Crack cocaine makes you feel like a new man; the only problem is the new guy wants more cocaine.
That maxim, part of a 1990s public service campaign in the United States, conveys a hard truth: crack delivers an intense, but brief high that can trigger powerful cravings for more stimulation.
Crack invaded inner cities in the mid-1980s, offering a cheap alternative to the powdered form of cocaine. More than two decades later, crack remains a central feature of the drug landscape in Ottawa and other North American cities.
The physiology of crack use helps to explain why it has become so firmly entrenched.
Crack speeds delivery of cocaine’s powerful chemical impact. When a rock of crack is heated — usually in a small glass pipe — it produces smoke that’s drawn into the lungs. The lungs are super efficient at transferring the vapourized cocaine from air sacs (alveoli) to tiny blood vessels (capillaries).
Once in the bloodstream, the drug is whisked to the brain’s main pleasure centre within seconds.
That centre, known as the ventral tegmantal area (VTA), is made up neurons in the middle of the brain. The centre is vital to the survival of the human species since it generates a pleasurable sensation for behaviour that sustains people — eating, drinking … sex.
An evolutionary feature, the system reinforces essential human behaviour with what amounts to brain candy: dopamine. That chemical messenger informs other parts of the brain’s reward circuit that the body’s fundamental needs are being met.
The cocaine molecule produced by smoking crack hijacks this reward system.
Cocaine overstimulates the circuit by preventing dopamine from being reabsorbed by those neurons that first issued the neurotransmitter. As a result, the brain is flooded with dopamine that continues to send its euphoric message to other neurons.
Crack’s impact on brain chemistry means users can also experience surges in confidence and energy. But the high, while quickly delivered, is fleeting: a typical hit lasts anywhere from five to 15 minutes.
While it works on the brain, cocaine also changes the body. Its short-term effects include constricted blood vessels, dilated pupils and an increase in the body’s heart rate, respiratory rate, temperature and blood pressure. Some people become agitated or nervous under influence of the drug.
In rare cases, first-time cocaine users can suffer fatal effects.
“Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest,” according to a 2009 research report by the U.S. National Institute on Drug Abuse. “Research has also revealed a potentially dangerous interaction between cocaine and alcohol. In fact, this mixture is the most common two-drug combination that results in drug-related death.”
Not everyone who smokes crack becomes addicted. But because the drug produces such a quick, intense high, it is dangerous, particularly to those with a genetic predisposition to addiction.
Studies have shown that people with naturally low dopamine levels — those with depression often suffer the condition — experience more intense highs from stimulants such as crack.
“So if you have a genetic predisposition, you get a bigger bang for your buck whenever you use the drug: You get a greater amount of dopamine released,” explains Dr. Peter Selby, clinical director at Toronto’s Centre for Addiction and Mental Health.
Cocaine can cause people to “crash” when they stop using it, he said, because they move quicky between euphoria and irritability. That can bring powerful cravings for more of the drug, which in turn can lead to binges and addiction.
The physiological effects of long-term crack use are profound.
The brain can develop an increased tolerance to the drug that requires users to smoke more crack to obtain the same high. Computer imaging has revealed that cocaine physically alters the brain: the number of available dopamine receptors is significantly reduced in an addict.
Chronic crack smokers are more likely to suffer panic, paranoia, hallucinations, depression, nausea and seizures.
That maxim, part of a 1990s public service campaign in the United States, conveys a hard truth: crack delivers an intense, but brief high that can trigger powerful cravings for more stimulation.
Crack invaded inner cities in the mid-1980s, offering a cheap alternative to the powdered form of cocaine. More than two decades later, crack remains a central feature of the drug landscape in Ottawa and other North American cities.
The physiology of crack use helps to explain why it has become so firmly entrenched.
Crack speeds delivery of cocaine’s powerful chemical impact. When a rock of crack is heated — usually in a small glass pipe — it produces smoke that’s drawn into the lungs. The lungs are super efficient at transferring the vapourized cocaine from air sacs (alveoli) to tiny blood vessels (capillaries).
Once in the bloodstream, the drug is whisked to the brain’s main pleasure centre within seconds.
That centre, known as the ventral tegmantal area (VTA), is made up neurons in the middle of the brain. The centre is vital to the survival of the human species since it generates a pleasurable sensation for behaviour that sustains people — eating, drinking … sex.
An evolutionary feature, the system reinforces essential human behaviour with what amounts to brain candy: dopamine. That chemical messenger informs other parts of the brain’s reward circuit that the body’s fundamental needs are being met.
The cocaine molecule produced by smoking crack hijacks this reward system.
Cocaine overstimulates the circuit by preventing dopamine from being reabsorbed by those neurons that first issued the neurotransmitter. As a result, the brain is flooded with dopamine that continues to send its euphoric message to other neurons.
Crack’s impact on brain chemistry means users can also experience surges in confidence and energy. But the high, while quickly delivered, is fleeting: a typical hit lasts anywhere from five to 15 minutes.
While it works on the brain, cocaine also changes the body. Its short-term effects include constricted blood vessels, dilated pupils and an increase in the body’s heart rate, respiratory rate, temperature and blood pressure. Some people become agitated or nervous under influence of the drug.
In rare cases, first-time cocaine users can suffer fatal effects.
“Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest,” according to a 2009 research report by the U.S. National Institute on Drug Abuse. “Research has also revealed a potentially dangerous interaction between cocaine and alcohol. In fact, this mixture is the most common two-drug combination that results in drug-related death.”
Not everyone who smokes crack becomes addicted. But because the drug produces such a quick, intense high, it is dangerous, particularly to those with a genetic predisposition to addiction.
Studies have shown that people with naturally low dopamine levels — those with depression often suffer the condition — experience more intense highs from stimulants such as crack.
“So if you have a genetic predisposition, you get a bigger bang for your buck whenever you use the drug: You get a greater amount of dopamine released,” explains Dr. Peter Selby, clinical director at Toronto’s Centre for Addiction and Mental Health.
Cocaine can cause people to “crash” when they stop using it, he said, because they move quicky between euphoria and irritability. That can bring powerful cravings for more of the drug, which in turn can lead to binges and addiction.
The physiological effects of long-term crack use are profound.
The brain can develop an increased tolerance to the drug that requires users to smoke more crack to obtain the same high. Computer imaging has revealed that cocaine physically alters the brain: the number of available dopamine receptors is significantly reduced in an addict.
Chronic crack smokers are more likely to suffer panic, paranoia, hallucinations, depression, nausea and seizures.
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