Stimulants have been used medicinally for thousands of years. Chinese physicians have used ma haung, a tea made from the herb Ephedra vulgaris, as a medicinal herb for 5000 years. Chat, another stimulant, was used 2000 years ago by Roman gladiators to overcome fatigue and thus fight longer during contests ( 1994). Coffee has been in existence since at least A.D. 900, when an Arabian medical book referred to it as useful for a variety of indications, including measles and lust reduction. Coffee drinking was so widespread that coffeehouses were common in England, Arabia, and France as early as the 1600s (2002)
Other drugs used historically for medicinal purposes include opiates, alcohol, and marijuana. Opiates were used as early as the third century B.C. as analgesics, to treat anxiety and psychotic disorders, and were even given to children to ease colic. Fermented honey (mead) may have been used since 8000 B.C. By 6400 B.C., beer and berry wine were being used by Neolithic humans ( 2002). Alcohol was also used to reduce anxiety and to help insomnia sufferers fall asleep ( 1999). By the 1500s, drugs were big business. Prior to the arrival of the Spanish in South America in 1518, the coca leaf had been chewed by the Incas in their religious ceremonies and was used as a medium for barter ( 1987;). As Spanish landlords realized that chewing the coca leaf reduced thirst, hunger, fatigue, and increased productivity, the practice of chewing the leaves was encouraged and soon became widespread ( 1994) Cocaine was extracted in 1859. Combined with the invention of the syringe in 1853 cocaine use began to increase in popularity. The extracts from the coca leaf were used in a range of medicinal drinks including CocaCola. Cocaine use was widespread; users included many prominent people, among them , who was one of cocaine’s greatest proponents ( 1999).
Opiates, cocaine, and alcohol were so widely used that, by the early 1900s, when there was great concern with drug use, many patented medicines containing these drugs were sold on the streets by peddlers. The ingredients of these snake oil concoctions were kept secret. No agency existed to regulate the contents or claims made about these drug cordials. When the medical community began to question the claims made about these elixirs, the conflict led to the Pure Food and Drug Act of 1906, which prohibited the distribution of food and drugs that were misbranded.
Another law that passed in the effort to control the manufacture and distribution of opiates was the Harrison Act of 1914. thought that the U.S. would improve its trading status with China by helping the Chinese control the importation of opium. In 1912, an international conference was held; at that time, Great Britain wanted to include controlling the importation of morphine, heroin, and cocaine as well. When all talks and compromises were over, the Harrison Act of 1914 was born; its intent was “to provide for the registration of, with collectors of internal revenue, and to impose a special tax upon all persons who produce, import, manufacture, compound, deal in, dispense, or give away opium or coca leaves, their cults, derivatives or preparation, and for other purposes” . The Harrison Act was meant to be solely a tax law and did not prevent the use or distribution of such drugs (, 2002). In the 1820s a “new drug” called marijuana (which had been used to make rope and clothing since grew it) came to the attention of Congress. Medicinal use of marijuana can be historically dated to the year 2737 B.C. when Emperor wrote a pharmacy book recommending the use of marijuana to treat “female weakness, gout, rheumatism, ben been, constipation, and absent mindedness” (1970). There is also a documented case of physicians using marijuana on a rabies patient to control the terror and excitement that the patient suffered. In the 1800s, American and European physicians used marijuana as a hypnotic, anticonvulsant, analgesic, and as treatment for migraine headaches ( 1992, 1993, 1995). It was not until the 1920s that marijuana became a concern in the U.S. In 1926, newspaper articles began associating marijuana use with violent crime (no evidence of this existed). , who was the U.S. Commissioner of Narcotics, reported in 1931 that marijuana use was not a problem. However, in a Congressional hearing in 1937, reported that marijuana trafficking had increased at such an alarming rate “that it has come to be the cause for the greatest national concern”. By this time, newspaper and magazine reports of marijuana had burgeoned to include, not only violent crimes being committed, but also police interviews stating as much. These reports were believed by the public but, in fact, there was no evidence provided to support their validity. This concern led to the passage of the Marijuana Tax Act in 1937. This act required the registration and taxation of those importing, buying, or selling marijuana, but did not make the possession of marijuana illegal.
The Spread of Methamphetamine Use in the U.S.
After the withdrawal of Desoxyn and methedrine from the pharmaceutical market, illicit methamphetamine laboratories emerged in San Francisco late in 1962. Motorcycle gangs took over the manufacture and distribution of methamphetamine in the mid-1960s spreading it north and south along the Pacific Coast. By the 1970s the use of methamphetamine had spread from the blue-collar workers to include college students, young professionals, minorities, and women. By the 1980s intensified law enforcement efforts that targeted the biker subculture, together with new, easier ways of producing methamphetamine, caused the production and distribution to move to the San Diego area. With the move to San Diego, Mexican traffickers became involved in the manufacture and distribution. Large amounts of the illicitly produced methamphetamine and precursor chemicals were smuggled in from Mexico to California, and distributed not only to the traditional market, but also to the southwestern and midwestern states (2000). Large amounts of the illicitly produced methamphetamine and precursor chemicals were smuggled in from Mexico to California, and distributed not only to the traditional market, but also to the southwestern and midwestern states (2000).
Hawaii and Ice
During the 1980s there was a surge in Hawaii of methamphetamine use when a smokeable, highly pure form of D-MA-hydrochloride (ice) became available, imported from Far East sources in the Philippines, Japan, Korea, and Taiwan ( 1997). During the 1990s use of ice in the Hawaiian Islands became rampant. The distribution of methamphetamine in Hawaii was gradually dominated by Mexico- and California-based trafficking organizations. These crime groups are supplemented in Hawaii by extended kinship networks, which sometimes include whole families or neighborhoods (1997). The use of ice in Honolulu had led to particularly serious physical and psychological problems and significant social disruption in poor working communities where it replaced marijuana which had become scarce and expensive due to eradication policies (NIDA, 1991-1994, summary).
There are thought to be several influences on the tremendous growth of ice in Honolulu after 1987. Residents were pushed away from marijuana, their staple drug of choice, and pulled toward ice by a well-organized marketing campaign by Asian distributors. Also, the overwhelming drug of choice, marijuana, which had been grown and used throughout the islands for many years, became the target of a government eradication campaign. This drove up prices and left locals without their customary smoke. Also very important, many locals derived either part of or their entire livelihood from marijuana production. Thus, when a new, easy-to-use smokeable product entered the market, one that at first seemed nonthreatening to youthful novitiates, i.e., ice, it was readily accepted.
Methamphetamine continues to be a major problem in Hawaii. Methamphetamine is readily available, with the majority of it converted into ice before it is distributed. In the past few years, ice-related crimes have increased as the drug has increased in popularity and availability. The Arrestee Drug Abuse Monitoring Program in 2001 revealed that 35.9% of males arrested from January to September 2001 tested positive for methamphetamine abuse. Further tests showed arrested males and females in Honolulu tested positive for methamphetamine at a higher rate than for marijuana (28.8%) and for cocaine (11.2%). Among 37 metropolitan areas, Honolulu has the highest percentage of arrested males testing positive for methamphetamine, according to a report from the U.S. Department of Justice. No other city approached 30%. Cities participating in the survey ranged from New York City and Philadelphia to San Diego and Seattle.
Effects of Methamphetamine Use
The cerebral damage caused by methamphetamine intoxication can be formidable. Prolonged use is associated with injury to the dopamine system. Essentially, continued methamphetamine use likely leads to axonic degeneration of the dopamine axon terminals in the striatum, frontal cortex, nucleus accumbens, and amygdala. Hypersensitization of neurons occurs, for example, in increasing sensitivity of D-1 receptors. It is important to note that changes in catecholamines alone cannot explain behavior in humans when they are methamphetamine intoxicated. Animal studies across several species demonstrate that high dosages of methamphetamine damage nerve cells . In rats, one high dose is enough to cause damage to neurons; prolonged administration increases the number of neurons that are killed off. In squirrels, a single dose of MDMA (which is structurally similar to methamphetamine and mescaline) in only slight doses significantly damages brain neurons that produce serotonin. Twelve to 18 months after exposure, serotonin-producing nerves grow abnormally or not at all. MDMA selectively damages serotonin neurons in virtually all species (1995).
Not surprisingly, high doses of methamphetamine can cause death. A male under arrest died with a blood content greater than 60 mg per litter after swallowing a “baggie” of methamphetamine. A toxic reaction in humans can occur at levels as low as 50 mg of pure methamphetamine for nontolerant users. Ischemic stroke is associated with methamphetamine inhalation (1999). Massive strokes are fairly common. The second author conducted a neuropsychological evaluation of a 30-year-old, previously normal, federal employee who suffered multiple strokes and a vascularizing dementia after a single methamphetamine intoxication. Although a family history of strokes for members in their 60s and 70s was revealed, representing a possible vulnerability for the client, methamphetamine appeared to cause the client’s strokes long before they would normally be expected, given his family history. Methamphetamine taken intranasally has caused caudal thalamic infarctions in an abuser . Ischemic stroke is associated with methamphetamine inhalation.
In sum, much of the data suggest there is no way of establishing a “safe” or “unsafe” level of methamphetamine for a particular person, or even for the same person with repeated doses. With other drugs, and certainly with alcohol, use of the particular substance must continue for a given time period (e.g., 12 months) and be accompanied by maladaptive behavior to qualify for a DSM-IV diagnosis of substance abuse. Preliminary data suggest that this is in marked contrast to methamphetamine abuse where a small number of intoxications can create catastrophic changes in physical and mental functioning. There are multiple factors, in addition to its untoward effects on nontolerant users, that cause the effects of methamphetamine to be unpredictable. The properties of methamphetamine itself can create unpredictable reactions. Further, there may be impurities in the drug. Methamphetamine manufactured in clandestine labs is frequently impure. Methamphetamine can be used to “cut” other drugs, which means that interactive effects must be considered. Also, a variety of toxic chemicals can be used as the precursors from which methamphetamine can be formed (e.g., ephedrine and pseudoephedrine, benzyl chloride, benzyl cyanide, methylamine); or as reagents, substances that react with precursors (e.g., hydriodic acid, iodine, mercuric chloride, sodium cyanohydridoborate); or as solvents (e.g., ethanol, ethyl chloroform, acetone). Residues of these substances may contaminate the final product.
There are two basic methods for producing methamphetamine, each of which requires 2 to 4 days to produce a batch. One method involves the reaction of phenyl-2-propanone (P-2-P), phenylacetine, and methylamine. The other method uses ephedrine as a precursor chemical, which does not necessitate use of a controlled precursor. This method, referred to as the ephedrine/red phosphorus method, requires the use of hydrogenator. Red phosphorus is on the list of less restricted chemicals in many states, and information that this chemical can be obtained from the fireworks and matchmaking industries has been widely disseminated on the Internet since 1996 ( ). The striking pad on match covers is about 40% red phosphorus and 30% antimony sulfide, with lesser amounts of glue, iron oxide, manganese dioxide, and glass powder. Some of these chemicals, alone or in combination, can cause toxic reactions in the methamphetamine user. In addition, the ephedrine/red phosphorus method often produces “garbage” methamphetamine. Unless simple precautions are followed, which are typically not followed by makers who are often chronic methamphetamine users themselves, high amounts of iodoephedrine and azirine are produced as contaminants.
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