The intent of this website is to provide general health resources and information. It is not intended to provide medical advice on personal health matters, which should be obtained directly from a healthcare provider. The material/references are offered solely in an educational context and are therefore designed to support, not replace, any relationship that may exist between a patient/site visitor and his/her existing physician. Please consult your doctor before starting, changing or discontinuing any medical treatment.
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The intent of this publication is to provide general health resources and information. It is not intended to provide medical advice on personal health matters, which should be obtained directly from a healthcare provider. The material/references are offered solely in an educational context and are therefore designed to support, not replace, any relationship that may exist between a patient/site visitor and his/her existing physician. Please consult your doctor before starting, changing or discontinuing any medical treatment.
Brecher, E. Licit and Illicit Drugs. Consumers Union.
This book was published in the seventies by the same people that produce the magazine Consumer Reports. It attempted to cut through the propaganda and hysteria of the time and present consumers with a factual report on drugs and their use/abuse. Many of the finest experts of the time (and now) contributed to this book (and then they proceeded to catch hell for not hewing to Richard Nixon's hard-line War on Drugs message). The book is out of print now, but you can still find a used copy now and then on Amazon.com.
Brizer D, Castaneda R. Addiction and Recovery for Beginners. Writers and Readers Publishing.
This is a humorous and inexpensive comic book that covers all the important points of drug effects, addiction and treatment. Perhaps it was intended for young adults, but I found it an exceptionally accurate, comprehensive and very enjoyable book. It takes an hour to read and leaves the reader with a fine start on addiction knowledge.
Inaba, D, Cohen, W. Uppers, Downers, and All Arounders. CNS Publications.
An excellent pictorial textbook at the high school or college level about the history and pharmacology relating to drug use and addiction. Written by the CEO of the Haight-Ashbury Free Clinics.
Kuhn C, Swartzwelder S, Wilson W. Buzzed. Norton.
This is the most intellectually honest book I’ve ever read on the topic of drugs. The authors of this book are all pharmacists, and they present refreshingly balanced information about each class of drugs, their effects and consequences. If brave enough to use it, this is a very good text for high school and college teachers looking to go beyond the “Just Say No’ platitudes regarding drugs and their effects.
Liska K. Drugs and the Human Body. Prentice Hall.
This is a small and inexpensive college textbook of interesting and accurate information on drug effects, drug addiction, and how these have influenced the history and sociology surrounding drugs. A very good survey text about addiction.
Ruden RA. The Craving Brain. Harper Collins.
Probably the easiest book to read that describes addiction’s impact on midbrain survival systems. Dr. Ruden’s chapters on his “Biobalance Approach” are less useful, but the first part of the book is worth its price.
Schuckit M. Educating Yourself About Alcohol and Drugs. Perseus Books.
This is one of the best books containing information on classes of drugs, mechanisms of drug abuse and addiction, and theories on addiction’s origins. Dr. Schuckit is the world's expert on the genetic mechanisms of addiction.
Weil A, Rosen W. From Chocolate to Morphine. Houghton Mifflin.
This is an exceptionally enlightened and balanced survey text about drugs and their effects. Dr. Andrew Weil, a physician famous for combining holistic approaches and nutrition, is an intelligent guide through the morass of ideology surrounding drug use.
Graham AW, Schultz TK, Wilford BB. Principles of Addiction Medicine. American Society of Addiction Medicine.
A large and expensive textbook best found at a medical school library. This book reflects more the philosophic orientation of the American Society of Addiction Medicine, a philosophy that leans heavily in favor of twelve-step programs. Still, it is an excellent sourcebook – second only to the Lowinson text – and has very good sections on pain relief in recovery.
Karch SB (Ed.). Drug Abuse Handbook. CRC Press.
An excellent reference text for a huge variety of information about drugs and drug abuse written from a forensic pathology/toxicology perspective
Lowinson J. ed. Substance Abuse: A Comprehensive Textbook. Williams and Wilkins.
This is one of the two main medical textbooks on addiction medicine (the other being the ASAM text). True to its title, it covers a wide range of topics from brain reward neurophysiology and the neurochemistry of individual drugs to the social and political issues concerning the treatment of addicts. At over one thousand pages, it is also an expensive book. The best place to read it without having to buy it is at a local medical school library.
Miller NS, Gold MS, Smith DE. Manual of Therapeutics for Addictions. Wiley-Liss.
A great handbook for medical and surgical residents to use in managing addicted patients in the hospital setting. Written by three superstars in the field of addiction medicine and the treatment industry.
Fernandez H. Heroin. Hazelden Press.
The best book I’ve found that compiles the history, effects and addiction process of this drug. It is a very good resource book, but to avoid triggers to relapse I recommend that newly sober heroin addicts avoid chapter five until further along in sobriety.
McCoy AW. The Politics of Heroin. Lawrence Hill Books.
An interesting but somewhat breathless investigation into the global traffic in heroin including the putative involvement of the CIA. Very good sections about the trafficking of heroin during the Vietnam War.
Streatfeild D. Cocaine: An Unauthorized Biography. St. Martin's Press.
A thorough and fascinating (if somewhat celebratory) examination of the history and politics surrounding the use of cocaine.
Barthelme S, Barthelme F. Double Down: Reflections on Gambling and Loss. Houghton Mifflin.
A moving memoir by two brothers concerning their accelerating addiction to gambling.
Beattie M. Codependent No More. Hazelden Press.
Although the precise nature of “codependency” is debated in feminist psychology, this book is the best description of the phenomenon available. It’s possible to wear out a highlighter while reading this book - that’s how powerful the identification of the reader to the codependent process can be. This book has sold in huge numbers and is a standard in pop psychology. It is an excellent book for the spouse or parent of the addict in early recovery to read since it will provide explanations for past painful events and introduce Al-Anon as a method of support.
Boskind-White, M. Bulimia/Anorexia. W. W. Norton and Company.
Carnes, P. Out of the Shadows. Hazelden Press.
Dr. Carnes is the leading expert in the emerging (and highly sensitive) topic of sexual addiction. Written from a humane perspective, this book explains the dynamics of the sexual behaviors that are commonly paired with chemical addiction - especially cocaine and methamphetamine.
Galanter M. Cults: Faith, Healing and Coercion. Oxford University Press.
An important description of a form of addiction that can be perpetrated by many dysfunctional "faith-based" treatment centers onto drug addicted patients.
Burns D. Feeling Good: the New Mood Therapy. Harper Collins
This is the easier-to-read version of Aaron Beck’s Cognitive Therapy of Substance Abuse. It explores the issues of faulty core beliefs that direct automatic thinking leading to intolerable feelings that trigger addictive behaviors. This is a good book for those in early recovery who are more rationally inclined and having trouble with the spiritual aspects of traditional recovery programs.
Coombs RH. Drug Impaired Professionals. Harvard University Press.
A compendium of the literature describing addiction in physicians, dentists, pharmacists, nurses, attorneys and airline pilots and the impaired professional programs run by most state licensing boards. This book is a good introduction to the concept of dealing with addiction from an occupational medicine perspective. Professional groups traditionally have very high success rates when carefully monitored in work settings, and lessons learned in this area of addiction medicine are important because they can be transferred to other addicts, regardless of their professional status.
Marlatt, GA. Harm Reduction: Pragmatic Strategies for Managing High-Risk Behaviors. Guilford Press.
One of my all-time favorite books. This book explains the philosophy and research behind the highly controversial public health approach to addiction known as Harm Reduction - a view that seeks to work with addicts even if they are not ready to stop drugs. This view is anathema to the traditional abstinence-based treatment approaches currently used in the United States today. Although it is respected and effective in other countries (it is, for instance, the official government policy on drug abuse in Canada and much of Europe), the hostility toward Harm Reduction borders on rabid. Dr. Marlatt slices through the misrepresentations and articulates the ethical and practical arguments for this approach.
Marlatt GA, Gordon JR. Relapse Prevention. Guilford Press.
The definitive text on the dynamic of relapse and the techniques to prevent it. This expansive book is written for professionals.
Miller W, Rollnick S. Motivational Interviewing. Guilford Press.
In my opinion, the most important addiction medicine book currently in print for professionals. Miller and Rollnick's approach marks an important shift away from the traditional, punitive tactics used in many treatment centers in the United States. The book is the jewel in the crown of addict/patient advocacy, and contains withering arguments against the concepts of denial and aggressive intervention. Whenever I am depressed about the things I see done to patients in treatment centers, I read the first chapter of this book - it never fails to inspire me. IT IS IMPORTANT TO NOTE that the authors have removed much of the revolutionary tone in their second edition (I think someone got to them), but you can still find the first edition used on Amazon.com.
Acker CJ. Creating the American Junkie. Johns Hopkins University Press.
An extremely important book. Dr. Acker chronicles the development of the - today unchallenged - idea that addicts are criminally-minded, disease-spreading sociopaths and demonstrates that this portrait of addicts was very consciously and carefully created during the period surrounding the enactment of the Harrison Narcotics Act in 1914. Dr. Acker's withering account of the complicity of psychoanalysts in stereotyping addicts as deviants is an absolute must-read for counselors, therapists and physicians before they practice confrontational therapies to "break down" the ego of addicted patients.
Baum, D. Smoke and MirrorsSmoke and Mirrors. Little, Brown and Company.
An excellent by a journalist for the Wall Street Journal about the escalation of the War on Drugs from the Nixon to the Clinton Administrations.
Gray, J. Why Our Drug Laws Have Failed and What We Can Do About It. Temple.
An analysis of the social and legal problems created by the Zero Tolerance/War On Drugs approach to addiction written by an Orange County Superior Court Judge.
Gray, M. Drug Crazy. Random House.
This book is a fascinating account of the attitudes of the individuals who established United States drug laws. It contains exceptionally interesting anecdotes about the history of drug policy in the United States.
Hentoff N. A Doctor Among the Addicts. Grove Press.
If you want to read about a true hero in addiction medicine, read Mr. Hentoff's book about Dr. Marie Nyswander. She talks about addicts as people, as patients and as valuable human beings - high or sober. And it's important to remember that this book was written in 1968! Dr. Nyswander and her colleague Dr. Robert Dole were two of a very small handful of doctors who were willing to bring heroin addicts into hospitals and treat them with dignity and kindness. Both of these pioneers are gone now, but I refer back to Hentoff's book for inspiration and a glimpse of what addiction medicine could be if only we followed Dr. Dole's and Dr. Nyswander's ideas.
Hodgson B. Opium: A Portrait of the Heavenly Deamon. Chronicle Books.
This is a beautiful pictorial of the history of opium use, but it might be too romantic for people in early recovery. It is a good book for the heroin addict on your Christmas list who already has ten years sober.
Lenson D. On Drugs, University of Minnesota Press.
This book is one of my favorites. Lenson analyses drug use and addiction from a phenomenological basis – through the experience of the addict. He deliberately avoids the standard neurophysiological, psychological, evangelical, confessional and literary approaches to the subject of drug use and addiction that make books in this genre so boring. His analysis of addiction as a pathology of consumerism is exciting and important.
Massing M. The Fix. University of California Press.
Extremely readable and insightful account of the origins of the Office of National Drug Control Policy under President Nixon and the formation of the cabinet position known as the “Drug Czar.” This book reveals the politics behind much of the United States’ policy toward addicts.
Musto, D. The American Disease: Origins of Narcotic Control. Oxford Press.
This book is an exhaustive review of the history and evolution of the legal sanctions and moral philosophy in the United States. Dr. Musto is the senior authority in this subject, making this a very important work. The book is commonly must-read in college courses about the sociology and history of American drug laws.
Musto, D. Drugs in America: A Documentary History. New York University Press.
An excellent anthology of primary source historical material relating to drug use and drug addiction in the United States over the last three hundred years.
Peele S, Brodsky, AM. The Truth About Addiction and Recovery. Fireside Books.
Written by a notorious opponent of the addiction treatment industry, Dr. Peele summarizes the strongest arguments against the "Disease Model" conceptualization of Addiction and the ideology of the recovery movement that claims it. Dr. Peele writes in the same style as Thomas Szasz and other anti-psychiatry libertarians, and denounces the “zealotry” and “coercive tactics” used by addiction treatment centers. I think this is an exceptionally important book for all addiction medicine clinicians to read. Peele's arguments are very strong and should be addressed. The addiction treatment industry ignores Peele at its own peril. Fortunately, good counter-arguments do exist to Peele’s positions.
Shavelson L. Hooked: Five Addicts Challenge Our Misguided Drug Rehab System. The New Press.
This book, written by a physician and photojournalist in Northern California, accurately describes the abusive tactics of the therapeutic community model of treatment to which addicts who cannot afford traditional treatment centers (i.e. Hazelden, Betty Ford) are exposed. It is an important documentation of this injustice, and a telling account of why it fails as a treatment method. Shavelson follows several addicts as they go through the addiction/treatment/relapse process and explores the reasons for their lack of success. He makes intelligent recommendations at the end of the book to change this pattern in the addict who is poor or mentally ill by changing the punitive aspects of treatment available to them.
Szasz T. Ceremonial Chemistry. Learning Publications.
Thomas Szasz is the intellectual father of the anti-psychiatry, libertarian movement against the addiction treatment industry and the Disease Model of addiction. Szasz claims that mental illness is a cultural construct more than a pathologic process (see his additional work The Myth of Mental Illness) and advocates for the elimination of drug laws entirely in favor of allowing addicts to “mature out” of their destructive behavior.
White, W. Slaying the Dragon. Chestnut Health Systems.
This book chronicles the evolution of early alcoholism treatment in the United States from patent medicine cures, mutual aid societies and inebriate asylums as well as the formation of Alcoholics Anonymous.
Dement, W. The Promise of Sleep. Living Planet Press.
A good book for patients in and out of recovery experiencing problems with sleep disorders. Written by the head of Stanford University's sleep lab, Dr. William Dement, who is arguably the leading expert on the subject. Explores in detail the elements of Sleep Hygiene which is used in addiction treatment centers as a non-pharmacological approach to insomnia in early sobriety.
Gorski TT. Staying Sober. Herald House/Independence Press.
The second book I would recommend to the addict in early recovery (the first being the Alcoholics Anonymous basic text). Gorksi combines the material from Marlatt and Gordon’s standard clinical text on relapse prevention with his own valuable insights. This book contains an excellent description of Post-Acute Withdrawal Syndrome as well as strategies to cope with it.
Gorski TT. Getting Love Right: Learning the Choices of Healthy Intimacy. Fireside Press.
Although frowned upon as a relapse trigger, romantic relationships in early recovery are common. If a relationship is going to happen, this book is probably the best way the help the recovering addict learn ways to avoid disaster. It is also a good book for long-established relationships with one or both members in early recovery.
Cheever S. My Name is Bill. Simon and Schuster.
A reverent but honest look into the life of William G. Wilson, the co-founder of Alcoholics Anonymous.
Kurtz E. Not God. Hazelden Press.
This is a semi-objective account of the origins of Alcoholics Anonymous from an academic historical approach. It explores the philosophical concepts at work in the twelve steps, and the significance of the twelve-step movement as a response to modernism.
LDS Family Services
Center for Substance Abuse Treatment
CSAT provides a library of Treatment Improvement Protocols which are publications designed to standardize understanding and management of common problems in addiction treatment. TIPs cover a range of subjects such as Substance Abuse Treatment for Persons with Co-Occurring Disorders (TIP 42) and Treatment of Adolescents with Substance Use Disorders (TIP 32). It is possible to build a fine addiction medicine library for free by downloading these TIPs and their accompanying TAPs (Technical Assistance Publications).
Treatment Improvement Protocols can be found here:
And Technical Assistance Publications can be found here
National Institute of Drug Abuse
The U.S. government-sponsored research arm of the National Institutes of Health. Although it often is influenced by the political agenda of the Executive Branch, the research funded by NIDA is of excellent quality - especially regarding neurophysiology and brain imaging.
National Institute on Alcohol Abuse and Alcoholism
Nature Neuroscience is the pre-eminent publication for the latest research on the brain. The Nov 2005 issue was devoted entirely to addiction and can be found here: http://www.nature.com/neuro/journal/v8/n11/index.html
Science Daily (regular updates on addiction topics)
Erowid is a beautiful library of information about psychoactive plants and chemicals. It is just about the best reference section on common drugs of abuse available on the internet (even if it does somewhat romanticize drugs).
Addiction Science Research and Education Center University of Texas, Austin
This is an excellent source of information and serves as the home site for Dr. Carlton Erickson, a popular lecturer on the neurophysiologic basis of addiction.
American Society of Addiction Medicine
The national professional society for medical doctors who practice addiction medicine. Also a good source for new treatments for addiction and legislative efforts for humane treatment of addicts.
Betty Ford Institute
The mission of the Betty Ford Institute is to conduct and support collaborative programs of prevention, education and research that will lead to a reduction in the devastating effects of addictive disease on individuals – especially parents and children in family settings – as well as on organizations and communities.
California Society of Addiction Medicine
The California state professional society for medical doctors who practice addiction medicine. A good source for new treatments for addiction and legislative efforts for humane treatment of addicts.
National Association of Addiction Treatment Providers
Faces and Voices of Recovery
The political action committee for Americans in recovery. An excellent site to keep up to date on the latest news regarding legislation regarding addiction and its treatment.
An excellent source of current information on new treatments for addiction, legislative efforts in public health, and reports about conflicts regarding the rights of addicted patients.
The “My Space” for people in recovery.
Amphetamine is the prototype drug for a large class of major CNS stimulants that share a basic Phenylethylamine structure. Phenylethylamine-type molecules include not only many amphetamine-related stimulant drugs, but the catecholamine neurotransmitters (epinephrine, norepinephrine and dopamine), entactogen drugs (MDMA, or “Ecstasy”), and the anti-depressants venlafaxine (Effexor) and buproprion (Wellbutrin). Because of their structural relation to the catecholamines, phenylethylamine drugs like amphetamines are sympathomimetic – meaning they stimulate the “fight-or-flight” sympathetic nervous system.
Amphetamines have a long history in medicine. Originally their sympathomimetic properties were employed for bronchodialation in asthmatic patients. Drugs such as methamphetamine also possess this property, one reason for the instantaneous cough on injection experienced by intravenous methamphetamine users. Amphetamine drugs have also been used in the treatment of obesity due to their ability to suppress appetite (anorectic), and for the treatment of attention-deficit disorder, as well as severe cases of narcolepsy.
Unlike the other major stimulant cocaine, which acts solely as a dopamine re-uptake inhibitor, amphetamines have multiple mechanisms of action. Like cocaine, amphetamines are also dopamine re-uptake inhibitors. They also cause the release of dopamine itself from pre-synaptic neurons, as well as the newly-synthesized pools of norephinephrine and (to a lesser degree) serotonin in brain neurons. Additionally, amphetamines in high doses also inhibit the enzyme Mono-Amine Oxidase (MAO), which ordinarily breaks down those same three catecholamine neurotransmitters. These different mechanisms combine to produce a powerful potentiation of the catecholamine-based sympathetic nervous system. The rewarding effects of amphetamines are due primarily to the exaggerated release of dopamine in the mesolimbic reward circuit of the brain.
LOW DOSES OF AMPHETAMINES
Arousal (often sexual in nature)
Increased Attention and Task Performance
Increased Heart Rate
Increased Blood Pressure
Increased Body Temperature
Mydriasis (Dilated Pupils)
MODERATE DOSES OF AMPHETAMINES
Hedonic Instability (variable and unpredictable drug reward)
Widened Sexual Repertoire
Socially Inappropriate Behavior (fight-seeking)
Repetitive Assembling and Disassembling Objects (“Projects”)
HIGH DOSES OF STIMULANTS
Hedonic Dysregulation (anhedonia)
Hypersexuality (genital injury, unsafe situations)
Social Withdrawal, Violence
Rhabdomyolysis (breakdown of muscle, release of proteins into bloodstream)
TOXIC/FATAL DOSES OF STIMULANTS
Suicide, “Death by Cop”
Cerebrovascular Accident (stroke)
A withdrawal phenomenon is observed in patients who suddenly stop taking amphetamines. Although not as life-threatening as the withdrawal from sedative/hypnotic medications, the patient can experience severe depression, hypersomnia (oversleeping), extreme hunger and craving for amphetamines.
Methamphetamine is synthesized when an extra methyl group is added to the amphetamine molecule. This makes the methamphetamine molecule more lipid soluble and thus increases its effects in the central nervous system over amphetamine. Methamphetamine was first synthesized in Japan in 1893 from ephedrine, a chemical found in the Chinese herb Ma-huang. Ephedrine has is a bronchodialator and was once sold over the counter as asthmatic inhalers. Like most amphetamine-like molecules, the “L” enantiomer of ephedrine is a less powerful sympathomimetic drug known as Pseudoephedrine (L stands for Levo-rotatory, for its ability to rotate polarized light to the left when passed through the molecule). L-ephedrine is sold over-the-counter as a nasal decongestant. It can be used to synthesize L-methamphetamine via a relatively easy process known as “cooking meth.” The purified, crystalline “L” enantiomer of methamphetamine has a wide vaporization phase and is therefore smokable. This form of crystal methamphetamine is often known as “ice” or “glass.”
Other phenylethylamine stimulants can be used as appetite-supressants (or “anorectics”). Phentermine and Fenfluramine used to be prescribed together as “Phen-Fen” in outpatient clinics (sometimes set up exclusively for that purpose). Because of the propensity for these moderate stimulants to produce pulmonary hypertension, their use is controversial for the purpose of weight loss. Phen-Fen was pulled from the market in the late 1990s.
Psychostimulants such as amphetamine and other phenylethylamines are also used for the treatment of Attention-Deficit Disorder. The most common drug prescribed for this purpose is methylphenidate (Ritalin, Concerta).
CLASS: MINOR STIMULANT
THERAPEUTIC EFFECTS: REDUCED FATIGUE, INCREASED ALERTNESS, AND FLUIDITY OF THOUGHT, IMPROVED COORDINATION
SIDE EFFECTS: IRRITABILITY, WITHDRAWAL HEADACHES
OVERDOSE: TACHYCARDIA, ANXIETY
LONG-TERM HEALTH EFFECTS: GENERALLY CONSIDERED SAFE FOR MOST PATIENTS
Caffeine is the most widely consumed psychoactive substance and been used by humans since pre-historic times. Caffeine is produced in the leaves, fruit and beans of over sixty different plants where it acts as a natural pesticide.
It is an ingredient in many beverages such as coffee, tea, chocolate, cola-flavored drinks, and in larger quantities in increasingly popular energy drinks.
Caffeine acts a minor CNS stimulant to produces alertness, ward off drowsiness, and increase the speed and clarity of thought. Caffeine works by blocking the neurotransmitter adenosine in the central nervous system, and by increasing the amount of cyclic-AMP in cells.
Caffeine content in foods & drugs (source: Center for Science in the Public Interest)
Starbucks Drip Coffee (grande): 320 mg
Starbucks Latte (grande): 150mg
Starbucks Espresso: 75mg
Tea (brewed): 50mg
Diet Coke: 47mg
Mountain Dew: 40mg
Monster Energy: 160mg
Red Bull: 80mg
Ben & Jerry’s Coffee Ice Cream: 68mg
Hershey’s Chocolate Bar: 9mg
NoDoz & Vivarin (1 tablet): 200mg
Excedrin (2 tablets): 130mg
Cannabindoid receptor antagonists
EXAMPLES: MARIJUANA, HASHISH, HASHISH OIL
THERAPEUTIC EFFECTS: RELAXATION, DECREASED MUSCLE SPASTICITY, DECREASED INTRAOCULAR PRESSURE
SIDE EFFECTS: IMPAIRED JUDGEMENT AND MEMORY, INCREASED HEART RATE AND APPETITE
DESIRED ABUSE EFFECTS: ELEVATED MOOD, MILD STIMULATION FOLLOWED BY SEDATION, DECREASED ANXIETY, LAUGHTER, CONTEMPLATION
OVERDOSE: HALLUCINATIONS, PARANOIA, PSYCHOSIS IN SOME PATIENTS, COMA IN CHILDREN
LONG-TERM HEALTH EFFECTS: AGGREVATION OF PULMONARY DISEASE, IMMUNE SYSTEM DYSFUNCTION
Cannabinoids are a large class of molecules similar in their structure to tetrahydrocannabinol, the active ingredient in cannabis (marijuana) and hashish. Upon burning cannabis leaves, a wide variety of cannabinoid compounds are liberated, most of which have psychoactive properties through their interaction with cannabinoid receptors in the central nervous system.
For many years, marijuana was considered to be psychologically addicting, not physically addicting the way alcohol and heroin. Since the discovery of physical cannabinoid receptors in the central nervous system, this distinction has lost its meaning. It appears that in many users, marijuana can in fact produce tolerance and a clinically observable withdrawal phenomenon. Also, due to individual differences, perhaps with a genetic basis, the response of some patients to marijuana can be distinctive, up to and including psychosis.
Nevertheless, and perhaps to the dismay of many parents, cannabinoids are considered one of the safer drug of abuse - at least by the pharmacologic definition of safety in which the effective dose of a drug is far less than the lethal dose of the drug (the lethal dose of marijuana has yet to be determined). This “pharmacologic” safety should not be confused with the overall safety of marijuana, which is quite real due to its effects on memory and its current classification by the Department of Justice as a Schedule I drug – defined as a drug so dangerous that it cannot be prescribed safely even by a doctor, and therefore has no legitimate medical use.
The issues surrounding the concept of “medical marijuana” are complex and nearly impossible to divorce from political and personal considerations. The active ingredient in marijuana, tetrahydrocannabinol, is available as a Schedule II medication, but its efficacy appears to be far less than smoked marijuana cigarettes. This may be due to some process in the pyrolysis (burning) of cannabis leaves that cannot be reproduced when the medication is in tablet form. The clinical evidence for marijuana’s effectiveness over other available medications for conditions such as glaucoma, nausea secondary to chemotherapy, and wasting syndrome due to HIV/AIDS is equivocal and highly contested. Marijuana does have demonstrated efficacy over other medications in the treatment of spastic muscular disorders such as muscular dystrophy and neurological disorders such as multiple sclerosis. The effort at the state level to legislate “compassionate use” of marijuana ignores the prevailing enforcement authority of the federal government, which recognizes no such utility.
Cannabinoids can be classified as either exogenous – those coming from plants and often self-administered for recreational purposes, or endogenous – those peptides manufactured by the body that have activity at CB (cannabinoid) receptors. The main endogenous cannabinoid is named Anandamide (“ananda” being the Sanskrit word for “bliss”).
The presently known cannabinoid receptors are divided into two classes, CB1 and CB2. CB1 receptors are found primarily in the brain. CB1 agonists produce the mood altering and anti-convulsant effects usually associated with marijuana. CB2 receptors have been found in the spleen and throughout the immune system and may be responsible for the anti-inflammatory effects of marijuana.
There are a number of synthetic cannabinoids used in medicine for their analgesic, anti-emetic (nausea) and appetite-stimulating effects. Dronabinol (Marinol) is a Schedule III cannabinoid mediction used in the treatment of cancer pain and nausea and anorexia associated with chemotherapy. Rimonibant is a cannabinoid receport antagonist that blocks the CB1 receptor and initially showed some promise as an anti-obesity drug. Its association with suicide in patients taking the medication has delayed its FDA approval for this purpose.
Free base cocaine
Route of administration
Along with the amphetamines, cocaine is a major stimulant – as opposed to the two minor stimulants, nicotine and caffeine. Cocaine is produced by two Central and South American shrubs: Erythroxylon coca, and Erythroxylon novogranatense. The vast majority of the world’s cocaine comes from Erythroxylon coca. There is a long history of cocaine use in South America in the form of chewing coca leaves drinking coca leaf tea. Leaves are chewed with a pinch of an alkaline substance – usually lime – to liberate the cocaine from the leaves. Among the Incas, the use of coca leaves was limited to royalty.
During the 1800s, organic chemists succeeded in extracting alkaloids from plant products such as opium and coca leaves. In the United States, cocaine was mass-produced and sold as a key ingredient in many “health tonics” – including
It was soon recognized as a severely addictive drug. Today, cocaine is used only rarely as a local anesthetic for the upper respiratory tract (nose, sinuses, pharynx). It is no longer used for anesthesia during eye surgery due to its tendency to produce corneal ulcerations. Cocaine is a key ingredient in Brompton Cocktail, a combination of cocaine, morphine and alcohol given to cancer patients in the final hours of their life to elevate their mood and provide some last minute sociability with family and friends before death. Today, this use fallen from favor among palliative care physicians.
Cocaine is produced by crushing coca leaves in a mixture of sulfuric acid and an organic solvent (often acetone or benzene, but sometimes gasoline or kerosene). After this crushing and mixing process – called “maceration” - an alkaline chemical is added (sodium hydroxide or lime) to make coca paste (which is 40 to 70% cocaine in its base form). Hydrochloric acid is then added to precipitate out the salt of the cocaine (cocaine hydrochloride), which is then filtered, dried, compressed and packaged for export.
Cocaine exists in two forms: as a salt, and as a base. The cocaine salt is almost always cocaine hydrochloride. It is a white powder that is highly soluble in water: nearly 2 grams can dissolve in 1 ml of water, or two “eight-balls” (each an eighth of an ounce of cocaine) in a teaspoon of water. Being water-soluble, the salt can be eaten, “snorted,” or injected, but it has a very narrow vaporization temperature, so cocaine hydrochloride cannot be smoked with any real efficiency. Cocaine base – also known as the “free base” form of cocaine – is not soluble in water, but has a much wider vaporization temperature phase. It can therefore be smoked readily. Crack cocaine is a base form of cocaine in which cocaine hydrochloride is dissolved in water and heated. A weakly alkaline chemical is then added – usually ammonia or sodium bicarbonate (baking soda) – that converts the cocaine to an oily solid. This base form is then collected for smoking. The innovation of crack cocaine was a marketing revolution for the drug. Since it can be packaged in small, single-dose vials and sold for small sums of money (five to ten to twenty dollars), crack cocaine became available to middle-income and poor populations. It was no longer a drug only for the affluent.
When cut into small pieces, crack cocaine looks like a tiny white chiclet. In larger amounts, it can resemble a macadamia nut. Cocaine is often smoked through a “stem” – a four-inch glass cylinder sold in many convenience stores, usually as a container for a small artificial rose. One end of the cylinder is stuffed with a scouring pad (classically the “Chore Boy” brand is used). A small piece of crack cocaine – a “rock” – is heated very carefully so as to melt it onto the wire mesh of the scouring pad inside the stem and then into a cocaine vapor without overheating. When smoked, the residual water in the cocaine base makes a crackling sound – thus the name “crack” cocaine.
To decrease its volume for smuggling, pure cocaine hydrochloride is often tightly compressed into bricks. This highly prized form of cocaine appears flaky and iridescent, and is known on the street as “fish-scale” cocaine.
Cocaine is a powerful vasocontrictor. If injected outside a vein it can cause painless but disfiguring ulcerations which heal very slowly and often leave permanent scarring.
Cocaine can also be administered through the rectum, the vagina, or through the urethra. This administration provides fast absorption but can lead to injuries, nerve damage and ulceration.
If a person uses cocaine and alcohol simultaneously, the two drugs form a third drug in the bloodstream called cocaethylene. Cocaethylene has a much longer half-life (and therefore longer duration of action) than cocaine or alcohol alone. It has been postulated that this chemical leads to an intoxication that involves considerably more paranoia and social violence than cocaine or alcohol alone.
Cocaine is metabolized by the liver to the metabolite benzoyl-ecognine. It is this metabolite that is detected in the urine, blood, skin or hair follicle by drug tests and is considered evidence of cocaine intoxication.
Cocaine is a powerful sympathomimetic drug, meaning it stimulates the sympathetic (the “fight-or-flight”) nervous system, mobilizing the body’s mechanisms for short bursts of energy in the service of defense or attack.
Sympathomimetic drugs produce:
The opposite counterpart of the “fight or flight” sympathetic nervous system is the “feed and breed” parasympathetic nervous system. High doses of cocaine also decrease the influence of the parasympathic nervous system to produce:
Cocaine produces its “sympathetic discharge” through the release of several chemicals in the brain and body known as monoamines. These include dopamine, epinephrine, norepinephrine, and serotonin.
The main reason for cocaine’s potential for abuse and addiction is it’s profound ability to increase amounts of dopamine in pleasure areas of the limbic brain.
The effects of cocaine are dose-dependent: The following are the signs and symptoms experienced from cocaine use in escalating doses:
LOW DOSES OF COCAINE:
INCREASED ATTENTION AND TASK PERFORMANCE
INCREASED MOTOR ACTIVITY/MOVEMENT
INCREASED HEART RATE AND BLOOD PRESSURE
INCREASED BODY TEMPERATURE
MYDRIASIS (DILATED PUPILS)
MODERATE DOSES OF COCAINE:
REPETITIVE TASKS SUCH AS ASSEMBLING & DISASSEMBLING OBJECTS
HYPERPYREXIA (VERY HIGH BODY TEMPERATURE)
HIGH DOSES OF COCAINE:
HYPERSEXUALITY – OFTEN RESULTING IN GENITAL INJURY & UNSAFE SITUATIONS
TOXIC DOSES OF COCAINE:
AUDITORY HALLUCINATIONS (HEARING VOICES, WHISPERING)
VISUAL HALLUCINATIONS (SEEING FIGURES IN TREES AND SHADOWS)
PROVOKING LAW ENFORCEMENT OFFICIALS INTO LETHAL DEFENSE (AKA “DEATH BY COP”)
RHABDOMYOLYSIS (BREAKDOWN OF MUSCLE LEADING TO TOXIC LEVELS OF MUSCLE PROTEINS INTO THE BLOODSTREAM)
RENAL FAILURE AND HEMATURIA (BLOOD IN URINE)
CHRONIC USE OF COCAINE:
PSYCHOMOTOR AGITATION (MUSCLE TWITCHES AND LIMB JERKS)
ANOREXIA (LOSS OF APPETITE)
COGNITIVE IMPAIRMENT (DIFFICULTY FINDING WORDS, CONFUSION)
HYPERSOMNIA OR INSOMNIA
Medications for cocaine addiction:
Disulfiram (Antabuse) is a drug commonly used to treat alcoholics. It blocks an enzyme, acetaldehyde dehydrogenase, that causes the accumulation of acetaldehyde – a metabolite of alcohol – in the bloodstream resulting in nausea, headache and flushing. The hope is that the alcoholic will be dissuaded from drinking due to these unpleasant effects. Recent research suggests that disulfiram may be helpful in reducing cravings for cocaine.
Since the cocaine molecule is antigenic - the human immune system produces antibodies to it – it could be possible to produce a cocaine vaccine, which would prevent the drug from reaching the brain.
Baclofen is a medication used for spasticity in
A major neuro-hormone involved in the brain’s stress response and relapse is Corticotropin Releasing Factor (CRF). CRF antagonists have been shown to block relapse in cocaine-addicted mice that are stressed and then re-exposed to cocaine after a period of abstinence.
CLASS: DISSOCIANTS (NMDA ANTAGONISTS)
EXAMPLES: PHENCYCLIDINE (PCP), KETAMINE, DEXTROMETHORPHAN
THERAPEUTIC EFFECTS: DISSOCIATIVE ANESTHESIA IN CHILDREN
SIDE EFFECTS: PSYCHOTOMIMESIS
DESIRED ABUSE EFFECTS: MOOD ALTERATION, DEPERSONALIZATION
OVERDOSE: AGITATION, PSYCHOSIS, DELIRIUM, SEIZURES, COMA
LONG-TERM HEALTH EFFECTS: NEUROTOXICITY, OLNEY’S LESIONS
Dissociants are drugs that have a limited and specific use in medicine as anesthetics.. They are also used recreationally for their unique mood altering effects. Dissociants work by binding to and antagonizing NMDA receptors in the central nervous system. They produce a characteristic feeling of dissociation or depersonalization: a sense of being separated from one’s body, and even an experience of observing oneself from a distance.
Initially, this tendency to produce a dissociated or cataleptic state in which the patient is quiet and unconcerned that he is undergoing surgery gave the NMDA antagonists some promise as anesthetics since they did not risk airway problems as many other anesthetics do. However, as these drugs wear off they can cause a severe emergence delirium as well as psychotomimesis in which the person experiences a schizophrenic-like state of disorientation, agitation, hallucinations, and paranoia.
Phencyclidine (PCP, Angel Dust, Sherm) used to be classified as a hallucinogen, but a more accurate description is as the prototypical dissociative anesthetic. It’s notoriously unpredictable and potentially severe emergence delirium has made it a particularly feared drug by the general public.
Ketamine (Ketalar) is a dissociative anesthetic used in children. It is often administered orally as a pre-operative anesthetic or in clinics for sedation during laceration repairs or for minor procedures. It is considered safe in children, but in adolescents and adults it produces the same emergence problems as PCP. Ketamine is also commonly used in veterinary medicine as a sedative or tranquilizer for agitated pets or larger animals such as horses undergoing surgical procedures. This drug is often stolen or diverted from veterinary clinics for recreational use, but Ketamine should not be confused with another veterinary tranquilizer, Acepromazine (Atravet) which is toxic to humans.
Dextromethorphan (DXM) is a weak opioid receptor agonist sold as a moderately-effective over-the-counter cough suppressant. In high doses however, dextromethorphan is a NMDA antagonist, and produces effects similar to PCP and Ketamine but more mild.
The use of Robitussin cough syrup for recreational purposes is common among adolescents and teenagers, and is known as “Robo-tripping.” Dextromethorphan-containing Coricidin tablets are often referred to as “skittles” because of their resemblance to the red variety of this candy.
“Entactogen” is a novel term to describe a small class of psychoactive and abusable drugs consisting of two variants of methamphetamine: MDA (3,4-methylenedioxyamphetamine) and MDMA (3,4-methylenedioxymethamphetamine, also known as “Ecstasy,” or “X”). These two drugs differ only in the substitution of one methyl group on one carbon on the phenylethylamine backbone molecule. Being less lipid soluble and therefore less active in the central nervous system, MDA is reported to be less euphoric but more “psychedelic” than MDMA due to greater affinity for certain serotonin receptors.
Entactogens are so named because of their ability to produce visual disturbances and hallucinations, intensified tactile sensations, and a perceived increase in appreciation for music and desire to dance. These two drugs are sometimes also called empathogens due to their ability to produce feelings of increased openness and interpersonal closeness and understanding (empathy).
The fact that the structure of MDA and MDMA is very similar to methamphetamine gives these drugs many of the same effects of this stimulant. But these molecules also have activity at serotonin receptors and produce similar effects to the entheogens. It is not inaccurate to say that MDA and MDMA exist structurally and pharmacologically between methamphetamine and the entheogens.
Both drugs have been investigated for their utility in psychotherapy, but the catagorization by the Department of Justice of this drug into Schedule one effectively ended this research.
Earlier medical research explored the potential of MDA and MDMA as drugs for Parkinson’s Disease, depression, obesity and even cough suppression. The United States Army also explored their use as truth drugs for interrogation purposes.
Lysergic acid diethylamide
EXAMPLES: LSD, PSILOCYBIN, MESCALINE, DMT
DESIRED ABUSE EFFECTS: PERCEPTUAL AND PSYCHIC DISTORTIONS INCLUDING INTENSELY COLORED VISUAL HALLUCINATIONS, EUPHORIA, HEIGHTENING OF HEARING AND EVALUATIVE THOUGHT PROCESSES, MOOD AND THOUGHT CHANGES WITH RELATIVELY LITTLE COGNITIVE IMPAIRMENT
SIDE EFFECTS: NAUSEA, DIZZINESS, ANXIETY, PSYCHOSIS
LONG-TERM HEALTH EFFECTS: MAY RESULT IN HALLUCINOGEN-PERSISTENT PERCEPTUAL DISORDER
“Entheogen” are drugs that generate new theological or mystical experiences. This word is preferred over the term ‘hallucinogen” due to its imprecise and political/social controversy. Entheogens belong to a wide variety of chemicals, many of them found in plants, that produce hallucinatory and revelatory experiences that are often interpreted by the user (but not by others) as being deeply profound and even life-changing.
Entheogens are agonists or agonist-antagonists at serotonin receptors (specifically the 5-HT2A receptor). Their effects can be divided into distorted perceptions (altered shapes, colors, heightened sense of hearing), psychic disturbances (alterations in mood and thought, depersonalization) and somatic disturbances (nausea, blurred vision, dizziness).
The entheogens can be divided into two main classes: (1) Indolealkylamines, which include the Ergolines, derived from the Rye fungus Ergot, and the Alkyltryptamines: and (2) the Phenylalkylamines, which include the Phenyltheylamines, and the Phenylisopropylamines. The Ergolines include LSD which is made from the Lysergic Acid found in the Ergot fungus. The Alkyltryptamines include Psilocin and its phosphate ester Psilocybin, both of which are found in certain species of mushroom. Another Alkyltryptamine is DMT (N,N-dimethyltryptamine), an entheogen that is not orally active but must be smoked or injected. DMT has a rapid onset and a short duration (less than thirty minutes). A variant of DMT known as bufotenine is found in the skin of certain frogs.
Entheogens are notorious for producing “flashbacks,” or a return of the drug experience many days or even months after the use of the drug. Many think this experience is due to the drug being released from body fat stores, but there is no evidence that this phenomenon is due to the drug itself. The occurance of these flashbacks – technically known as Hallucinogen Persistent Perceptual Disorder – does not seem to be related to dose of the entheogen taken, nor to frequency or duration of use. These experiences often occur when the individual changes from one sensory setting to another (for instance, walking into a darkened theater) or during sleep deprivation. Often these experiences create a great deal of anxiety in those who experience them. Of the Ergolines, LSD is extremely potent and sold as blotter paper dipped with small amounts of the drug, while Harmaline (aka Ayahuasca) is far weaker and used in South American Indian religious ceremonies. The most famous Phenyltheylamine entheogen is Mescaline is an even weaker entheogen found in Peyote cactus.
EXAMPLES: NITROUS OXIDE, AMYL NITRATE, ORGANIC SOLVENTS
THERAPEUTIC EFFECTS: ANESTHESIA, ANALGESIA DURING ANESTHESIA
SIDE EFFECTS: NAUSEA, DIZZINESS, HEADACHE, CONFUSION, VITAMIN B12 DEFICIENCY (NITROUS OXIDE)
DESIRED ABUSE EFFECTS: EUPHORIA, LIGHTHEADEDNESS, DEPERSONALIZATION, HALLUCINATIONS
OVERDOSE: VOMITING, FAINTING, COMA, DEATH DUE TO ANOXIA (LACK OF OXYGEN)
LONG-TERM HEALTH EFFECTS: NON-REVERSABLE NEUROTOXICITY
Inhalants constitute a wide variety of household cleaning products, industrial chemicals, and anesthetics that are gases or produce fumes that create varying kinds of mood alteration. Many of these chemicals are profoundly neurotoxic, making inhalant use particularly dangerous compared to other drugs of abuse and of great public health concern, especially since inhalant abuse is common in children, adolescents and the impoverished.
Nitrous oxide, also known as “laughing gas,” is an anesthetic gas used in dentistry and surgery as an adjunct to other inhalational anesthetics such as Enflurane and Halothane and intravenous anesthetics such as propofol. When correctly administered with oxygen, nitrous oxide is safe, non-flammable and produces good analgesia (pain relief)
Its use was a major innovation in medicine and displaced older anesthetics such as chloroform, which is hepatotoxic, and ether, which is extraordinarily flammable.
Nitrous oxide is used recreationally for an instantaneous but short-acting high consisting mainly of visual and auditory disturbances, lightheadedness, euphoria and dissociation.
The dissociative effects of nitrous oxide may be due to its antagonism of the NMDA receptor. The precise mechanism of nitrous oxide is not known.
Amyl nitrite is a potent vasodilator that, when inhaled, produces a profound drop in blood pressure and increase in heart rate that users experience as an instantaneous lightheadedness and euphoria, or “rush.” Other effects are flushing, headache and relaxation of involuntary muscle tone, all of which pass as quickly as they came on.
Amyl nitrite comes in small ampules which can be cracked and snorted. When the drug is taken this way it is known as a “popper,” and is often used as part of casual heterosexual and homosexual encounters to heighten sexual gratification. Amyl nitrite is used in medicine for the rapid relief of angina pectoris, and as an antidote in cyanide poisoning.
When inhaled, volatile organic solvents such as toluene, chloroform, acetone and ether can produce lightheadedness and euphoria. Many of these chemicals are found in industrial products and household cleaners such as model airplane glue, typewriter correction fluid and computer dusters. Users will soak a rag with the chemical or pour some into a soda bottle, hold it to their nose or mouth and breath deeply, a practice called “huffing.” These drugs are particularly dangerous, even compared to most drugs of abuse, and can be associated with sudden death.
CLASS: MINOR STIMULANT
DESIRED ABUSE EFFECTS: MILD STIMULATION, INCREASED ATTENTION AND CONCENTRATION, DECREASE IN ANXIETY, DECREASED APPETITE
SIDE EFFECTS: NAUSEA, VOMITING, DIZZINESS, INCREASED HEART RATE
OVERDOSE: TREMORS, SEIZURES, RESPIRATORY ARREST, DEATH IS RARE BUT POSSIBLE
LONG-TERM HEALTH EFFECTS: INTRAUTERINE GROWTH RETARDATION IN PREGNANCY,
Nicotine is a minor stimulant found in several plants but mainly in the tobacco plant. It is a natural insecticide, and several nicotine derivatives are used as commercial insecticides. Nicotine in very high doses has many of the same effects as nerve agents used in chemical warfare.
Nicotine binds to nicotinic receptors on specific cells in the central nervous system, which then produce an increase in the release of the neurotransmitter acetylcholine eventually resulting in the release of ephinephrine.
While nicotine is classified as a stimulant, many regular users claim it produces relaxation and calmness. Whether or not these feelings are actually the reduction of withdrawal symptoms is debatable.
Regular nicotine use produces tolerance, requiring the user to self-administer increasing amounts of nicotine (for example, by smoking more cigarettes) to receive the same effects. Should the user stop his nicotine intake (for example, by quitting smoking), a powerful withdrawal syndrome will occur.
OPIATES/OPIOIDS (aka NARCOTICS)
CODEINE (TYLENOL #2, #3, #4)
DIACETYL MORPHINE (HEROIN)
HYDROCODONE (VICODIN, NORCO, LORTAB)
OXYCODONE (PERCOCET, PERCODAN, OXYCONTIN)
PROPOXYPHENE (DARVON, DARVOCET)
FENTANYL (DURIGESIC PATCHES, ACTIC LOZENGES)
ANALGESIA (PAIN RELIEF)
DECREASED COUGH (ANTI-TUSSIVE)
DECREASED GASTROINTESTINAL MOTILITY
ABDOMINAL PAIN DUE TO SPASM OF THE BILE DUCT
CONSTRICTION OF THE PUPILS (MIOSIS)
ITCHING AND HIVES
DESIRED ABUSE EFFECTS:
LONG-TERM HEALTH EFFECTS:
An opioid is a drug molecule that can bind to an opioid receptor. Receptors are proteins that float on a cell’s surface membrane. They have a specific shape – just like lock of a door has a specific shape. The opioid molecule has a complimentary shape that fits the opioid receptor – just as a key fits into a lock. When the opioid binds to the opioid receptor, it triggers changes in the cell that then produce the effect of the opioid drug.
If an opioid binds to the opioid receptor and turns it on, it is an opioid agonist. If it binds to the receptor and turns it off, it is an opioid antagonist.
The most famous opioid agonist is morphine. It is the prototypical opioid by which all other opioids are measured. There are opioid medications that are stronger than morphine and longer acting than morphine, but no opioid has been found to be more effective at relieving pain than morphine.
There are two opioid antagonists: naloxone (Narcan), which is used by injection in emergency settings to reverse heroin overdose, and naltrexone which has many of the same opioid-blocking actions as naloxone but can be taken orally (as ReVia) or administered as a long-acting injection (as Vivitrol).
There are also molecules that can bind to opioid receptors and turn them on a little bit and off a little bit at the same time. These opioids are called agonist-antagonists. They are also sometimes called partial opioid agonists. The most famous opioid agonist-antagonist is burprenorphine. It is the main ingredient in Subutex and Suboxone.
There are three main classes of opioid receptors: mu opioid receptors, delta opioid receptors, and kappa opioid receptors.
When bound by an agonist, the mu-opioid receptor (MOR) produces the classic opioid effects associated with morphine and heroin. These include analgesia (decreased pain), sedation, euphoria, decreased gastrointestinal tract motility, and decreased cough reflex. These effects make opioids useful in the treatment of pain, diarrhea and severe cough. Higher doses of opioid drugs like morphine cause additional mu-opioid receptor effects such as constipation, constricted (“pin-hole” or “pinned”) pupils, sleepiness (“nodding out”), nausea and vomiting, urinary retention, decreased heart rate and blood pressure, itching and hives. Overdoses of morphine can cause dangerous effects mediated by mu-opioid receptors such as coma, respiratory depression, cardiovascular collapse and death. Long-term use of morphine can produce irregular menstruation in women, erectile dysfunction in men, and decreased sexual drive (libido) in both men and women.
Delta opioid receptors are involved in analgesia in the brain. Endogenous opioids called enkephalins bind to delta opioid receptors with high affinity.
Like mu and delta receptors, kappa opioid receptors produce analgesia, but they act in the spinal cord, not the brain. Also, binding of kappa opioid receptors causes dysphoria, not euphoria.
Opioids have no ceiling dose. It is possible to
Opioids are not intrinsically toxic
The term “narcotic” is often used in legal settings to include all illicit and/or illegal controlled substances such as heroin, marijuana, and cocaine. From a pharmacologic standpoint, this is inaccurate. Only opioids are true narcotics.
Opiates are those drugs that come directly from the opium poppy. They include morphine, codeine and thebaine. Once separated out of raw opium, morphine can be further processed into heroin. Thebaine is not used as a medication, but can be chemically converted into a number of opioids that are used as medications such as oxymorphone, oxycodone, buprenorphine, naltrexone and naloxone.
Opiates and opioids have the ability to produce tolerance. This means that the dose needed to produce a given drug effect increases with continued use of the drug. Heroin addicts need to use more and more heroin to reach the same high as well as stave off withdrawal symptoms. If a person is tolerant to the effects of opioids, any sudden decrease in their dose of opioids or cessation of opioid use will result in withdrawal symptoms. As a rule, the withdrawal symptoms the addict experiences are the exact opposite of those effects of the original opioid drug.
MUSCLE CRAMPS, BONE PAIN
CHILLS AND “GOOSEFLESH”
PROLONGED WITHDRAWAL SYMPTOMS:
Many long-term opioid users will experience withdrawal symptoms weeks or even months after their cessation of use and medical detoxification.
Opioid drugs include:
Propoxyphene is a schedule IV long-acting opioid analgesic marketed in tablet-form by Eli Lilly as the medication Darvon. It also comes as a preparation combined with acetominophen known as Darvocet. Any time the suffix “-ocet” is found in the name of a an analgesic medication, it means the medication is a of an opioid plus acetominophen – the active ingredient in Tylenol. Opioids prescribed as tablets are often combined with acetominophen because the two medications together have greater analgesic potency with fewer side effects than if used alone. Very often in overdoses of opioids in tablet form, the concern for the patient’s welfare comes not from the toxicity of the opioid but from the acetominophen (at high doses, acetominophen is highly toxic to the liver).
Hydrocodone is a schedule III short-acting opioid analgesic medication marketed in tablet form in combination with acetominophen as Vicodin, Lortab, Norco and generic preparations. For patients with liver disease who cannot take acetominophen, hydrocodone can be combined with ibuprofen – the medication in Motrin and Advil – to make the medication Vicoprofen. Hydrocodone was the number one most-prescribed drug in the United States in 2003. In 2005, hydrocodone had dropped to the number three spot.
Oxycodone is a schedule II short-acting opioid analgesic medication used for moderate to severe pain. It commonly comes combined with acetominophen in 5mg and 7.5mg (of oxydocone) preparations either in generic form or as Percocet. Percodan is oxycodone combined with aspirin in lieu of acetominophen. Since these tablets need to be taken frequently to achieve steady pain relief, and since the toxicity of acetominophen is a concern, an acetominophen-free, time-release tablet – OxyContin – has been marketed by Purdue Pharma for moderate to severe pain. OxyContin is designed to be taken by mouth every twelve hours, and comes in preparations of 10mg (round, white tablets with a “10” imprinted on one side and an “OC” on the other), 20mg (round, light orange tablets), 40mg (round, light pink tablets), 80mg (round, light green tablets) and 120mg (blue capsules). It was not long before recreational users realized that crushing the tablets rendered the time-release preparation inert, thereby liberating the entire dose of oxycodone to be used by nasal insufflation (“snorting”) or by intravenous injection.
Meperidine (Demerol) is a short-acting schedule II opioid analgesic most often administered in emergency room settings by IM or IV injection. Its prolonged use is limited by the accumulation of its metabolite normeperidine, with can induce seizures. It is a common drug of abuse among addicted health-care professionals.
Methadone is a long-acting medication (half-life 48 to 72 hours) used for the relief of moderate to severe pain in patients with such illnesses as cancer. Methadone can also be used as a medication for the treatment of opioid addiction as either a detoxification medication or as substitution. The goal of substitution or maintenance therapy is to increase survival rates in heroin addicted patients, decrease viral hepatitis and HIV infection rates, block heroin cravings and heroin overdose, and promote healthy pregnancy outcome relative to heroin use. In meeting these goals, methadone has been quite successful. The complaint about methadone is that the use of other drugs such as cocaine and benzodiazepines often continues. From an abstinence-based recovery viewpoint, methadone is simply switching an addiction to heroin to an addiction to methadone. From a public health viewpoint, methadone is an effective treatment for heroin addiction that can decrease criminal recidivism and allow the addict to resume a normal life (including the procurement of a job, housing, and healthcare). Methadone substitution therapy is a very controversial subject in the recovery community.
L-AAM (levo-alpha-acetylmethadol) is an even longer-acting opioid (half-life of 2.6 days) that was intended to replace methadone. It never caught on.
Hydromorphone is a potent schedule II opioid analgesic marketed under the name Dilaudid and used for moderate to severe pain.
Oxymorphone is an especially potent schedule II opioid analgesic (8x more potent than morphine) used in the treatment of severe pain.
Fentanyl is a short-acting superpotent schedule II opioid analgesic usually used as part of anesthesia in hospital operating rooms. It is also used in dental surgery and minor day surgery procedures. Fentanyl is 80 to 100 times more potent than morphine. Fentanyl also comes as a transdermal patch (Durigesic) that can be replaced every 72 hours for the control of severe pain in cancer patients. For breakthrough pain, fentanyl also can be prescribed as a lollipop (Actic).
Sufentanil (Sufenta) is an ultra-short acting schedule II super-opioid analgesic that is used exclusively by anesthesiologists. Sufentanil is five to ten times more potent than Fentanyl.
Carfentanil is 10,000 times the potency of not used in human medicine. It is used in veterinary medicine as a bear, moose and buffalo tranquilizer.
Heroin is a short-acting (half-life 6 to 8 hours) schedule I opioid that is illegal for use in the United States. It is used in the UK as a pain reliever and as a medication for substitution in the treatment of heroin addiction.
There are an estimated half-million heroin addicts in the United States, although the number varies depending on the purity of heroin available for illicit sale at any given time. Heroin (aka Diacetylmorphine and Diamorphine) was independently invented and sold by the Bayer company in the late 1800s as a cough medicine. Heroin is produced from morphine extracted from raw opium that has been acetylated - a chemical conversion in which two acetyl groups are exchanged for the hydroxyl groups on the morphine molecule. Heroin – 3,6-diacetylmorphine – is three times more potent than morphine, and by virtue of its two acetyl groups, is a much more lipophilic molecule than morphine. This means it can traverse cell membranes readily. This allows the heroin molecule to cross the blood-brain barrier faster than morphine or many other opioids. The result of this speed of distribution produces a “rush” of euphoria even greater than that of morphine, considerably increasing heroin’s potential for addiction. Once inside the brain, the heroin molecule is two large to fit into the mu opioid receptor. Enzymes in the brain cleave the acetyl groups from the molecule, which is now once again morphine. Technically speaking, there is no such thing as a “heroin high” due to the inability of the heroin molecule to bind to the mu opioid receptor. Heroin is simply a “prodrug” – and a rapid delivery method – for morphine.
Buprenorphine is a partial mu-opioid receptor agonist. It was approved for the treatment of opioid addiction by the Drug Abuse Treatment Act (DATA) in 2000. The protocols for the medical use of this potentially abusable drug are very strict, and only physicians who have passed a special certification course are allowed to prescribe buprenorpine in the course of treating opioid addicts. A key provision of DATA is that burprenorphine can be prescribed in the privacy of a doctor’s office (known as OBOT: Office-based Opioid Therapy), enhancing compliance by avoiding the problems associated with daily visits to a methadone clinic.
For the purposes of treatment for opioid addiction, buprenorphine comes in two preparations. Subutex is buprenorphine as a sublingual tablet. The patient holds the tablet under his/her tongue and the medication is absorbed through the mucosal surface. Suboxone is also a sublingual preparation of buprenorphine plus naloxone
As a detoxification medication, buprenorphine can provide relief from cravings and withdrawal symptoms. It is important to remember that in the tolerant opioid addict, the administration of buprenorphine
Buprenorphine can also be used as a maintenance medication (also known as opioid substitution therapy). In maintenance, buprenorphine is given daily to decrease cravings for heroin or other abusable opioids, and – at high enough doses – block the high from these abusable opioids should they be used. Unlike most other opioids, buprenorphine has a “speed limit” in that doses over 32mg cannot increase the effects of the drug.
Buprenorphine has many of the advantages of methadone (good craving reduction, blockade of other opioids) while avoiding some of its pitfalls (excessive euphoria and sedation, potential for overdose).
Tramadol (Ultram) is an analgesic originally purported by its manufacturer to be a non-opioid. It has since been found to be a weak mu-opioid agonist, while it exerts its analgesic effects primarily through modulation of the GABA, noradrenergic and serotonergic systems in the brain. Tramadol is available by prescription in the United States but is not listed as a controlled substance by the DEA. A withdrawal syndrome has been described for patients who suddenly stop taking tramadol. Tramadol is also a serotonin-reuptake inhibitor and should be prescribed carefully in patients taking SRI-antidepressants since an overdose could result in a toxic state known as serotonin syndrome. Tramadol should never be taken in combination with MAOI anti-depressants.
ALCOHOL, BARBITURATES, BENZODIAZEPINES, GHB
DECREASED ANXIETY (SEDATION)
INDUCTION OF SLEEP (HYPNOSIS)
CENTRAL NERVOUS SYSTEM DEPRESSANTS
DECREASED COORDINATION & REACTION TIME
DECREASED IMPULSE CONTROL
ANTEROGRADE AMNESIA (“BLACKOUTS”)
DESIRED ABUSE EFFECTS:
FEELING OF WELL-BEING
RESPIRATORY DEPRESSION (SHALLOW, SLOW BREATHING) WITHDRAWAL SEIZURES
LONG-TERM HEALTH EFFECTS:
FETAL-ALCOHOL SYNDROME (ALCOHO
Sedative/Hypnotics are drugs that decrease anxiety (sedative) and induce sleep (hypnotic). As such they are an extremely useful class of medications and are extensively used in medicine. All of these drugs exert their action by enhancing the inhibitory neurotransmitter GABA (Gamma-AminoButyric Acid) in the brain.
This is a VERY LARGE class of medications that includes alcohol, chloral hydrate, barbiturates (ex. phenobarbital), benzodiazepines (ex. diazepam), GHB and many of the newer prescription sleep aids. Sedative/hypnotic drugs are widely abused, and several are so notorious for their addictive potential, for example methaqualone (Quaalude), that they are banned and no longer used in medicine.
All of these medications have the ability to produce “anterograde amnesia” meaning that they can cause users to be unable to recall events after a certain blood plasma level of the drug is reached. Another term for anterograde amnesia is a “blackout.” Because of this property of sedative/hypnotic drug, they can be used as “date rape” drugs.
Of particular concern with Sedative/Hypnotics is that if taken in overdose amounts, these drugs can suppress breathing, especially when combined with other drugs such as opioids. It is common that sedative/hypnotics in pill form (benzodiazepines, barbiturates, and other sleep aids such as Ambien) are combined with alcohol. Taken together, these drugs often have a synergistic effect, meaning that their effects in combination are several times greater than if the effects of each individual drug were simply added together. This synergistic effect has lead to many inadvertent overdoses and death.
Sedative/hypnotics as a class tend to produce the phenomenon of tolerance, meaning that as more drug is used over time, more drug is required to produce the same effect. In tolerance, the body tries to counter-act the effect of the drug by removing receptors or producing its own chemicals that produce an opposite effect of the drug. This requires the user to ingest increasing amounts of the drug with continued use. If the user should stop the drug abruptly, they are likely to experience withdrawal symptoms. As a rule, the withdrawal symptoms experienced are the exact opposite of the effects of the original drug (extreme anxiety instead of sedation, prolonged insomnia instead of hypnosis). Sudden cessation of some sedative/hypnotics after long periods of use can cause withdrawal symptoms severe enough to be life threatening. The standard treatment for severe withdrawal is to ease the patient’s symptoms by providing tapering or decreasing doses of another sedative/hypnotic drug (usually a benzodiazepine) over a period of several days.
GABA stands for for Gamma-AminoButyric Acid, and is one of the main inhibitory chemical neurotransmitters in the brain (inhibitory meaning that it turns things down). It is also known a 4-aminobutyrate.
There are three main types of GABA receptors – GABA-A, GABA-B and GABA-C receptors. GABA-A receptors exist on the pre-synaptic nerve cell membrane. When bound by GABA, these receptors open ion channels on the membrane that let negatively-charged chloride ions (Cl-) into the nerve cell, making the cell less likely to depolarize and transmit a nerve impulse. These kind of receptors, in which the receptor is an ion channel itself, are called ionotropic. GABA-B receptors are metabotropic receptors, where the receptors are coupled to a protein inside the cell called a G-protein. When the GABA-B receptor is bound, the G-protein acts as an intermediary to open ion channels on the cell membrane that let positively-charged potassium ions (K+) into the cell. GABA-C receptors, like GABA-A receptors, are ionotropic
GABA is made by brain cells from the amino acid glutamate, which oddly enough is itself an excitatory neurotransmitter in the brain. This synthesis requires vitamin B6.
Setting aside the history of alcohol production, the astounding varieties of alcoholic beverages, and the complex ritualization of their use, alcohol is interesting as a drug simply because it’s a very special molecule.
Alcohol – also known as ethyl alcohol, or ethanol – has two carbon atoms and an oxygen atom, and all three of these atoms have hydrogen atoms around them. This means that one half of the molecule is a hydrocarbon. Hydrocarbons are lipophilic – they “like” to be around lipids and oils. Lipophilic molecules distribute quite nicely in fatty tissues. The other half of the molecule – the half with the oxygen atom - has a little electrical charge. This makes that half of the molecule hydrophilic – it “likes” to be around water. Hydrophilic molecules distribute themselves throughout the fluids of the body. This special blend of “fat liking” and “water liking” qualities in the same molecule, combined with the fact that the alcohol molecule is small in size, means that alcohol can get absolutely everywhere in the body. This is one reason that in severe alcoholics you can see the effects of alcohol in every organ and kind of tissue examined.
Along with heat and carbon dioxide, yeast produce alcohol as a waste product during their consumption of simple sugars in a process known as fermentation.
Chloral hydrate is a Schedule IV sedative/hypnotic medication. Once used extensively in hospitals for insomnia or pre-operative sedation, it has largely been replaced by newer sedative/hypnotic medications such as benzodiazepines. It is occasionally used in addiction treatment as a sedative in patients undergoing detoxification for alcohol.
Anytime halogen atoms (chorine, fluorine for example) are added to a drug molecule, it becomes more potent (for instance, sucralonse, aka “Splenda,” is chlorinated sugar, and is several hundred times sweeter than regular table sugar). The same is true for alcohol. If you add three chlorine atoms and an extra hydroxyl (-OH) group to ethanol, you get chloral hydrate. It is a potent medication, and was the purported ingredient in the notorious drug-laced “knockout” drink known as a “Mickey Finn” – which was given to unsuspecting victims in order to rob them.
Barbiturates are powerful sedative/hypnotic drugs that used to be widely used in medicine. Their clinical utility was limited by the fact that in very high doses they suppress breathing to the point of respiratory arrest. Barbiturates are especially dangerous when taken with alcohol and this combination been implicated in many accidental deaths (legendary guitarist Jimi Hendrix died of aspiration pneumonia after consuming wine and secobarbital) and even to commit suicide (the Heaven’s Gate cultists committed mass suicide in 1997 by ingesting a deliberately lethal combination of vodka and phenobarbital). Many barbiturates also can be hepatotoxic (damaging to the liver). Barbiturates were almost completely replaced by benzodiazepines, which are much safer in overdose (relative to barbiturates).
Barbiturates bind to the GABA-A receptor and increase the duration that the GABA ion channels are open, thus potentiating the effect of GABA, the main inhibitory neurotransmitter in the central nervous system.
Phenobarbital (Luminal) is a long-acting schedule IV barbiturate sedative/hypnotic medication often used today in medicine as an anti-convulsant in the treatment of seizure disorders.
Amobarbital (Amytal) is a schedule II barbiturate sedative/hypnotic medication
Secobarbital (Seconal) is a schedule II barbiturate sedative/hypnotic medication
Thiopental (Pentothal) is an ultra-short acting barbiturate administered intravenously to induce anesthesia at the beginning of surgical operations. It is the drug an anesthesiologist is using when he or she says, “Now count backward from 100” and the patient is unconscious before they get to “98.” The anesthesiologist then quickly places an endotracheal tube, begins mechanical ventilation with a respirator, and administers other longer-acting intravenous or inhalational anesthetics, which then take over by the time the thiopental wears off. Thiopental is used to execute prisoners by lethal injection. In order to produce rapid unconsciousness and respiratory depression extremely high doses of this drug are given along with norcuronium (a muscle paralyzing drug), and potassium chloride (to produce cardiac arrest).
Butabarbital is a schedule III barbiturate sedative/hypnotic medication.
Pentobarbital (Nembutal) is a schedule II barbiturate sedative/hypnotic medication.
Benzodiazepines are the dominant class of sedative/hypnotic medications currently used in clinical medicine. They have a wide clinical utility as sedatives and anxiolytics (medications that decrease or “cut” anxiety), hypnotics, anti-convulsants, muscle relaxants, and amnestics. Benzodiazepines largely replaced the barbiturates due to their greater relative safety since they are far less likely to suppress respiration in overdose.
Chlordiazepoxide (Librium) is a schedule III sedative/hypnotic medication.
Diazepam (Valium) is a schedule III sedative/hypnotic medication.
Alprazolam (Xanax) is a schedule III sedative/hypnotic medication.
Clonazepam (Klonopin) is a schedule III sedative/hypnotic medication.
Triazolam (Halcion) is a short-acting, schedule IV hypnotic medication.
Temazepam (Restoril) is a schedule IV hypnotic medication.
Lorazepam (Ativan) is a schedule IV sedative/hypnotic medication.
Oxazepam (Serax) is a schedule IV hypnotic medication.
Many benzodiazepines are converted by the body into metabolites that are themselves active benzodiazepines, giving them a longer duration of effect. For instance, diazepam is converted to oxazepam prior to being converted to a more water soluble metabolite which can be excreted in the urine.
Flunitrazepam (Rohypnol) is a benzodiazepine that was never approved by the FDA for clinical use in the United States due to its tendency to be abused and its ability to produce blackouts. This drug, known on the street as “Roofies,” is perhaps the most notorious “date rape” drug next to GHB.
Flumazenil (Romazicon) is an antagonist at the benzodiazepine receptor and is used to reverse the effects of a benzodiazepine overdose.
GHB (Gamma-hydroxybutyrate) occurs naturally in the brain as the immediate metabolic precursor of GABA. A Schedule III controlled substance, it is prescribed under the trade name Xyrem to prevent the symptom of cataplexy (sleep paralysis) as part of the larger treatment of narcolepsy. GHB is also an illicit drug of abuse and so is a Schedule I controlled substance as well – the only drug to occupy two different schedules based on its formulation. GHB is primarily a GABA-B agonist, in contrast to benzodiazepines, which are mainly GABA-A agonists.
The use of GHB (and its pro-drug GBL, gamma-butyrolactone) became popular in the weight-lifting community because of its purported ability to prolong Stage IV sleep during which growth hormone is secreted.
GHB is used recreationally to produce effects similar to those of alcohol: intoxication, euphoria, increased libido and sociability. It comes in powder and liquid form and is salty to taste. GHB is commonly used in combination with other drugs of abuse such as methamphetamine, MDMA (”Ecstasy”) and alcohol. GHB is dangerous as a drug of abuse due to its low therapeutic index – meaning that the dose that produces intoxication and the dose that causes overdose are very close. Of particular concern in GHB overdose are coma, aspiration pneumonia, decreased heart rate and seizures. It is vital that persons who have overdosed on GHB are not left unattended and put in contact with emergency services as soon as possible.
GHB is notorious for its use as a “date-rape” drug. GHB can be slipped into an unsuspecting victim’s drink, perhaps at a party. Often the victim’s sense of caution is lowered due to the use of alcohol and other drugs.
Zolpidem (Ambien) is a fast-onset, short-acting schedule IV hypnotic medication that is distinct from benzodiazepine drugs but still binds to GABA-A receptors and potentiates GABA in the brain. Zolpidem is designed to decrease sleep latency (the time it takes to get to sleep) without prolonged sedation by acting quickly (within ten to fifteen minutes of ingestion) and wearing off within hours. Unfortunately, this creates problems for patients waking-up late at night unable to get back to sleep. For this reason, the manufacturer produced Ambien CR: one half of the tablet is a normal dose to help induce sleep, and the other half is a time-release preparation of zolpidem to keep the patient asleep throughout the night. This medication can produce anterograde amnesia in some users to include blackouts and sleepwalking.
As a drug of abuse, users experience effects similar to benzodiazepines or alcohol: euphoria, decreased anxiety and social inhibitions, increased impulsivity, sedation and sleep. Some users report visual hallucinations, and in certain at-risk patients psychosis is possible. Contrary to popular belief, zolpidem can produce addiction – including tolerance and withdrawal seizures.
Nonbenzodiazepine hypnotic medications similar to zolpidem include zalepon (Sonata) and eszopiclone (Lunesta).
Ramelton (Rozeram) is a newer hypnotic medication that is purported by its manufacturer to be non-addicting. As such, it is not a controlled substance. Ramelton binds to melatonin receptors instead of GABA receptors, like other hypnotic medications. Melatonin is believed to be a chemical in the brain responsible for the circadian (daily sleep/wake) cycle.
Baclofen is a GABA-B agonist used in the treatment of spastic muscle disorders such as those that accompany patients with spinal cord injuries, multiple sclerosis and amyotrophic lateral sclerosis (aka Lou Gehrig’s Disease). Baclofen works primarily in the spinal cord. Preliminary research suggests that Baclofen may be helpful in reducing cocaine cravings.
Some antihistamines such as hydroxizine (Atarax), (Vistaril, Phenergan) and diphenhydramine (Benadryl) cause drowsiness and are sometimes used as hypnotic (sleep inducing) medications. Their use is not without some risk of relapse in recovering alcoholics, and should only be used with great caution and under the supervision of a physician certified in addiction medicine.
INCREASED MUSCLE MASS AND STRENGTH
INCREASED MOTIVATION AND TRAINING INTENSITY
INCREASED OPTIMISM AND CONFIDENCE
FASTER HEALING FROM INJURY (AND THUS INCREASED TRAINING FREQUENCY)
DECREASED BODY FAT
FEMINIZATION DUE TO INCREASED CIRCULATING ESTROGENS GYNECOMASTIA
RAPID WEIGHT GAIN AND STRIA (“STRETCH MARKS”)
DAMAGE TO TENDONS
DECREASED SPERM COUNT, INFERTILITY
CHANGE IN LIPID PROFILE (INCREASED LDL, DECREASED HDL)
IN ADOLESCENTS: PREMATURE CLOSURE OF EPIPHYSEAL GROWTH PLATES
PERSONALITY CHANGES (IMPULSIVITY, NARCISSISM, LACK OF EMPATHY)
COGNITIVE IMPAIRMENT (DISTRACTIBILITY, CONFUSION, FORGETFULLNESS)
DEPRESSED MOOD (ESP. DURING WITHDRAWAL)
INCREASED CONCENTRATION OF RED BLOOD CELLS
LIVER DISEASE (CHOLESTATIC JAUNDICE, HEPATOCELLULAR ADENOMAS)
COMPLICATIONS OF INJECTION DRUG USE
Anabolic-androgenic steroids (AASs, or steroids) are drugs that (1) build muscle by increasing protein synthesis (“anabolic”), and (2) promote the expression of male sex characteristics because they closely resemble testosterone (“androgenic”). In medicine, AASs are used to treat hormone deficiency diseases such as hypogonadism, Turner’s Syndrome and Kleinfelter’s Syndrome. Anabolic-androgenic steroids differ from catabolic steroids like predisone, which are used in medicine to reduce inflammation.
According to the DEA, there are an estimated one million illicit steroid abusers in the United States. The population of steroid abusers can be divided into three groups: athletes, aesthetes and occupational elites. Athletes use very high doses of steroids (amounts far higher than the body can normally produce) to increase their performance during competitive events. Steroids not only build muscle strength and size, they increase stamina and foster a confident, aggressive frame of mind for competition. Aesthetes use lower doses of steroid in an attempt to improve their appearance by adding body weight and increasing musculature. Occupational elites are those users in specific jobs such as bodyguards, nightclub bouncers, and law enforcement or corrections officers who use steroids in order to project a more intimidating physique. Steroid use is also extraordinarily common in school-age boys and girls – with studies quoting a prevalence of 2.5% to as high as 6.6% in male high-school seniors. This is especially concerning since steroids are primarily administered by injection, and needle-sharing is likely in this high-risk group.
Steroids do not follow the typical patterns of abuse seen with other drugs. There is little immediate reinforcement for the user at the time of administration. Animals do not self-administer steroid drugs like they do cocaine or heroin, and humans cannot distinguish between an injection of steroid and a placebo. The psychological rewards of the drug often come later when the user is exercising or training, or observing the results of such efforts in a mirror, or when the user receives attention and admiration from others due to his/her physique. Many steroid abusers feel a lack of self-esteem if their musculature is not grossly overdeveloped. In this way, anabolic-androgenic steroid addiction contains many of the features observed in other body-dysmorphic disorders such as anorexia or bulimia.
Experienced users know that steroid drugs have to be used carefully to allow for maximal muscle growth while avoiding the unwanted side effects of over-masculinization, while at the same time escaping detection of use by drug testing. To achieve these goals, highly elaborate schedules, meticulous protocols and intricate rituals accompany the illicit use of steroid drugs – often learned and practiced in the complex social cultures of professional athletics, body-building competitions and training gyms. Different brands of steroids are favored for their abilities to produce increased muscle buildup, produce greater strength, enhance recovery after exercise or injury, or harden newly-gained muscle. These fastidious administration schedules and encyclopedic knowledge of steroid physiology are passed from person to person and from group to group.
The use of steroids includes such practices as “cycling,” “stacking” and “pyramiding.” “Cycling” refers to the use of a particular steroid for a period of time (usually two to three months) then stopping and switching to another steroid for a similar period of time. This technique is designed to circumvent the problem of tolerance – the phenomenon that a particular steroid will begin to lose its effectiveness as the user’s body compensates for its artificially high levels. Often these “cycles” will overlap so that the user is taking two or even three different steroids at one time. This “stacking” of the steroid drugs produces greater results while lessening unwanted side effects and tolerance. Steroids cycles are often administered in a “pyramid” dosing schedule – starting small, working up to a peak dose, and then tapering off – timed precisely so that as one steroid schedule is ending another drug pyramid is beginning. These tapering doses are also used to escape detection. In contrast to all other classes of drugs, the effects of steroids can continue long after their administration and even after the drug has cleared from the urine.
Steroids are commonly injected intramuscularly. This avoids the immediate metabolism by the liver of steroids that are taken orally, allowing much greater blood levels of steroid and greater effects. Exogenously administered steroids increase the level of circulating estrogens and may cause female sex characteristics to develop, such as gynecomastia. To decrease this risk of feminization, anti-estrogens are added into the mix.
When heavy users stop taking steroid drugs, a significant withdrawal phenomenon can occur which includes depressed mood,
In addition to steroids, athletes often administer other drugs such as CNS stimulants, opioids, and diuretics that provide additional enhancement of performance, physical appearance, or that combat the side effects of chronic steroid use.
CNS Stimulants such as ephedrine and very high doses of caffeine increase alertness and aggressiveness for competitive events.
Nalbuphine (trade name: Nubain) is a partial opioid agonist used in medicine as an analgesic, but is commonly abused in weightlifting cultures. This opioid is favored over other opioids medications such as hydrocodone for its purported ability to allow athletes to return to training quickly following an injury.
Diuretics such as furosemide (Lasix) and spironolactone are commonly used in medicine to decrease blood pressure by causing the kidneys to excrete more water. These drugs are used by body-builders to give a more “cut” appearance in competition. They are also used to dilute the urine with excess water in the attempt to hide drug use on testing.
Beta-blockers such as Propranolol – used in archery and riflery to decrease heart rate and maximize ability to shoot between beats
Erythropoetin (EPO) is a hormone used by the body to increase the production of red blood cells (RBCs). It can be used by athletes to boost the blood’s the oxygen carrying capacity, which translates into an advantage of increased endurance during competitive events, especially at higher altitudes. Synthetic erythropoetin is made via recombinant DNA technology and sold commercially as Epogen by the pharmaceutical corporation Amgen.
Another tactic employed by athletes is to purposefully remove one’s own blood (called “auto-phlebotomy”) and store it for transfusion back to the donor (called “auto-transfusion”) prior to a competitive event, boosting endurance. This practice is known as “blood packing,” and is particularly hard to detect since many well-conditioned athletes already have a high concentration of red blood cells.