Effects of Substance Abuse on Mental Health Essay
Substance related disorders Definitions and terms Use This is when a person drinks alcohol or swallows smoke, sniffs or injects a mind altering substance. Abuse This is when a person is using alcohol or drugs for the purpose of intoxication or in the case of prescription for purpose beyond their intended use. Dependence It is the continuing use of alcohol or drugs despite adverse consequences to ones physical, social and psychological wellbeing Addiction This describes that state when the person experiences severe psychological and behavioral dependence on drugs or alcohol Withdrawal effects
These are the adverse physical and psychological symptoms that occur when a person ceases using a substance Detoxification It is the process of safely or effectively withdrawing a person from an addictive substance usually under medical supervision Relapse This is the reoccurrence of alcohol or drug dependent behavior in an individual who has previously achieved a maintained abstinence for a significant time beyond the period of detoxification Intoxication It is the psychological and physical effects of the substance which h disappear when a substance is eliminated Tolerance
The state in which repeated administration leads to decreasing the effects Dependence syndrome A person is said to have dependence syndrome they experience three of the following characteristics in the past twelve months 1. a strong desire of compulsion to take the drug 2. difficulty in refraining from using the substance, stopping using it or limiting the amount taken 3. a physiological withdrawal state when substance use has stopped or been reduced 4. Evidence of tolerance a state in which an increasing dose of the substance required to produce the effects originally produced by lower dose. . Persistence use of the substance despite clear evidence of harm. Co morbidity This is a situation where mental disorder are in part a by product of long tern substance abuse, for others the mental disorder itself predisposes to alcohol or drug abuse Categories of substance-related disorders according to DSMIV-TR A . Substance-use disorder • Substance abuse This is a maladaptive pattern of substance use manifested by recurrent and significant adverse consequences related to repeated use of substance. DSM-IV-TR Criteria for substance abuse
A maladaptive pattern of substance use leading to clinically significant impairment or distress as manifested by one or more of the following occurring within a 12 month period; 1. Recurrent substance use resulting in a failure to fulfill major role obligation at work school or home 2. Recurrent substance use in situation which it is physically hazardous e. g. driving. 3. recurrent substance –related legal problems 4. Continued substance use despite having recurrent social or interpersonal problems caused by exacerbated by the effects of the substance. • Substance dependence
This is physical or psychological dependence. Physical dependence is evidenced by a cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues use of substance despite the problems Psychological dependence is when the individual has overwhelming desire to repeat the use of a particular drug to produce pleasure or avoid discomfort. DSM-IV-TR Criteria for substance dependence At least three of the following characteristics must be present for a diagnosis of substance dependence 1. evidence of tolerance 2. evidence of withdrawal symptoms 3. he substance is taken for longer period of time or in large amount than expected 4. There is unsuccessful desire to cut down or control the substance use. 5. a great deal of time is spent in activates to obtain the substance 6. social, occupational activities are given up due to substance use 7. the substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problems B. Substance –induced disorders Substance intoxication This is the development of a reversible –specific syndrome caused by the recent ingestion of a substance.
The change of behaviors in that time is due to effects of the drug in the CNS. DSMIV. TR Criteria for substance intoxication 1. the development of reversible substance specific syndrome caused by recent ingestion of a substance 2. clinically maladaptive behavior or psychological changes caused by the effect of the substance 3. the symptoms are not caused by any medical condition Substance withdrawal This is development of a substance specific maladaptive behavior changes with physiological and cognitive disturbance due to cessation of or reduction in heavy and prolonged substance use.
DSM-IV0TR Criteria for substance withdrawal 1. the development of a substance specific syndrome caused by the cessation of heavy and prolonged substance use 2. the substance specific syndrome causes clinically significant distress or impairment in social, occupational or any other important areas of functioning 3. The symptoms are not caused by a general condition. Predisposing factor to substance abuse disorder 1. Biological factors Genetics Hereditary factor are involved in the development of substance use disorder. This is very much evident with the alcoholism.
According to the American academy of child and aldolesece1999 children born of alcoholics are four times more likely to become alcoholic. Other studies have shown that male biological offspring of alcoholic father have four times the incidence of alcoholism then the offspring of non alcoholic (Francis and Franklin, 1994) 2. Biochemical factors It is hypothesized that alcohol may produce morphine like substance in the brain that is responsible for the alcohol addiction. 3. psychological factors Developmental influence Individual with punitive superego turn to alcohol to diminish unconscious anxiety.
It also serves to increase feeling of power and self worth. 4. personality Some personality increase tendency to addictive behaviour. people with ant social behavior and depressive styles are more prone to substance abuse in an attempt to treat the symptoms of discomfort 5. social cultural factors Social learning The effects of modeling, imitation whereby the individual involved learn from one another the use a substance. Conditioning The effect of a substance that creates a pleasurable experience to the user encourages the user to use it again and again.
The addictive property of the substance conditions the individual to seek the repeated use of the substance. 6. cultural and ethnic influence some factor within individual culture help establish pattern of substance use by molding attitudes ,influencing pattern of consumption based on cultural acceptance and determining availability of the substance e. g. French and Italians consider wine as essential part of their meal been for the children and so the possibility of effects associated with life long consumption may occur.
The following are the psychoactive substances associated with substance-use and substance –induced disorder 1. alcohol 2. amphetamine 3. caffeine 4. cocaine 5. cannabis 6. hallucinogens 7. inhalants 8. nicotine 9. opioids 10. phencyclidine 11. Sedatives, hypnotics. or anxiolytics . Alcohol Alcohol is a natural substance formed by the reaction of fermenting sugar with yeast spores. It is a sedative found in various preparations like wine, liquor and beer. Alcohol produces sedative effects by suppressing the central nervous system.
This make the individual to have a feeling of relaxation, emotion and mood swing tat can range from angry outburst and cognitive impairment such as reduced concentration or attention span, impaired judgment and memory loss. The intensity of the CNS impairment depends on how much alcohol is consumed in a given period of time and rapidly the body metabolizes it Intoxication is determined by the level of alcohol in the blood called alcohol blood level. Biological body response to alcohol Alcohol makes neuronal membrane more permeable to potassium and chloride ions and closes sodium and calcium channels.
This increased permeability causes elevated blood pressure and heart rate. Alcohol is metabolized in the liver as carbohydrate into carbon dioxide and water. Alcohol is converted by alcohol dehydrogenase into acetaldehyde which is converted to acetic acid by aldhyde dehydrogenase. the body is capable of metabolizing 15dl of alcohol per minute . Rapid intake of alcohol can cause accumulation of acetaldehyde which then combines with neurotransmitters dopamine and serotonin and this contribute to the alcohol dependency Co morbities It is associated with anxiety, phobias and obsessive compulsive disorder
DSMIV-TR classification of alcohol related disorder • Alcohol dependence • Alcohol abuse • Alcohol intoxication • Alcohol withdrawal delirium • Alcohol induced disorder • Alcohol-induced psychotic disorder • Alcohol –induced amnesia disorder Jellinek (1952) outlined four phases through which the alcoholics patterns of drinking progresses PHASE I. THE PREALCHOLIC PHASE This phase is characterized by use of alcohol to relieve the daily stress of life. As a child the individual may have observed parent and enjoy the effects. The child learns that use of alcohol helps to relieve stress and tolerance develops. PHASE II
This begin with the person (period of amnesia) following a period of drinking. The person drinks preoccupied with drinking rapid gulping of drinks later he feels guilty of the action of drinking. PHASE III THE CRUCIAL PHASE The person has lost control and is psychologically dependent on alcohol. The person focus is drinking day in day out. The person falls ill because he is only taking alcohol no feeding. The person is ready to loose what he has but maintain the addiction. The person become dysfunctional PHASE IV CHRONIC PHASE There is physical and emotional disintegration; this is evidenced by helplessness and self pity.
Abstinence from alcohol results in a terrifying syndrome of symptoms like hallucinations, tremors, convulsions, and pani Alcohol dependence This is a pattern of compulsive use defined by the presence of three or more major areas of impairment related to alcohol occurring within the same 12months. these area include tolerance or withdrawal, spending most time in taking the substance, returning to use despite physical and psychological effects repeated unsuccessful attempt to stop the substance Alcohol abuse This is diagnosed when alcohol is used in very hazardous situation.
It differs from dependence in that it does not include tolerance and withdrawal or compulsive use pattern. Alcohol abuse includes continuous heavy drinking, weekend intoxication or binges interspersed with periods of sobriety. Alcohol intoxication This is also called simple drunkenness; it is a recent ingestion of a sulfficent amount of alcohol to produce acute maladaptive behaviors changes Mild intoxication produce a feeling of relaxation while moderate the patient experience slurred speech, uncondination, unsteady gait flushed face. In severe intoxication leads to withdrawn behavior psychomotor retardation and may progress to coma
Alcohol-induced psychotic disorder The patient in this state experience persistent hallucination without delirium following a decrease in alcohol consumption in an alcohol dependent person. The patient is treated with benzodiazepines e. g. lorazepam1-2 mg orally on daily basis. Alcohol withdrawal This occurs within 4-12 hours of cessation or reduction in heavy and prolonged several days or longer alcohol use. the patient develop tremors of the hands tongue or eyelids nausea and vomiting malaise or weakness tachycardia sweating elevated blood pressure anxiety ,depressed mood hallucination illusion headache and insomnia.
Alcohol withdrawal delirium (delirium tremens) This occur after recent cessation of or reduction in severe heavy alcohol use in medically compromised patient with long history of dependence It is characterized by delirium. Marked autonomic activity like tachycardia, sweating, fever, anxiety and insomnia. The patient has vivid hallucinations tremors fever seizures that develop before delirium, paranoid delusion, tactile hallucinations. Management The patient is observed constantly in a quiet room to avoid much stimulation.
The patient is put on IV fluid to correct electrolytes imbalance and hydrate the patient. Incase of any coexisting medical problem like infection they are treated. Vital signs are taken every 6 hours. Administration of thiamine 100mg three times a day Folic acid 1mg orally daily Magnesium sulphate 1g i. m every 6 hours for 2 days to these patients with post withdrawal seizures. Alcohol –induced amnesia disorder In this situation the toxic effect of alcohol to the brain causes atrophy of the frontal cortex and eventually chronic brain syndrome.
Most people with this condition have history of heavy alcohol abuse There are two types of his disorder • Wernickes syndrome This occurs due to thiamine deficiency in alcoholics. It causes oculomotor dysfunction, ataxia and confusion. The patient may also present with confabulation, lethargy, mild delirium and photophobia. Management The patient is treated with thiamine100mg -300mg a day until the opthamoplegia resolves. • Korsakoffs syndrome Also called korsakoff psychosis. This is a chronic condition related to alcohol dependence. There is severe thiamine deficiency.
It is characterized by retrograde and anterograde amnesia. Confabulation is a key feature of psychosis Management Long term oral administration of thiamine50-100 mg of thiamine a day Treatment modalities for alcoholic disorder 1. pharmacotherapy Benzodiazepine These are long acting CNS depressants that produce sedation and reduce anxiety symptoms so they help overcome the symptoms of alcohol withdrawal Diazepam can be given 5mg -10mg two to four hours to prevent development of delirium tremens or chlordiazepoxide hydrchloride25mg-100mg every 4hours.
Dislfirum This is used as adjuvant therapy to help deter some individual from taking alcohol while using treatment modalities to learn new coping skill to alter abuse behavior The mode of action is that it inhibits acetaldehyde dehydrgenase hence leading to the accumulation of acetahydehyde that causes adverse effects to the patient e. g. nausea vomiting hypotension diarrhea. These effects discourage patient from taking alcohol. The dosage is 100-200mg/day Anticonvulsants E. g. carbamazepine is used for the management of withdrawal seizures. . Self help groups 1. alcoholic anonymous(AA) They hold group meetings at which members obtaining support from one another. They share their experiences and focus on substance and loss of control over the ability to dink. 2. Al-Anon This provides support for the spouse of excessive drinkers. 3. Al Ateen It provides support to teenage children whose parents are alcoholics. 3. Adequate nutrition and supplemental vitamins Multivitamins therapy This involve oral administration of thiamine to prevent neuropathy, onfusion and encephalopathy It is usually given 100mg four times a day orally or given iv infusion with glucose Folic acid deficiency is corrected with administration of folic 20mg daily Magnesium is given prophylactic ally if patient has history of withdrawal seizures; it also enhances the body response to thiamine and reduces seizure activity. The dosage is 1. 0 g i. m four times daily for two days. Other managements include Individual therapy / Counseling Group therapy INHALANTS AND SOLVENTS The term “inhalants” refers to chemical vapors or gases that produce a “high” when they are breathed in.
Most of the substances used as inhalants, such as glue, gasoline, cleaning solvents and aerosols, have legitimate everyday uses, but they were never meant for human consumption. Inhalants are cheap, legal and easy to get. They have a high potential for abuse especially by children and young adults. Most of the people who use solvents and aerosols are young – between 10 and 16 years old. Many try inhalants only once or twice, or use them only on occasion. But some people use heavily and may continue using into adulthood. Chronic solvent users are usually in their 20s.
Solvent use is associated with poverty, difficulty at school, lack of opportunity, problems at home and a high incidence of substance use in the family. There are hundreds of different kinds of inhalants, roughly dividing into four different types: • Volatile solvents: These are the most commonly abused type of inhalants. “Volatile” means they evaporate when exposed to air, and “solvent” means they dissolve many other substances. Examples of solvents used as inhalants include benzene, toluene, xylene, acetone, naptha and hexane.
Products such as gasoline, cleaning fluids, paint thinners, hobby glue, and correction fluid and felt-tip markers contain a mixture of different types of solvents. • Aerosol or spray cans: Hair spray, spray paint, cooking spray and other aerosol products contain pressurized liquids or gases such as fluorocarbon and butane. Some aerosol products also contain solvents. • Gases: This includes some medical anesthetics, such as nitrous oxide (laughing gas), chloroform, halothane and ether, as well as gases found in commercially available products, such as butane lighters and propane tanks. Nitrites: Amyl nitrite, butyl nitrite and cyclohexyl nitrite (also known as “poppers”) are different from other inhalants in effect and availability. They are sold as “room odourizer” or “video head cleaner. ” Amyl nitrite is used medically to treat cyanide poisoning. Most of these inhalants and solvents that are abused have different street names by which they are identified i. e. glue, gas, sniff (solvents); whippets (nitrous oxide); poppers, room odourizers, VCR cleaner – some sold under “brand” names such as Rush, Bolt, Kix (nitrites). SOURCES OF INHALANTS
Many inhalants are widely available as commercial products. It is hard to prevent their use because these products are found in many homes and workplaces. Some manufacturers taint their products to try to make them less appealing to use as inhalants, but this has not prevented use. Stores may refuse to sell certain products to minors or people who are intoxicated, although there is no proper legislation to enforce this. Solvent and aerosol products on the store shelf, in the kitchen cupboard or in the workshop would not be noticed by most people as dangerous drugs.
When solvents are used as drugs, they are either inhaled directly from the container (sniffed), from a soaked rag held to the face (huffed) or from a bag (bagged). Sometimes people spray aerosols into a bag or balloon and then inhale the gas. Nitrous oxide or other anesthetic gases intended for medical use are contained in a gas tank; nitrous oxide is also found in whipped cream dispensers. Because nitrous oxide is pressurized and can be very cold, it is often inhaled from a balloon. Nitrites are clear yellow liquids that are inhaled directly from the bottle or from a cloth. EFFECTS OF INHALANTS
The effect of inhalants varies greatly among different people depending on a number of factors: • Age • Sensitivity to the drug being used • Quantity of the drug used • Duration and frequency of abusing the drug • The method used to take the drug • The environment one is in at the time of abusing the drug • Pre-existing medical or psychiatric conditions • Potential drug interactions with alcohol or other drugs (illicit, prescription, over-the-counter or herbal). All inhalants are absorbed through the lungs and travel quickly in the blood to the brain. This produces an immediate and brief intoxication.
Different types of inhalants produce different effects. Inhaled solvents usually produce an alcohol-like effect, but with more distortion of perception, such as the shape, size and color of objects, and distortion of time and space. New users may be initially excited, then become drowsy and fall asleep. People who use solvents more often may feel euphoric, exhilarated and have vivid fantasies. Some feel giddy, outgoing and confident. Physical effects may include dizziness, nausea, vomiting, blurred vision, sneezing and coughing, staggering, slow reflexes and sensitivity to light.
Nitrous oxide produces a dreamy mental state, loss of motor control, hallucinations and an increased threshold for pain. Nitrites dilate blood vessels and relax muscles. The heartbeat quickens and blood rushes to the head, creating a “rush. ” Nitrites also cause headaches, dizziness, nausea and flushing. Some men use nitrites during sex for the drugs’ capacity to relax muscles and promote blood flow. Several breaths of solvents will produce a high within a few minutes of use. This high may last up to 45 minutes, if no more breaths are taken.
Some people continue to take additional breaths to sustain the effects for several hours. As the effects wear off, the person may feel drowsy and have a hangover with a mild-to-severe headache for up to several days. The effects of nitrous oxide and nitrites are immediate, and wear off within a few minutes. INTOXICATION STATES Inhalants use is dangerous in many ways: • Suffocation: Solvents are often sniffed from a plastic bag, which is held firmly around the nose and mouth. People who use solvents sometimes pass out with the bag still in place, and suffocate due to lack of oxygen.
Choking on vomit when unconscious is another major cause of inhalant-related death. • Recklessness: Sniffing reduces inhibition and affects the way people feel about themselves and the world around them. It makes some people feel powerful, which has led to dangerous and destructive behaviour that caused serious harm. Others don’t get “high” when they sniff; they get depressed. Self-destructive or suicidal behaviour are common among people who use solvents. Most inhalants are highly flammable; recklessness with lit cigarettes and flames while using inhalants has caused tragic accidents. • Sudden sniffing death (SSD):
Prolonged sniffing of highly concentrated inhalants can cause a rapid and irregular heartbeat, leading to death from heart failure. SSD can occur after only one sniffing session, and when stress or strenuous exercise follows several deep inhalations. • Serious health problems: People who use solvents regularly for a long time can damage their liver, kidneys, lungs, heart, brain, bones and blood. Sometimes this damage heals when drug use is stopped; sometimes it is permanent. • Fetal solvent syndrome: Use of solvents during pregnancy, especially chronic use, can result in premature birth, birth defects or stillbirth. Frostbite: Nitrous oxide is extremely cold as it is released from the cylinder and can freeze skin. In addition, pressure in the tank can damage the lungs. • Nerve damage: High levels of nitrous oxide use, even with adequate oxygen, have been shown to damage nerves. This can cause numbness, weakness and loss of balance. • Unsafe sexual practices: An increased risk of contracting HIV and hepatitis is associated with nitrite use. • Weakened immune system: Recent animal research shows that nitrites may impair the immune system thereby predisposing their users to infectious diseases.
The long-term effects of inhalants vary depending on which inhalant is used. Some of the possible effects are bloodshot eyes, sores on the nose and mouth, nosebleeds, pale skin, excessive thirst and weight loss. People who use inhalants over a long term may also be confused, tired, depressed, irritable, hostile and paranoid and have trouble concentrating, remembering and thinking clearly. Heavy solvent use can result in numbness, weakness, tremors and a lack of co-ordination in the arms and legs. Some long-term effects may be reversible, but others are permanent.
When inhaled, solvents are carried by the blood and stored in fat tissue in the body. Internal organs that have high blood circulation and that are rich in fat tissue, such as the brain, liver and kidney, are particularly affected. If inhalant use is stopped, damage to the liver and kidneys may heal, but damage to the brain is almost always permanent. Studies using scans of people’s brains after chronic long-term solvent use show that solvent use can cause the brain to atrophy, or shrink, which can severely affect thinking, memory and movement control.
Inhalant use can also result in permanent hearing loss and damage to bone marrow. ADDICTION, TOLERANCE AND WITHDRAWAL STATES Most inhalant use is experimental and occasional. However, people who use inhalants regularly can develop “tolerance. ” This means that more and more of the substance are needed to produce the same effects. Regular use also leads to a persistent craving for the high, which makes it hard to stop using. When regular use is stopped, withdrawal symptoms may include nausea, loss of appetite, tremors, anxiety, depression and paranoia. STIMULANTS
Stimulants also called psychostimulants are psychoactive drugs which induce temporary improvements in either mental or physical function or both. All stimulants work by increasing dopamine levels in the brain, a chemical neurotransmitter associated with pleasure, movement, and attention. The therapeutic effect of stimulants is achieved by slow and steady increases of dopamine, which are similar to the natural production of the chemical by the brain. The doses prescribed by physicians start low and increase gradually until a therapeutic effect is reached.
However, when taken in doses and routes other than those prescribed, stimulants can increase brain dopamine in a rapid and highly amplified manner as do most other drugs of abuse disrupting normal communication between brain cells, producing euphoria, and increasing the risk of addiction. Examples of these kinds of effects may include enhanced alertness, wakefulness, and locomotion, among others. Due to their effects typically having an “up” quality to them, stimulants are also occasionally referred to as “uppers”.
Depressants or “downers”, which decrease mental and/or physical function, are in stark contrast to stimulants and are considered to be their functional opposites. Stimulants produce a wide variety of different kinds of effects by enhancing the activity of the central and peripheral nervous systems. Common effects, which vary depending on the substance in question, may include enhanced alertness, awareness, wakefulness, endurance, productivity, and motivation, increased arousal, locomotion, heart rate, and blood pressure, and the perception of a diminished requirement for food and sleep.
Many stimulants are also capable of improving mood and relieving anxiety, and some can even induce feelings of euphoria. It should be noted, however, that many of these drugs are also capable of causing anxiety, even the ones that may paradoxically reduce it to a degree at the same time. Stimulants exert their effects through a number of different pharmacological mechanisms, the most prominent of which include facilitation of norepinephrine (noradrenaline) and/or dopamine activity (e. g. , via monoamine transporter inhibition or reversal), adenosine receptor antagonism, and nicotinic acetylcholine receptor agonism.
Stimulants include: • Caffeine • Nicotine • Amphetamine • Methylenedioxymethamphetamine (MDMA)/ Ecstacy • Cocaine CAFFEINE Caffeine is a bitter, white crystalline xanthine alkaloid that is a psychoactive stimulant drug. Caffeine was discovered by a German chemist, Friedrich Ferdinand Runge, in 1819. He coined the term kaffein, a chemical compound in coffee, which in English became caffeine. Humans have consumed caffeine since the Stone Age. Early peoples found that chewing the seeds, bark, or leaves of certain plants had the effects of easing fatigue, stimulating awareness, and elevating one’s mood.
Only much later was it found that the effect of caffeine was increased by steeping such plants in hot water. Many cultures have legends that attribute the discovery of such plants to people living many thousands of years ago. Caffeine is found in varying quantities in the beans, leaves, and fruit of some plants, where it acts as a natural pesticide that paralyzes and kills certain insects feeding on the plants. It is most commonly consumed by humans in infusions extracted from the cherries of the coffee plant and the leaves of the tea bush, as well as from various foods and drinks containing products derived from the kola nut.
Other sources include yerba mate, guarana berries, and the Yaupon Holly. Global consumption of caffeine has been estimated at 120,000 tonnes per year, making it the world’s most popular psychoactive substance. This number equates to one serving of a caffeine beverage for every person, per day. Caffeine is a central nervous system and metabolic stimulant, and is used both recreationally and medically to reduce physical fatigue and restore mental alertness when unusual weakness or drowsiness occurs. Caffeine and other methylxanthine derivatives are also used on newborns to treat apnea and correct irregular heartbeats.
Caffeine stimulates the central nervous system first at the higher levels, resulting in increased alertness and wakefulness, faster and clearer flow of thought, increased focus, and better general body coordination, and later at the spinal cord level at higher doses. MECHANISM OF ACTION In humans, caffeine is a central nervous system (CNS) stimulant, having the effect of temporarily warding off drowsiness and restoring alertness. Beverages containing caffeine, such as coffee, tea, soft drinks, and energy drinks, enjoy great popularity.
Caffeine is the world’s most widely consumed psychoactive substance, but, unlike many other psychoactive substances, it is legal and unregulated in nearly all jurisdictions. Caffeine has diuretic properties, at least when administered in sufficient doses to subjects that do not have a tolerance for it. Regular users, however, develop a strong tolerance to this effect, and studies have generally failed to support the common notion that ordinary consumption of caffeinated beverages contributes significantly to dehydration.
Caffeine from coffee or other beverages is absorbed by the stomach and small intestine within 45 minutes of ingestion and then distributed throughout all tissues of the body. It is eliminated by first-order kinetics. Caffeine readily crosses the blood–brain barrier that separates the bloodstream from the interior of the brain. Once in the brain, the principal mode of action is as a nonselective antagonist of adenosine receptors. The caffeine molecule is structurally similar to adenosine, and binds to adenosine receptors on the surface of cells without activating them (an “antagonist” mechanism of action).
Therefore, caffeine acts as a competitive inhibitor. Adenosine is found in every part of the body, because it plays a role in the fundamental ATP-related energy metabolism. By counteracting adenosine, caffeine reduces resting cerebral blood flow between 22% and 30%. Caffeine also has a generally disinhibitory effect on neural activity. It has not been shown, however, how these effects cause increases in arousal and alertness. EFFECTS WHEN TAKEN IN MODERATION The precise amount of caffeine necessary to produce effects varies from person to person depending on body size and degree of tolerance to caffeine.
It takes less than an hour for caffeine to begin affecting the body and a mild dose wears off in three to four hours. Consumption of caffeine does not eliminate the need for sleep; it only temporarily reduces the sensation of being tired throughout the day. In general, 25 to 50 milligrams of caffeine is sufficient for most people to report increased alertness and arousal as well as subjectively lower levels of fatigue. With these effects, caffeine is an ergogenic, increasing a person’s capability for mental or physical labor.
A study conducted in 1979 showed a 7% increase in distance cycled over a period of two hours in subjects that consumed caffeine compared to control subjects. Other studies attained much more dramatic results; one particular study of trained runners showed a 44% increase in “race-pace” endurance, as well as a 51% increase in cycling endurance, after a dosage of 9 milligrams of caffeine per kilogram of body weight. Additional studies have reported similar effects. Another study found 5. milligrams of caffeine per kilogram of body mass resulted in subjects cycling 29% longer during high-intensity circuits. Caffeine citrate has proven to be of short and long term benefit in treating the breathing disorders of apnea of prematurity and bronchopulmonary dysplasia in premature infants. The only short-term risk associated with caffeine citrate treatment is a temporary reduction in weight gain during the therapy, and longer term studies (18 to 21 months) have shown lasting benefits of treatment of premature infants with caffeine.
Caffeine relaxes the internal anal sphincter muscles and thus should be avoided by those with fecal incontinence. TOLERANCE AND WITHDRAWAL Because caffeine is primarily an antagonist of the central nervous system’s receptors for the neurotransmitter adenosine, the bodies of individuals that regularly consume caffeine adapt to the continuous presence of the drug by substantially increasing the number of adenosine receptors in the central nervous system.
This increase in the number of the adenosine receptors makes the body much more sensitive to adenosine, with two primary consequences. First, the stimulatory effects of caffeine are substantially reduced, a phenomenon known as a tolerance adaptation. Second, because these adaptive responses to caffeine make individuals much more sensitive to adenosine, a reduction in caffeine intake will effectively increase the normal physiological effects of adenosine, resulting in unwelcome withdrawal symptoms in tolerant users.
Other research questions the idea that up-regulation of adenosine receptors is responsible for tolerance to the locomotor stimulant effects of caffeine, noting, among other things, that this tolerance is insurmountable by higher doses of caffeine (it should be surmountable if tolerance were due to an increase in receptors), and that the increase in adenosine receptor number is modest and does not explain the large tolerance that develops to caffeine. Caffeine tolerance develops very quickly, especially among heavy coffee and energy drink consumers.
Complete tolerance to sleep disruption effects of caffeine develops after consuming 400 mg of caffeine 3 times a day for 7 days. Complete tolerance to subjective effects of caffeine was observed to develop after consuming 300 mg 3 times per day for 18 days, and possibly even earlier. In another experiment, complete tolerance of caffeine was observed when the subject consumed 750–1200 mg per day while incomplete tolerance to caffeine has been observed in those that consume more average doses of caffeine.
Because adenosine, in part, serves to regulate blood pressure by causing vasodilation, the increased effects of adenosine due to caffeine withdrawal cause the blood vessels of the head to dilate, leading to an excess of blood in the head and causing a headache and nausea. Reduced catecholamine activity may cause feelings of fatigue and drowsiness. A reduction in serotonin levels when caffeine use is stopped can cause anxiety, irritability, inability to concentrate, and diminished motivation to initiate or to complete daily tasks; in extreme cases it may cause mild depression.
Together, these effects have come to be known as a “crash”. Withdrawal symptoms — possibly including headache, irritability, an inability to concentrate, drowsiness, insomnia and pain in the stomach, upper body, and joints may appear within 12 to 24 hours after discontinuation of caffeine intake, peak at roughly 48 hours, and usually last from one to five days, representing the time required for the number of adenosine receptors in the brain to revert to “normal” levels, uninfluenced by caffeine consumption. Analgesics, such as aspirin, can relieve the pain symptoms, as can a small dose of caffeine.
Most effective is a combination of both an analgesic and a small amount of caffeine. This is not the only case in which caffeine increases the effectiveness of a drug. Caffeine makes pain relievers 40% more effective in relieving headaches and helps the body absorb headache medications more quickly, bringing faster relief. For this reason, many over-the-counter headache drugs include caffeine in their formula. It is also used with ergotamine in the treatment of migraine and cluster headaches as well as to overcome the drowsiness caused by antihistamines. OVERUSE
In large amounts, and especially over extended periods of time, caffeine can lead to a condition known as caffeinism. Caffeinism usually combines caffeine dependency with a wide range of unpleasant physical and mental conditions including nervousness, irritability, anxiety, tremulousness, muscle twitching (hyperreflexia), insomnia, headaches, respiratory alkalosis, and heart palpitations. Furthermore, because caffeine increases the production of stomach acid, high usage over time can lead to peptic ulcers, erosive esophagitis and gastroesophageal reflux disease.
There are four caffeine-induced psychiatric disorders recognized by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition: caffeine intoxication, caffeine-induced anxiety disorder, caffeine-induced sleep disorder, and caffeine-related disorder not otherwise specified (NOS). Caffeine intoxication An acute overdose of caffeine, usually in excess of about 300 milligrams, dependent on body weight and level of caffeine tolerance, can result in a state of central nervous system over-stimulation called caffeine intoxication (DSM-IV 305. 90), or colloquially the “caffeine jitters”. In cases of extreme overdose, death can result.
The median lethal dose given orally, is 192 milligrams per kilogram in rats. The LD50 of caffeine in humans is dependent on weight and individual sensitivity and estimated to be about 150 to 200 milligrams per kilogram of body mass, roughly 80 to 100 cups of coffee for an average adult taken within a limited time frame that is dependent on half-life. Though achieving lethal dose with caffeine would be exceptionally difficult with regular coffee, there have been reported deaths from overdosing on caffeine pills, with serious symptoms of overdose requiring hospitalization occurring from as little as 2 grams of caffeine.
An exception to this would be taking a drug such as fluvoxamine, which blocks the liver enzyme responsible for the metabolism of caffeine, thus increasing the central effects and blood concentrations of caffeine dramatically at 5-fold. It is not contraindicated, but highly advisable to minimize the intake of caffeinated beverages, as drinking one cup of coffee will have the same effect as drinking five under normal conditions. Death typically occurs due to ventricular fibrillation brought about by effects of caffeine on the cardiovascular system.
Treatment of severe caffeine intoxication is generally supportive, providing treatment of the immediate symptoms, but if the patient has very high serum levels of caffeine then peritoneal dialysis, hemodialysis, or hemofiltration may be required. Anxiety and sleep disorders Two infrequently diagnosed caffeine-induced disorders that are recognized by the American Psychological Association (APA) are caffeine-induced sleep disorder and caffeine-induced anxiety disorder, which can result from long-term excessive caffeine intake.
In the case of caffeine-induced sleep disorder, an individual regularly ingests high doses of caffeine sufficient to induce a significant disturbance in his or her sleep, sufficiently severe to warrant clinical attention. [In some individuals, the large amounts of caffeine can induce anxiety severe enough to necessitate clinical attention. This caffeine-induced anxiety disorder can take many forms, from generalized anxiety to panic attacks, obsessive-compulsive symptoms, or even phobic symptoms.
Because this condition can mimic organic mental disorders, such as panic disorder, generalized anxiety disorder, bipolar disorder, or even schizophrenia, a number of medical professionals believe caffeine-intoxicated people are routinely misdiagnosed and unnecessarily medicated when the treatment for caffeine-induced psychosis would simply be to stop further caffeine intake. A study in the British Journal of Addiction concluded that caffeinism, although infrequently diagnosed, may afflict as many as one person in ten of the population. Co administration of theanine was shown to greatly reduce this caffeine-induced anxiety.
Effects on memory and learning Anhydrous caffeine An array of studies found that caffeine could have nootropic effects, inducing certain changes in memory and learning. Researchers have found that long-term consumption of low dose caffeine slowed hippocampus-dependent learning and impaired long-term memory in mice. Caffeine consumption for 4 weeks also significantly reduced hippocampal neurogenesis compared to controls during the experiment. The conclusion was that long-term consumption of caffeine could inhibit hippocampus-dependent learning and memory partially through inhibition of hippocampal neurogenesis.
In another study, caffeine was added to rat neurons in vitro. The dendritic spines (a part of the brain cell used in forming connections between neurons) taken from the hippocampus (a part of the brain associated with memory) grew by 33% and new spines formed. After an hour or two, however, these cells returned to their original shape Another study showed that human subjects after receiving 100 milligrams of caffeine had increased activity in brain regions located in the frontal lobe, where a part of the working memory network is located, and the anterior cingulate cortex, a part of the brain that controls attention.
The caffeinated subjects also performed better on the memory tasks. However, a different study showed that caffeine could impair short-term memory and increase the likelihood of the tip of the tongue phenomenon. The study allowed the researchers to suggest that caffeine could aid short-term memory when the information to be recalled is related to the current train of thought, but also to hypothesize that caffeine hinders short-term memory when the train of thought is unrelated.
In essence, caffeine consumption increases mental performance related to focused thought while it may decrease broad-range thinking abilities. NICOTINE Nicotine is the active chemical constituent in tobacco, of which is available in many forms, including cigarettes, cigars, and chewing tobacco, among others. Nicotine is used widely throughout the world for its stimulating effects. It is named after the tobacco plant Nicotiana tabacum which in turn is named after Jean Nicot de Villemain, French ambassador in Portugal, who sent tobacco and seeds from Brazil to Paris in 1560 and promoted their medicinal use.
Nicotine was first isolated from the tobacco plant in 1828 by German chemists Posselt & Reimann, who considered it a poison. Its chemical empirical formula was described by Melsens in 1843, its structure was discovered by Garry Pinner in 1893, and it was first synthesized by A. Pictet and Crepieux in 1904. In low concentrations (an average cigarette yields about 1 mg of absorbed nicotine), the substance acts as a stimulant in mammals and is the main factor responsible for the dependence-forming properties of tobacco smoking.
The pharmacological and behavioral characteristics that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine. As nicotine enters the body, it is distributed quickly through the bloodstream and can cross the blood-brain barrier. On average it takes about seven seconds for the substance to reach the brain when inhaled. The half life of nicotine in the body is around two hours. The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used.
For chewing tobacco, dipping tobacco, snus and snuff, which are held in the mouth between the lip and gum, or taken in the nose, the amount released into the body tends to be much greater than smoked tobacco. Nicotine is metabolized in the liver by cytochrome P450 enzymes. A major metabolite is cotinine. Other primary metabolites include nicotine N’-oxide, nornicotine, nicotine isomethonium ion, 2-hydroxynicotine and nicotine glucuronide. Gluconuration and oxidative metabolism of nicotine to cotinine are both inhibited by menthol, an additive to mentholated cigarettes, thus increasing the half-life of nicotine in vivo.
MECHANISM OF ACTION/ EFFECTS OF NICOTINE Nicotine acts on the nicotinic acetylcholine receptors, specifically the ganglion type nicotinic receptor and one CNS nicotinic receptor. The former is present in the adrenal medulla and elsewhere, while the latter is present in the central nervous system (CNS). In small concentrations, nicotine increases the activity of these receptors. Nicotine also has effects on a variety of other neurotransmitters through less direct mechanisms. IN CNS
By binding to nicotinic acetylcholine receptors, nicotine increases the levels of several neurotransmitters acting as a sort of “volume control”. It is thought that increased levels of dopamine in the reward circuits of the brain are responsible for the euphoria and relaxation and eventual addiction caused by nicotine consumption. Nicotine has a higher affinity for acetylcholine receptors in the brain than those in skeletal muscles, though at toxic doses it can induce contractions and respiratory paralysis. Nicotine’s selectivity is thought to be due to a particular amino acid difference on these receptor subtypes.
Tobacco smoke contains the monoamine oxidase inhibitors harman, norharman,anabasine, anatabine, and nornicotine. These compounds significantly decrease MAO activity in smokers. MAO enzymes break down monoaminergic neurotransmitters such as dopamine, norepinephrine, and serotonin. Chronic nicotine exposure via tobacco smoking up-regulates alpha 4beta2 nAChR in cerebellum and brainstem regions but not habenulopeduncular structures. Alpha4beta2 and alpha6beta2 receptors, present in the ventral tegmental area, play a crucial role in mediating the reinforcement effects of nicotine.
IN PNS Nicotine also activates the sympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulates the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and norepinephrine) into the bloodstream. Nicotine also has an affinity for melanin-containing tissues due to its precursor function in melanin synthesis or its irreversible binding of melanin and nicotine.
This has been suggested to underlie the increased nicotine dependence and lower smoking cessation rates in darker pigmented individuals. IN ADRENAL MEDULLA By binding to ganglion type nicotinic receptors in the adrenal medulla, nicotine increases flow of adrenaline (epinephrine), a stimulating hormone. By binding to the receptors, it causes cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and thus the release of epinephrine (and norepinephrine) into the bloodstream.
The release of epinephrine (adrenaline) causes an increase in heart rate, blood pressure and respiration, as well as higher blood glucose levels. PSYCHOACTIVE EFFECTS Nicotine’s mood-altering effects are different by report: in particular it is both a stimulant and a relaxant. First causing a release of glucose from the liver and epinephrine (adrenaline) from the adrenal medulla, it causes stimulation. Users report feelings of relaxation, sharpness, calmness, and alertness. By reducing the appetite and raising the metabolism, some smokers may lose weight as a consequence.
When a cigarette is smoked, nicotine-rich blood passes from the lungs to the brain within seven seconds and immediately stimulates the release of many chemical messengers including acetylcholine, norepinephrine, epinephrine, vasopressin, arginine, dopamine, autocrine agents, and beta-endorphin. This release of neurotransmitters and hormones is responsible for most of nicotine’s effects. Nicotine appears to enhance concentration and memory due to the increase of acetylcholine. It also appears to enhance alertness due to the increases of acetylcholine and norepinephrine.
Arousal is increased by the increase of norepinephrine. Pain is reduced by the increases of acetylcholine and beta-endorphin. Anxiety is reduced by the increase of beta-endorphin. Nicotine also extends the duration of positive effects of dopamine and increases sensitivity in brain reward systems. Most cigarettes (in the smoke inhaled) contain 1 to 3 milligrams of nicotine. Research suggests that, when smokers wish to achieve a stimulating effect, they take short quick puffs, which produce a low level of blood nicotine. This stimulates nerve transmission.
When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of nerve impulses, producing a mild sedative effect. At low doses, nicotine potently enhances the actions of norepinephrine and dopamine in the brain, causing a drug effect typical of those of psychostimulants. At higher doses, nicotine enhances the effect of serotonin and opiate activity, producing a calming, pain-killing effect. Nicotine is unique in comparison to most drugs, as its profile changes from stimulant to sedative/pain killer in increasing dosages and use similar to ethanol.
DEPENDENCE AND WITHDRAWAL STATES Technically, nicotine is not significantly addictive, as when it’s administered alone, it does not produce significant reinforcing properties. However, only after co-administration with an MAOI, such as those found in tobacco, nicotine produces significant behavioral sensitization, a measure of addiction potential. Modern research shows that nicotine acts on the brain to produce a number of effects. Specifically, its’ addictive nature has been found to show that nicotine activates reward pathways; the circuitry within the brain that regulates feelings of pleasure and euphoria.
Increasing the levels of dopamine within the reward circuits in the brain, nicotine acts as a chemical with intense addictive qualities. In many studies it has been shown to be more addictive than cocaine and heroin, though chronic treatment has an opposite effect on reward thresholds. Like other physically addictive drugs, nicotine causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. In addition, the sensitivity of nicotinic acetylcholine receptors decreases.
To compensate for this compensatory mechanism, the brain in turn up-regulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. The net effect is an increase in reward pathway sensitivity, opposite of other drugs of abuse such as cocaine and heroin, which reduce reward pathway sensitivity. This neuronal brain alteration persists for months after administration ceases. Due to an increase in reward pathway sensitivity, nicotine withdrawal is relatively mild compared to alcohol or heroin withdrawal.
Nicotine also has the potential to cause dependence in many animals other than humans. Mice have been administered nicotine and exhibit withdrawal reactions when its administration is stopped. A study found that nicotine exposure in adolescent mice retards the growth of the dopamine system, thus increasing the risk of substance abuse during adolescence. INTOXICATION STATE 0. 5-1. 0 mg/kg can be a lethal dosage for adult humans. Nicotine has a high toxicity in comparison to many other alkaloids such as cocaine.
It is impossible however to overdose on nicotine through smoking alone though a person can overdose on nicotine through a combination of nicotine patches, nicotine gum, and/or tobacco smoking at the same time. Spilling an extremely high concentration of nicotine onto the skin can result in intoxication or even death since nicotine readily passes into the bloodstream from dermal contact. The carcinogenic properties of nicotine in standalone form, separate from tobacco smoke, have not been evaluated by the IARC, and it has not been assigned to an official carcinogen group.
The currently available literature indicates that nicotine, on its own, does not promote the development of cancer in healthy tissue and has no mutagenic properties. However, nicotine and the increased cholinergic activity it causes have been shown to impede apoptosis, one of the methods by which the body destroys unwanted cells i. e. programmed cell death. Since apoptosis helps to remove mutated or damaged cells that may eventually become cancerous, the inhibitory actions of nicotine may create a more favorable environment for cancer to develop, though this also remains to be proven.
The teratogenic properties of nicotine have not yet been adequately researched, and while the likelihood of birth defects caused by nicotine is believed to be very small or nonexistent. COCAINE Cocaine (benzoylmethylecgonine) is a crystalline tropane alkaloid that is obtained from the leaves of the coca plant. The name comes from “coca” in addition to the alkaloid suffix -ine, forming cocaine. It is a stimulant of the central nervous system and an appetite suppressant.
Specifically, it is a serotonin-norepinephrine-dopamine reuptake inhibitor, which mediates functionality of such as an exogenous catecholamine transporter ligand. Because of the way it affects the mesolimbic reward pathway, cocaine is addictive. Cocaine is a powerful nervous system stimulant. Its effects can last from 15-30 minutes to an hour, depending upon the method of ingestion. It increases alertness, feelings of well-being and euphoria, energy and motor activity, feelings of competence and sexuality. Athletic performance may be enhanced.
Anxiety, paranoia and restlessness are also frequent. With excessive dosage, tremors, convulsions and increased body temperature are observed. Forms of cocaine SALTS Cocaine, like many alkaloids can form many different salts, such as hydrochloride (HCl) and sulfate (-SO4). Different salts have different solvency in solvents. Its hydrochloride, like many alkaloid hydrochloride is polar and is soluble in water. BASIC As the name implies, “freebase” is the base form of cocaine, as opposed to the salt form. It is practically insoluble in water whereas hydrochloride salt is water soluble.
Smoking freebase cocaine has the additional effect of releasing methylecgonidine into the user’s system due to the pyrolysis of the substance (a side effect which insufflating or injecting powder cocaine does not create). Some research suggests that smoking freebase cocaine can be even more cardiotoxic than other routes of administration because of methylecgonidine’s effects on lung tissue and liver tissue. Pure cocaine is prepared by neutralizing its compounding salt with an alkaline solution which will precipitate to non-polar basic cocaine.
It is further refined through aqueous-solvent Liquid-liquid extraction. CRACK COCAINE Crack is a lower purity form of free-base cocaine and contains sodium bicarbonate as impurity. Freebase and crack are often administered by smoking. The origin of the name is from the crackling sound (hence the onomatopoeic “crack”) produced when cocaine containing impurities are heated. COCA LEAF INFUSIONS Coca herbal infusion (also referred to as Coca tea) is used in coca-leaf producing countries much as any herbal medicinal infusion would elsewhere in the world.
The free and legal commercialization of dried coca leaves under the form of filtration bags to be used as “coca tea” has been actively promoted by the governments of Peru and Bolivia for many years as a drink having medicinal powers. Visitors to the city of Cuzco in Peru, and La Paz in Bolivia are greeted with the offering of coca leaf infusions (prepared in tea pots with whole coca leaves) purportedly to help the newly-arrived traveler overcome the malaise of high altitude sickness. The effects of drinking coca tea are a mild stimulation and mood lift.
It does not produce any significant numbing of the mouth nor does it give a rush like snorting cocaine. In order to prevent the demonization of this product, its promoters publicize the unproven concept that much of the effect of the ingestion of coca leaf infusion would come from the secondary alkaloids, as being not only quantitatively different from pure cocaine but also qualitatively different. It has been promoted as an adjuvant for the treatment of cocaine dependence. The cocaine metabolite benzoylecgonine can be detected in the urine of people a few hours after drinking one cup of coca leaf infusion.
ROUTES OF ADMINISTRATION ORAL A spoon containing baking soda, cocaine, and a small amount of water. Used in a “poor-man’s” crack-cocaine production. Many users rub the powder along the gum line, or onto a cigarette filter which is then smoked, which numbs the gums and teeth – hence the colloquial names of “numbies”, “gummers” or “cocoa puffs” for this type of administration. This is mostly done with the small amounts of cocaine remaining on a surface after insufflation. Another oral method is to wrap up some cocaine in rolling paper and swallow it.
This is sometimes called a “snow bomb. ” COCA LEAF Coca leaves are typically mixed with an alkaline substance (such as lime) and chewed into a wad that is retained in the mouth between gum and cheek (much in the same as chewing tobacco is chewed) and sucked of its juices. The juices are absorbed slowly by the mucous membrane of the inner cheek and by the gastrointestinal tract when swallowed. Alternatively, coca leaves can be infused in liquid and consumed like tea. Ingesting coca leaves generally is an inefficient means of administering cocaine.
Advocates of the consumption of the coca leaf state that coca leaf consumption should not be criminalized as it is not actual cocaine, and consequently it is not properly the illicit drug. Because cocaine is hydrolyzed and rendered inactive in the acidic stomach, it is not readily absorbed when ingested alone. Only when mixed with a highly alkaline substance (such as lime) can it be absorbed into the bloodstream through the stomach. The efficiency of absorption of orally administered cocaine is limited by two additional factors. First, the drug is partly catabolized by the liver.
Second, capillaries in the mouth and esophagus constrict after contact with the drug, reducing the surface area over which the drug can be absorbed. Nevertheless, cocaine metabolites can be detected in the urine of subjects that have sipped even one cup of coca leaf infusion. Therefore, this is an actual additional form of administration of cocaine, albeit an inefficient one. Orally administered cocaine takes approximately 30 minutes to enter the bloodstream. Typically, only a third of an oral dose is absorbed, although absorption has been shown to reach 60% in controlled settings.
Given the slow rate of absorption, maximum physiological and psychotropic effects are attained approximately 60 minutes after cocaine is administered by ingestion. While the onset of these effects is slow, the effects are sustained for approximately 60 minutes after their peak is attained. Contrary to popular belief, both ingestion and insufflation result in approximately the same proportion of the drug being absorbed: 30 to 60%. Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects. Snorting cocaine produces maximum physiological effects within 40 minutes nd maximum psychotropic effects within 20 minutes, however, a more realistic activation period is closer to 5 to 10 minutes, which is similar to ingestion of cocaine. Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40 – 60 minutes after the peak effects are attained. INSUFFLATION Insufflation (known colloquially as “snorting,” “sniffing,” or “blowing”) is the most common method of ingestion of recreational powdered cocaine in the Western world. The drug coats and is absorbed through the mucous membranes lining the sinuses.
When insufflating cocaine, absorption through the nasal membranes is approximately 30–60%, with higher doses leading to increased absorption efficiency. Any material not directly absorbed through the mucous membranes is collected in mucus and swallowed (this “drip” is considered pleasant by some and unpleasant by others). In a study of cocaine users, the average time taken to reach peak subjective effects was 14. 6 minutes. Any damage to the inside of the nose is because cocaine highly constricts blood vessels and therefore blood and oxygen/nutrient flow to that area is reduced.
Rolled up banknotes, hollowed-out pens, cut straws, pointed ends of keys, specialized spoons, long fingernails, and (clean) tampon applicators are often used to insufflate cocaine. Such devices are often called “tooters” by users. The cocaine typically is poured onto a flat, hard surface (such as a mirror, CD case or book) and divided into “bumps”, “lines” or “rails”, and then insufflated. As tolerance builds rapidly in the short-term (hours), many lines are often snorted to produce greater effects. INJECTION Drug injection provides the highest blood levels of drug in the shortest amount of time.
Subjective effects not commonly shared with other methods of administration include a ringing in the ears moments after injection (usually when in excess of 120 milligrams) lasting 2 to 5 minutes including tinnitus & audio distortion. This is colloquially referred to as a “bell ringer” In a study of cocaine users; the average time taken to reach peak subjective effects was 3. 1 minutes. The euphoria passes quickly. Aside from the toxic effects of cocaine, there is also danger of circulatory emboli from the insoluble substances that may be used to cut the drug.
As with all injected illicit substances, there is a risk of the user contracting blood-borne infections if sterile injecting equipment is not available or used. An injected mixture of cocaine and heroin, known as “speedball” is a particularly dangerous combination, as the converse effects of the drugs actually complement each other, but may also mask the symptoms of an overdose. It has been responsible for numerous deaths, including celebrities such as John Belushi, Chris Farley, Mitch Hedberg, River Phoenix and Layne Staley. INHALATION Inhalation or smoking is one of the several means cocaine is administered.
Cocaine is smoked by inhaling the vapor by sublimating solid cocaine by heating. In a 2000 Brookhaven National Laboratory medical department study, based on self reports of 32 abusers who participated in the study, “peak high” was found at mean of 1. 4min +/- 0. 5 minutes. Smoking freebase or crack cocaine is most often accomplished using a pipe made from a small glass tube, often taken from “Love roses,” small glass tubes with a paper rose that are promoted as romantic gifts. These are sometimes called “stems”, “horns”, “blasters” and “straight shooters”.
A small piece of clean heavy copper or occasionally stainless steel scouring pad often called a “brillo” (actual Brillo pads contain soap, and are not used), or “chore”, named for Chore Boy brand copper scouring pads, – serves as a reduction base and flow modulator in which the “rock” can be melted and boiled to vapor. Crack smokers also sometimes smoke through a soda can with small holes in the bottom. Crack is smoked by placing it at the end of the pipe; a flame held close to it produces vapor, which is then inhaled by the smoker.
The effects, felt almost immediately after smoking, are very i