Alcohol and drugs week 1
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Alcohol and drugs week 1
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- Drug Detection Times Drug Time Table Drug detection times indicate the period after you last used a drug. Drug testing can reveal its presence or resulting metabolites in your specimen. Drug detection times are affected by frequency of use, type of specimen, test method, cutoff levels , metabolism , and other factors. The time table below was designed to help you understand the variety of drugs, their common names, medical usage, and the period of time they may be detected in the body. It includes commonly-abused drugs, such as marijuana, cocaine, hash, methamphetamine and other amphetamines. The detection periods refer to Urine, Blood and Saliva specimens. All substances will remain in the hair follicle until the specified period of usage is cut off. Most hair tests will test for a period of 90 to 120 days depending on growth. The urinalysis test is the most commonly-used drug testing method in today. Stimulants Amphetamine Biphetamine, Dexedrine; Black Beauties, White Crosses Attention deficit hyperactivity disorder (ADHD), obesity, narcolepsy 2-5 days Cocaine Coke, Crack, Snow Local anesthetic, vasoconstrictor 2-5 days Methamphetamine Desoxyn; Crank, Crystal, Glass, Ice, Speed ADHD, obesity, narcolepsy 3-5 days Methylphenidate Ritalin ADHD, narcolepsy 1-2 days Nicotine Habitrol patch, Nicorette gum, Nicotrol spray, Prostep patch; Cigars, Cigarettes, Smokeless tobacco, Snuff, Spit tobacco Treatment for nicotine dependence 4-10 days Hallucinogens and Other Compounds LSD Acid, Microdot None 7-10 days Mescaline Buttons, Cactus, Mesc, Peyote None 5-7 days Phencyclidine & Analogs PCP; Angel Dust, Boat, Hog, Love Boat Anesthetic (veterinary) 2-8 days Psilocybin Magic Mushroom, Purple Passion, Shrooms None 5-7 days Amphetamine variants DOB, DOM, MDA, MDMA; Adam, Ecstasy, STP, XTC None 5-7 days Marijuana Blunt, Grass, Herb, Pot, Reefer, Chronic, Smoke, Weed Limited, Analgesic Hashish Hash Limited, Analgesic Tetrahydrocannabinol Marinol, THC Antiemetic Anabolic Steroids Testosterone (T/E ratio), Stanazolol, Nandrolone Hormone Replacement Therapy Oral: up to 3 weeks (for testosterone and others); Injected: up to 3 months (Nandrolone up to 9 months) Opiates and Morphine Derivatives Codeine Tylenol w/codeine, Robitussin A-C, Empirin w/codeine, Fiorinal w/codeine Analgesic, antitussive 5-7 days Heroin Diacetylmorphine; Horse, Smack None 5-7 days Methadone Amidone, Dolophine, Methadose Analgesic, treatment for opiate dependence 5-7 days Morphine Roxanol, Duramorph Analgesic 5-7 days Opium Laudanum, Paregoric; Dover's Powder Analgesic, antidiarrheal 5-7 days Depressants Alcohol Beer, Wine, Liquor Antidote for methanol poisoning 24-48 hours Barbiturates Amytal, Nembutal, Seconal, Phenobarbital; Barbs Anesthetic, anticonvulsant, hypnotic, sedative 2 days - 4 weeks Benzodiazepines Ativan, Halcion, Librium, Rohypnol, Valium; Roofies, Tranks, Xanax Antianxiety, anticonvulsant, hypnotic, sedative 7-10 days Methaqualone Quaalude, Ludes None 2 weeks Marijuana Detection Time Based on Usage Usage at 1 time only 5-8 days Usage at 2-4 times per month 11-18 days Usage at 2-4 times week 23-35 days Usage at 5-6 times per week 33-48 days Daily Usage 49-63 days
- Absorption: methods include through the mouth, skin and nose. This method is quick for administering drugs but can lead to irritation of skin or membranes. Drugs include cocaine, amphetamine, methamphetamine, nicotine, snuff, cocoa leaves. Oral: ingestion by swallowing or consuming in eating or drinking. This method has a slow absorption time which means there is a possibility of rejecting poisons and overdoses. Disadvantages include the slow absorption time which leads to no immediate effect. Examples include medications in pill form, marijuana baked in food, amphetamine, methamphetamine, barbiturates, LSD, PCP, opium, methadone, codeine, caffeine, and alcohol. Inhalation: ingestion by burning a drug and breathing smoke-borne particles into the lungs. Very fast absorption time; disadvantages include the effect of the drug being limited to the time during which the drug is being inhaled, risk of emphysema, asthma and lung cancer, and lung and throat irritation over chronic use. Examples include nicotine, marijuana, hashish, methamphetamine, ice, free-base cocaine, crack, PCP, heroine and opium. Injection: using a syringe to inject drugs intravenously (in a vein), intramuscularly (in a large muscle) or subcutaneously (just under the skin). Intravenous injection has an extremely fast absorption time and leads to immediate effects but it cannot be undone and there is a risk of allergic reaction. PCP, methamphetamine, heroin, methadone and morphine are intravenous drugs. Intramuscular injection is quicker than intravenous injection but it has a slower absorption rate than intravenous and there is a risk of piercing a vein by accident. Vaccine inoculations are given this way. Subcutaneous injection is the easiest of all injection techniques but it has a slower absorption time and there is a risk of skin irritation and deterioration. Heroin and other narcotics are injected this way.
- Drugs exit the body most commonly through excretion in the urine after a series of actions in the liver and kidneys. Elimination also occurs through excretion in exhaled breath, feces, sweat, saliva, or breast milk. Drugs are excreted from the body at different rates.
- Excerpt from http://www.stopaddiction.com/narconon_alcohol_metabolism.html Metabolism is the body's process of converting ingested substances (anything we eat or drink) to other compounds. Metabolism results in some substances becoming more toxic, and some less toxic, than those originally ingested. Metabolism involves a number of processes, one of which is referred to as oxidation (combining with oxygen). Through oxidation, alcohol is detoxified and removed from the blood, preventing the alcohol from accumulating and destroying cells and organs. A minute amount of alcohol escapes metabolism and is excreted unchanged in the breath and in urine. Until all the alcohol consumed has been metabolized, it is distributed throughout the body, affecting the brain and other tissues. By understanding alcohol metabolism, we can learn how the body can dispose of alcohol, and discern some of the factors that influence this process. Studying alcohol metabolism also can help us to understand how this process influences the metabolism of food, hormones, and medications (drugs). Blood Alcohol Concentration (BAC) 100 mg% is the "legal" level (BAC) of intoxication in most States. 50 mg% is the level at which deterioration of driving skills begins. (JAMA 255:522-527, 1986.) If the same number of drinks are consumed over a longer period of time, a peron's BAC will be lower. The Metabolic Process When alcohol is consumed, it passes from the stomach and intestines into the blood, a process referred to as absorption. Alcohol is then metabolized by enzymes, which are body chemicals that break down other chemicals. In the liver, an enzyme called alcohol dehydrogenase (ADH) mediates the conversion of alcohol to acetaldehyde. Acetaldehyde is rapidly converted to acetate by other enzymes and is eventually metabolized to carbon dioxide and water. Alcohol also is metabolized in the liver by the enzyme cytochrome P450IIE1 (CYP2E1), which may be increased after chronic drinking. Most of the alcohol consumed is metabolized in the liver, but the small quantity that remains unmetabolized permits alcohol concentration to be measured in breath and urine. The liver can metabolize only a certain amount of alcohol per hour, regardless of the amount that has been consumed. The rate of alcohol metabolism depends, in part, on the amount of metabolizing enzymes in the liver, which varies among individuals and appears to have genetic determinants. In general, after the consumption of one standard drink, the amount of alcohol in the drinker's blood (blood alcohol concentration, or BAC) peaks within 30 to 45 minutes. (A standard drink is defined as 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80-proof distilled spirits, all of which contain the same amount of alcohol.) Alcohol is metabolized more slowly than it is absorbed. Since the metabolism of alcohol is slow, consumption needs to be controlled to prevent accumulation in the body and intoxication. Factors Influencing Alcohol Absorption and Metabolism Food. A number of factors influence the absorption process, including the presence of food and the type of food in the gastrointestinal tract when alcohol is consumed. The rate at which alcohol is absorbed depends on how quickly the stomach empties its contents into the intestine. The higher the dietary fat content, the more time this emptying will require and the longer the process of absorption will take. One study found that subjects who drank alcohol after a meal that included fat, protein, and carbohydrates absorbed the alcohol about three times more slowly than when they consumed alcohol on an empty stomach. Gender. Women absorb and metabolize alcohol differently from men. They have higher BAC's after consuming the same amount of alcohol as men and are more susceptible to alcoholic liver disease, heart muscle damage, and brain damage. The difference in BAC's between women and men has been attributed to women's smaller amount of body water, likened to dropping the same amount of alcohol into a smaller pail of water. An additional factor contributing to the difference in BAC's may be that women have lower activity of the alcohol metabolizing enzyme ADH in the stomach, causing a larger proportion of the ingested alcohol to reach the blood. The combination of these factors may render women more vulnerable than men to alcohol-induced liver and heart damage. Body Weight. Although alcohol has a relatively high caloric value, 7.1 Calories per gram (as a point of reference, 1 gram of carbohydrate contains 4.5 Calories, and 1 gram of fat contains 9 Calories), alcohol consumption does not necessarily result in increased body weight. An analysis of data collected from the first National Health and Nutrition Examination Survey (NHANES I) found that although drinkers had significantly higher intakes of total calories than nondrinkers, drinkers were not more obese than nondrinkers. In fact, women drinkers had significantly lower body weight than nondrinkers. As alcohol intake among men increased, their body weight decreased. An analysis of data from the second National Health and Nutrition Examination Survey (NHANES II) and other large national studies found similar results for women, although the relationship between drinking and body weight for men is inconsistent. Although moderate doses of alcohol added to the diets of lean men and women do not seem to lead to weight gain, some studies have reported weight gain when alcohol is added to the diets of overweight persons. When chronic heavy drinkers substitute alcohol for carbohydrates in their diets, they lose weight and weigh less than their nondrinking counterparts. Furthermore, when chronic heavy drinkers add alcohol to an otherwise normal diet, they do not gain weight. Sex Hormones. Alcohol metabolism alters the balance of reproductive hormones in men and women. In men, alcohol metabolism contributes to testicular injury and impairs testosterone synthesis and sperm production. In a study of normal healthy men who received 220 grams of alcohol daily for 4 weeks, testosterone levels declined after only 5 days and continued to fall throughout the study period. Prolonged testosterone deficiency may contribute to feminization in males, for example, breast enlargement. In addition, alcohol may interfere with normal sperm structure and movement by inhibiting the metabolism of vitamin A, which is essential for sperm development. In women, alcohol metabolism may contribute to increased production of a form of estrogen called estradiol (which contributes to increased bone density and reduced risk of coronary artery disease) and to decreased estradiol metabolism, resulting in elevated estradiol levels. One research review indicates that estradiol levels increased in premenopausal women who consumed slightly more than enough alcohol to reach the legal limit of alcohol (BAC of 0.10 percent) acutely. A study of the effect of alcohol on estradiol levels in postmenopausal women found that in women wearing estradiol skin patches, acute alcohol consumption significantly elevated estradiol levels over the short term.
- Acetylcholine: there are two types of receptor sites that are sensitive to acetylcholine: muscarinic receptors and nicotinic receptors. Active in the parasympathetic autonomic nervous system, cerebral cortex, and peripheral somatic nerves. Deficiencies in acetylcholine have been tied to Alzheimer’s disease. Norepinephrine: the principal neurotransmitter for sympathetic autonomic activation. Helps regulate our mood states. Dopamine: affects motor control, emotionality, and produces the drug-craving feelings that encourage compulsive drug taking behavior. Endorphins: endogenous substance with effects similar to narcotic analgesics. Endorphins mimic the effects of morphine and other opiate drugs. GABA (Gamma aminobutyric acid): inhibitory neurotransmitter in the brain. Anti-anxiety drugs tend to facilitate the activity of GABA in the brain. Serotonin: related to emotionality and sleep patterns.
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- The following is the text version of the article listed above. Psychoactive Drugs and Athletic Performance Thomas L. Schwenk, MD THE PHYSICIAN AND SPORTSMEDICINE - VOL 25 - NO. 1 - JANUARY 97 In Brief: Some psychoactive drugs have actual performance-enhancing side effects. However, many actually decrease performance, primarily because of adverse cardiovascular effects and impaired judgment. Athletes and nonathletes alike may be knowingly or unknowingly exposed to psychoactive substances if they use over-the-counter, recreational, or prescription drugs. P sychoactive drug use by athletes is extraordinarily common, in particular high utilization of smokeless tobacco; alcohol, including binge drinking; and marijuana. At least one study (3) showed that the use of alcohol by athletes was greater than that by sedentary college students. Table 1. Prevalence of Psychoactive Drug Use Among 1,117 Male High School Athletes in the Chicago Area Drug Percent Using Beer 67.6 OTC drugs 56.7 Wine/whiskey 54.5 Oral smokeless tobacco 32 Cigarettes 27.9 Caffeine 27.1 Marijuana 18.5 Narcotics 9.9 Hallucinogens 9.2 Inhalants 4.9 Amphetamines 3.8 Cocaine 2.4 Anabolic steroids 2.2 Adapted from Forman et al (1). Over-the-Counter Drugs Alpha-adrenergic agents. These drugs are constituents of many over-the-counter medications, some of which are used for weight loss (phenylpropanolamine hydrochloride) and to treat asthma and upper respiratory infections (ephedrine/pseudoephedrine, phenylephrine, and epinephrine). Their primary effect is autonomic cardiac stimulation as well as an amphetamine-like central nervous system (CNS) stimulation. Possible side effects at commonly used dosages include tachycardia, headache, dizziness, hypertension, anorexia (hence their use by athletes in appearance sports), irritability, anxiety, mania, and, at high doses, psychosis. Although touted to assist in increasing endurance and reaction time, research (4,5) has demonstrated no effect of these drugs on strength, endurance, reaction time, anaerobic capacity, or recovery time after prolonged exercise. All systemic use has been banned by the IOC, but topical use is permitted (eg, oxymetazoline hydrochloride and phenylephrine nasal spray). Caffeine. This substance has been used as stimulant since the Stone Age. The average consumption in the United States is 206 mg per day; 10% of the adult population consumes more than 1,000 mg per day (7). A dose of 80 to 200 mg leads to increased alertness, shortened reaction time, and improved concentration, but the response varies greatly among individuals. At doses over 250 mg (2 to 3 cups of coffee), the nonhabitual user usually experiences a headache and nervousness. For habitual users, abstinence for as little as 24 hours leads to a withdrawal syndrome of headache, irritability, insomnia, and depression. The physiologic effects of caffeine include diuresis (waterloss), gastric acid release, smooth muscle relaxation, increased contractility of skeletal muscle, increased lipolysis, and increased heart rate, blood pressure, oxygen consumption, and metabolic rate. Moderate exercise leads to increased peak plasma concentrations, which explains the experience of many recreational runners who find an additional stimulant effect from the usual consumption of coffee following a morning run. Urinary clearance of caffeine is slowed by oral contraceptives and alcohol. The effect of caffeine on short-duration, high-intensity performance is negligible at levels under the IOC limit. Caffeine has been shown to increase exercise time during graded incremental performance, but the practical significance of this finding is unclear because of the high dosages used (9). However, during prolonged endurance exercise, the benefits of caffeine are more clear. Studies (7,9) have shown a 7% increase in work output and a 19% increase in exercise time with caffeine use; the proposed explanation is that caffeine enhances lipolysis and free fatty acid release, which would spare muscle glycogen use. Another suggested explanation for caffeine's enhancement of endurance exercise is CNS stimulation. The only consistent benefit of caffeine is in submaximal, prolonged endurance exercise, but there is controversy as to whether this benefit is realized at the concentrations allowed by the IOC (maximum urinary concentration of 12 micrograms/mL, equal to 8 cups of coffee in 2 to 3 hours) and the NCAA (maximum urinary concentration of 15 micrograms/mL) (6). Some athletes have approached or exceeded the IOC threshold despite seemingly minimal caffeine intake, and athletes should be advised of this possibility. Caffeine is the only substance for which the IOC has set a urinary threshold. Remember: Urinary clearance of caffeine is slowed by oral contraceptives and alcohol. Nicotine. Exposure to nicotine occurs with both cigarette smoking and smokeless tobacco use. The toxicity of tobacco smoke, with its approximately 4,000 chemical constituents, is well known. A fact that can be useful in educating athletes about the hazards of tobacco smoke is that carbon monoxide is a prominent ingredient might cause mild lethargy (10). Smokeless tobacco is used by 20% to 60% of male college athletes (use varies among sports and is highest in baseball) and 5% to 10% of female college athletes (highest in softball) (1,2). The CNS stimulation and skeletal muscle relaxation produced by nicotine cause athletes to underestimate muscle tension related to athletic performance but do not decrease the rating of perceived exertion (7). Reaction time is not affected. Vasoconstriction leads to an increased heart rate and blood pressure and a decreased stroke volume (by as much as 30% to 40%) (7,8). Nicotine yields no proved benefit in any athletic endeavor, and hence it is not banned by the IOC or NCAA. However, the NCAA has mounted an intense antitobacco campaign and has set regulations regarding use during competition. Melatonin. This substance is marketed as a "natural" sleep agent and is available in dosages of 1 to 3 mg. At this level, its purported benefits are shortened sleep onset and decreased time to stage 2 sleep without a "hangover" the next morning. Anecdotal reports suggest widespread use by athletes, especially when traveling, but controlled studies of its effects are sparse (11). Recreational Drugs Alcohol. Alcohol produces euphoria followed by depression (8). Alcohol has long been used as a prerace stimulant (sometimes laced with strychnine), and its prominence in sports promotion and marketing is obvious. College athletes express more negative attitudes about alcohol use than nonathletes do, but this may reflect only socially acceptable responses on questionnaires, since they show the same drinking behaviors, particularly binge drinking, as nonathletes (13). Limited evidence suggests increased isometric muscle strength at low doses of alcohol because of CNS disinhibition of neuromuscular impulses. Other significant effects include impaired gluconeogenesis, lowered resting muscle glycogen levels, poor temperature regulation, diuresis, and direct cardiotoxicity, all of which impair athletic performance . For unclear reasons, alcohol produces an increase in VO2 at submaximal exercise intensity but has no effect on VO2 max, resulting in decreased exercise time to exhaustion and decreased performance in middle-distance running events (7,14). Athletes engaged in activities that require precise fine motor control, will experience decreased hand-eye coordination and impaired judgment and tracking; this results in a less smooth release in archery, increased reaction time, and confusion. Marijuana. Tetrahydrocannabinol (THC), the active ingredient, causes sedation and euphoria at low doses and hallucinations and psychosis at high doses. Its effects on athletic performance are increased reaction time, decreased fine-motor coordination, and increased heart rate. These effects, along with the vasodilating effect, cause an athlete to reach maximal heart rate at a lower than normal intensity of exercise, resulting in a decreased maximal work capacity. Chronic marijuana use has been associated with decreased motivation to perform and to give a maximal effort as well as with decreased circulating testosterone levels (8) Cocaine. Cocaine is more addictive than amphetamine, and withdrawal produces fatigue, lack of motivation, and depression. Cocaine is notable for distorting the user's perception of reality; for example, an athlete may perceive increased performance and decreased fatigue in the face of actual decreased performance in both strength and endurance activities. Cocaine produces a negative effect on glycogenolysis, which affects athletic performance. Its more important adverse effects include paranoid psychosis, seizures, hypertension-related CNS bleeding in the presence of vascular malformations, coronary artery vasoconstriction and myocardial toxicity leading to arrhythmias and ischemia, and sudden death (14,15). Cocaine use, including its use as a local anesthetic, is banned by both the NCAA and the IOC. Methylenedioxymethamphetamine (ecstasy, MDMA, XTC). Whether it offers any benefits as a stimulant in sports is unknown. Recreational use may be revealed by amphetamine drug testing. Prescription Drugs Anabolic steroids. The metabolic and hormonal effects of anabolic steroids will not be addressed here, but there are significant psychological effects that deserve brief mention. While lacking controlled studies, the literature is full of case reports and case series describing depression, suicidal ideation, psychosis, delirium, mania, aggression, and homicidal behavior as a consequence of anabolic steroid use. Benzodiazepines. (Valium, Xanax) BZDs are often used to relax muscles following an injury, such as a lumbosacral strain, but there is no evidence that they have an effect on specific muscles, only a CNS-mediated relaxation effect. BZDs alter sleep by increasing total time asleep, reducing sleep latency, and decreasing total time in rapid-eye-movement (REM) sleep; however, the number of REM cycles is increased, resulting in more dreams. Conversely, BZD withdrawal often results in nightmares or bizarre dreams. The half-life of all BZDs and their metabolites is 6 to 20 hours or more. BZDs are sometimes used by athletes as a sleep aid, particularly during travel to competitions to prevent jet lag, but the predictable morning-after hangover results in a prolonged reaction time and dulled senses (4). Their use is banned by some sports federations and by the US Olympic Committee (USOC), although not specifically by the IOC. Their use is absolutely contraindicated for underwater divers. Gamma-aminobutyric acid (GABA). This substance is widely available in natural food and health catalogs and is rumored to be used for its anxiolytic effect, but little more is known because of inadequate testing methods. Narcotics. Narcotics are used primarily to relieve pain and to enable an athlete to compete despite painful injuries. They have no helpful effect on exercise tolerance or VO2 max. Narcotics that are banned, including morphine and meperidine, are banned because they impair judgment and hence the ability to perceive dangerous situations (14,15). Codeine, dihydrocodeine bitartrate, and dextromethorphan hydrobromide are not currently banned by the USOC (codeine was a banned substance until 1994) (6). Narcotic analgesics (other than heroin) are not banned by the NCAA, but since one of the metabolites of codeine is morphine, a positive drug test is possible. The recent highly publicized treatment of pro football quarterback Brett Favre for hydrocodone addiction and reports of the ready availability of unlimited quantities of addictive narcotics in team locker rooms and training facilities suggest the extent to which these drugs have become a part of athletic culture. Beta-adrenergic agents. Clenbuterol is the most notorious of the beta-adrenergic agents, which have been found to have anabolic properties. Several studies of laboratory animals and livestock have demonstrated marked increases (13% to 65%) in muscle mass with clenbuterol as well as with several other long-acting beta-agonists (7). These anabolic effects are not mediated through testosterone, growth hormone, or insulin. Beta-adrenergic agents are illicitly used to maintain anabolic effects after steroid use is discontinued; their potency is approximately 25% of that of anabolic steroids. They also enhance lipid metabolism, increase lipolysis, decrease fat deposition, and increase lean body mass and the lean-to-fat ratio. Clenbuterol has the longest half-life of all the commonly available beta-agonists (35 hours, compared with 5 hours for albuterol sulfate) and is considered to be the most potent by athletes (7). A long half-life may be necessary to produce an anabolic effect, but human studies have shown a 14% to 18% increase in hamstring and quadriceps muscle strength at oral albuterol dosages of 8 mg twice a day (a dose at which most humans have significant side effects). Side effects of clenbuterol are the expected ones for a beta-agonist: tachycardia, palpitations, muscle tension, headache, and dizziness. These drugs are most commonly used therapeutically in inhaled form to treat asthma. Approximately 10% to 15% of athletes at most levels of competition have exercise-induced bronchospasm, and an additional few have more severe inflammatory forms of asthma. The use of all beta-adrenergic agents in inhaled form was permitted by the IOC until 1992, when the anabolic properties of these drugs were quantified. At that time, all long-acting inhaled and oral forms, including clenbuterol (available only in Europe and for veterinary use), were banned by the IOC and were classified as "stimulants" and "other anabolic agents." Inhaled albuterol and terbutaline sulfate are permitted by the IOC after approval subject to verified medical indication. Use of salmeterol in inhaled form also is now permitted by the IOC, since studies have demonstrated a negligible anabolic effect (6,17). Beta-adrenergic antagonists (beta-blockers). Beta-blockers are commonly used to treat hypertension, angina, arrhythmias, migraine headache, and anxiety and are frequently given after myocardial infarction. Their propensity to cross the blood-brain barrier also contributes to CNS-mediated side effects such as nightmares, depression, insomnia, and fatigue (8). Beta-blockers have no effect on strength or power, but they reduce available energy by decreasing insulin release, glycogenolysis, and lipolysis. Their inotropic and chronotropic effects, ie, decreased heart rate, stroke volume, cardiac output, and VO2 max, are undesirable for endurance athletes. Beta-blockers are commonly used to reduce performance anxiety in musicians, teachers, and business executives, although reports are mostly anecdotal, with a recommendation for a short-acting, low-dose preparation, such as propranolol hydrochloride 10 to 20 mg. In a double-blind, controlled crossover comparison of 40 mg nadolol (a beta-blocker) and 2 mg diazepam (anit-anxiety medicaiton), the measured psychological anxiety was the same with both medications, but technical performance was better with nadolol due to an attenuation of the expected increase in heart rate and tremor. Diazepam resulted in a deterioration of performance (18). Methylphenidate hydrochloride and related amphetamines. Methylphenidate hydrochloride is one of several structurally related amphetamines; its increased use in the treatment of patients who have attention deficit hyperactivity disorder (ADHD) has made it the amphetamine that most physicians encounter most often. Amphetamine use has been shown to increase the speed of learning new tasks and to increase physical energy, confidence, and ambition on a short-term basis. Amphetamines are highly addictive, particularly when absorbed through mucosal surfaces. Students are known to use sublingual absorption to enhance the stimulant effect of methylphenidate. Amphetamines are not known to enhance athletic performance, but enhanced confidence and aggression (possibly on a placebo basis) may lead to a 1% to 2% increase in short-term power activities. At elite levels of competition, such an improvement may be significant. Athletes who use amphetamines may be able to tolerate a longer period of anaerobic metabolism, although credible data on this effect are not available. Of greatest importance are the serious, and sometimes fatal, side effects of amphetamine use, such as heatstroke due to shunting of blood away from the skin. A more common problem is impaired judgment, which may cause the athlete to participate while injured, possibly leading to worse injuries and putting others at risk. Amphetamines are banned by both the IOC and the NCAA, although the NCAA does permit the use of methylphenidate for ADHD if this need is documented. The practical implementation of this exception has yet to be fully assessed because of the imprecision of ADHD diagnosis and the theoretical possibility that methylphenidate prescribed for legitimate purposes may be used inappropriately. Tricyclic antidepressants (TCAs). Imipramine, the first TCA, was developed for the treatment of psychotic agitation (8). All TCAs inhibit the neuronal uptake of norepinephrine and serotonin to various degrees. These drugs are most effective in the treatment of severe, melancholic, major depressive disorder, particularly with psychomotor agitation (because of its neuroleptic origins) and postpsychotic depression. They are also effective for obsessive-compulsive disorder (eg, clomipramine hydrochloride), panic disorder, generalized anxiety disorder, and posttraumatic stress disorder. Most TCAs (particularly amitriptyline hydrochloride) produce numerous side effects relating to multiple receptor systems; each drug in the class causes various degrees of antihistaminic, antimuscarinic, alpha-adrenergic-antagonistic, and anticholinergic effects. Tricyclic antidepressants reduce cardiac capacity and increase the risk of arrhythmias as a result of quinidine-like effects, such as QT prolongation. Some studies have demonstrated increased running or swimming time to exhaustion in rats given imipramine hydrochloride or desipramine hydrochloride. The side effects of TCAs, particularly cardiac conduction abnormalities, preclude their use by athletes with clinical depression. These drugs are banned by the IOC only for athletes in shooting events (including the modern pentathlon and biathlon) because of their anxiolytic effects. Fenfluramine hydrochloride. This is a serotonergic agent recently approved for the long-term treatment of obesity. It is chemically related to amphetamines but has a minimal stimulant effect and a low potential for abuse. This drug appeals to athletes such as gymnasts, wrestlers, and rowers because of its anorexigenic effect. Fenfluramine is not currently banned by any athletic organization or federation. Selective serotonin reuptake inhibitors (SSRIs). An SSRI is the first-line medication used to treat most patients with depression in the United States. Fluoxetine hydrochloride, with over $2 billion in annual sales, is the most frequently prescribed antidepressant (19). This class of psychiatric drug was the first designed with specific predetermined criteria in mind. SSRIs have a nearly exclusive effect on neuronal uptake of serotonin and minimal to no effect on the receptor systems affected by TCAs. SSRIs produce numerous but relatively minor side effects, including nausea, headache, diarrhea, dyspepsia, agitation, and tremulousness. Sexual dysfunction is the most troublesome side effect for many patients. The relative lack of serious side effects makes an SSRI a better choice than a TCA for the treatment of clinical depression in athletes. These drugs can produce ergogenic effects, including prolonged running time to exhaustion, decreased central fatigue, and enhanced motivation and self-esteem, which may improve training and performance (20,21) These drugs are banned by the IOC for shooting sports (including modern pentathlon and biathlon) because of their anxiolytic effects. Clinical Implications Psychoactive drug use among young athletes often results from these drugs' perceived, and sometimes actual, enhancement of performance. The use of many psychoactive drugs is regulated or banned by national and international sports federations, which does provide a deterrent effect. Primary care physicians must be mindful of both deliberate and unintentional psychoactive drug use among their young athletic patients and the potential for serious or life-threatening complications related to this use. References Forman ES, Dekker AH, Javors JR, et al: High-risk behaviors in teenage male athletes. 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Am J Addiction 1992;1: 100-114 Brukner P: Drugs in Sport. Canberra, Australia, Sports Medicine Australia, 1995 James I, Savage I: Beneficial effect of nadolol on anxiety-induced disturbances of performance in musicians: a comparison with diazepam and placebo. Am Heart J 1984;108(4 pt 2):1150-1155 Olfson M, Klerman GL: Trends in prescription of antidepressants by office-based psychiatrists. Am J Psychiatry 1993;150(4):571-577 Bailey SP, Davis JM, Ahlborn EN: Effect of increased brain serotonergic activity on endurance performance in the rat. Acta Physiol Scand 1992;145(1):75-76 Kramer PD: Listening to Prozac. New York City, Viking, 1993 Dr Schwenk is professor and chair in the Department of Family Practice at the University of Michigan Medical School in Ann Arbor. He is a fellow of the American College of Sports Medicine. Address correspondence to Thomas L. Schwenk, MD, Department of Family Practice, University of Michigan Medical Center, 1018 Fuller St, Ann Arbor, MI 48109.
- In 1970 the Comprehensive Drug Abuse Prevention and Control Act was passed into law. Title II of this law, the Controlled Substances Act, is the legal foundation of narcotics enforcement in the United States. The Controlled Substance Act regulates the manufacture and distribution of drugs, and places all drugs into one of five schedules. SCHEDULE I A: Drug has no current accepted medical use. B: Drug has a high potential for abuse. Class examples: Heroin, Methaqualone, LSD, Peyote, Psilocybin, Marijuana, Hashish, Hash Oil , and various amphetamine variants. SCHEDULE II A: Drug has current accepted medical use. B: Drug has high potential for abuse. Class examples: Dilaudid, Demerol, Methadone, Cocaine, PCP, Morphine and certain cannibis, amphetamine, and barbiturates types . SCHEDULE III A: Drug has current accepted medical use. B: Drug has medium potential for abuse. Class examples: Opium, Vicodan, Tylenol w/codeine and other narcotic, amphetamine, and barbiturate types. SCHEDULE IV A: Drug has current accepted medical use. B: Drug has low potential for abuse. Class Examples: Darvocet, Xanax, Valium, Halcyon, Ambien, Ativan, and other barbiturate types. SCHEDULE V A: Drug has accepted medical use. B: Drug has lowest potential for abuse. Class examples: Lomotil, Phenergan, and liquid suspensions. http://www.addictions.org/schedules.html