is associated with short highs, multiple doses are often taken resulting in two increased risks. First, as a party drug cocaine is often taken alongside alcohol, which when metabolized at the same time results in a new molecule cocaethylene. This molecule is able to react almost identically to cocaine, while taking a lot longer to metabolize. Taking several doses of cocaine alongside ethanol increases the cocaethylene concentrations and can lead to acute cocaine toxicity, resulting in seizures and heart failure(Hayase, 1999). Secondly due to its role as a dopamine reuptake inhibitor the increased use of cocaine has a higher capacity to cause addiction, increasing cravings for cocaine when addicted users are exposed to places or people associated with cocaine(Carey, 2008). It is the combination of increased risk and capacity to become addicted that makes cocaine such a potent toxin.