drug addiction and its negative effects essay

Drug Abuse and Its Negative Effects Essay

Introduction.

One of the consequences of using drugs is, eventually, an individual becoming addicted. Addiction refers to a neuropsychological disorder that involves persistently feeling an urge to engage in particular behaviors despite the significant harm or negative effects. The psychology that explains addiction covers many areas, such as an illness or personal problem, an effect of someone’s lifestyle, family history, or socioeconomic demographics. This paper aims to highlight what the field of psychology says about the negative effects of drugs and why people continue using despite the consequences.

Using drugs once does not necessarily mean someone will never consume them again. In most cases, the drugs contain elements that can cause a person to become addicted. From a psychological perspective, it is important to understand how people enter into addiction. At the root of addictive behavior is a level of emotional stress deeply hidden within someone’s subconscious mind, and addressing it becomes a challenge. To relieve stress, pleasure is discovered in excess (Bechara 100). An example is when people choose to drink alcohol to ease their pain and ultimately find fun.

Stopping the behavior is a danger to someone’s mental state as they fear returning thoughts of the initial source of emotional stress. When a person is addicted, it suggests they lack healthy coping methods for the problem. The only mechanisms are distracting as well as unhealthy such as substance usage. Individuals dealing with addiction do not care about what matters since what is important to them is the desire to do something when that stress appears (Bechara 101). Some can stop their behaviors as their emotional stress does not manifest as among the addictive behaviors. Meanwhile, for others, their drug usage indicates an issue they may not have known and needs treatment. This leads to associative learning, which refers to learning to do something according to a novel stimulus.

Associative Learning

It is regarded as associative learning when an individual finds and takes drugs and ultimately gets high. The concept can be further explained using Ivan Pavlov’s experiment, where he rang a bell to call a dog and then rewarded it with food (Fouyssac and David 3015). A specific part of the brain controls associative learning, which it does via a neurotransmitter named dopamine. Dopamine is produced naturally by the brain when an individual does something rewarding or pleasurable.

The dopamine effect is a survival mechanism whereby eating or drinking feels good. It ensures continuity of life, family, and species in general. The element’s production is among the key drivers behind sex since, as much as the act is rewarding and pleasurable simultaneously, it is needed for survival (Fouyssac and David 3015). The main effect is that it creates a memory of the experience, which pushes people to seek the feeling again. People forget about the negative effects of drugs due to the moments of pleasure. As mentioned earlier, it is most likely that someone who uses the drug once will consume it again. The feeling established, regardless of how long, is enough to convince a person to forget everything they know concerning the negative effects and pursue a minute or two of a great time.

The paper has highlighted what the field of psychology says about the negative effects of drugs and why people continue using despite the consequences. It has been established that, in most cases, individuals experience addiction due to the pursuit of stress relief. Using the logic of the dopamine effect, once someone experiences something pleasurable or rewarding to them, they are most likely to pursue that feeling again. Eventually, it becomes impossible to convince them against the drugs as their desire to end their problem is more than the need to remain healthy.

Works Cited

Bechara, Antoine, et al. “A Neurobehavioral Approach to Addiction: Implications for the Opioid Epidemic and the Psychology of Addiction.” Psychological Science in the Public Interest, vol. 20, no. 2, 2019, p. 96–127.

Fouyssac, Maxime, and David Belin. “Beyond Drug‐Induced Alteration of Glutamate Homeostasis, Astrocytes May Contribute to Dopamine‐Dependent Intrastriatal Functional Shifts That Underlie the Development of Drug Addiction: A Working Hypothesis.” European Journal of Neuroscience, vol. 50, no. 6, 2019, p. 3014-3027.

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• Patient Care & Health Information
• Diseases & Conditions
• Drug addiction (substance use disorder)

Drug addiction, also called substance use disorder, is a disease that affects a person's brain and behavior and leads to an inability to control the use of a legal or illegal drug or medicine. Substances such as alcohol, marijuana and nicotine also are considered drugs. When you're addicted, you may continue using the drug despite the harm it causes.

Drug addiction can start with experimental use of a recreational drug in social situations, and, for some people, the drug use becomes more frequent. For others, particularly with opioids, drug addiction begins when they take prescribed medicines or receive them from others who have prescriptions.

The risk of addiction and how fast you become addicted varies by drug. Some drugs, such as opioid painkillers, have a higher risk and cause addiction more quickly than others.

As time passes, you may need larger doses of the drug to get high. Soon you may need the drug just to feel good. As your drug use increases, you may find that it's increasingly difficult to go without the drug. Attempts to stop drug use may cause intense cravings and make you feel physically ill. These are called withdrawal symptoms.

Help from your health care provider, family, friends, support groups or an organized treatment program can help you overcome your drug addiction and stay drug-free.

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Drug addiction symptoms or behaviors include, among others:

• Feeling that you have to use the drug regularly — daily or even several times a day
• Having intense urges for the drug that block out any other thoughts
• Over time, needing more of the drug to get the same effect
• Taking larger amounts of the drug over a longer period of time than you intended
• Making certain that you maintain a supply of the drug
• Spending money on the drug, even though you can't afford it
• Not meeting obligations and work responsibilities, or cutting back on social or recreational activities because of drug use
• Continuing to use the drug, even though you know it's causing problems in your life or causing you physical or psychological harm
• Doing things to get the drug that you normally wouldn't do, such as stealing
• Driving or doing other risky activities when you're under the influence of the drug
• Spending a good deal of time getting the drug, using the drug or recovering from the effects of the drug
• Failing in your attempts to stop using the drug
• Experiencing withdrawal symptoms when you attempt to stop taking the drug

Recognizing unhealthy drug use in family members

Sometimes it's difficult to distinguish normal teenage moodiness or anxiety from signs of drug use. Possible signs that your teenager or other family member is using drugs include:

• Problems at school or work — frequently missing school or work, a sudden disinterest in school activities or work, or a drop in grades or work performance
• Physical health issues — lack of energy and motivation, weight loss or gain, or red eyes
• Neglected appearance — lack of interest in clothing, grooming or looks
• Changes in behavior — major efforts to bar family members from entering the teenager's room or being secretive about going out with friends; or drastic changes in behavior and in relationships with family and friends
• Money issues — sudden requests for money without a reasonable explanation; or your discovery that money is missing or has been stolen or that items have disappeared from your home, indicating maybe they're being sold to support drug use

Recognizing signs of drug use or intoxication

Signs and symptoms of drug use or intoxication may vary, depending on the type of drug. Below you'll find several examples.

Marijuana, hashish and other cannabis-containing substances

People use cannabis by smoking, eating or inhaling a vaporized form of the drug. Cannabis often precedes or is used along with other substances, such as alcohol or illegal drugs, and is often the first drug tried.

Signs and symptoms of recent use can include:

• A sense of euphoria or feeling "high"
• A heightened sense of visual, auditory and taste perception
• Increased blood pressure and heart rate
• Decreased coordination
• Difficulty concentrating or remembering
• Slowed reaction time
• Anxiety or paranoid thinking
• Cannabis odor on clothes or yellow fingertips
• Major cravings for certain foods at unusual times

Long-term use is often associated with:

• Decreased mental sharpness
• Poor performance at school or at work
• Ongoing cough and frequent lung infections

K2, Spice and bath salts

Two groups of synthetic drugs — synthetic cannabinoids and substituted or synthetic cathinones — are illegal in most states. The effects of these drugs can be dangerous and unpredictable, as there is no quality control and some ingredients may not be known.

Synthetic cannabinoids, also called K2 or Spice, are sprayed on dried herbs and then smoked, but can be prepared as an herbal tea. A liquid form can be vaporized in electronic cigarettes. Despite manufacturer claims, these are chemical compounds rather than "natural" or harmless products. These drugs can produce a "high" similar to marijuana and have become a popular but dangerous alternative.

• Elevated mood
• An altered sense of visual, auditory and taste perception
• Extreme anxiety or agitation
• Hallucinations
• Increased heart rate and blood pressure or heart attack
• Violent behavior

Substituted cathinones, also called "bath salts," are mind-altering (psychoactive) substances similar to amphetamines such as ecstasy (MDMA) and cocaine. Packages are often labeled as other products to avoid detection.

Despite the name, these are not bath products such as Epsom salts. Substituted cathinones can be eaten, snorted, inhaled or injected and are highly addictive. These drugs can cause severe intoxication, which results in dangerous health effects or even death.

• Feeling "high"
• Increased sociability
• Increased energy and agitation
• Increased sex drive
• Increased heart rate and blood pressure
• Problems thinking clearly
• Loss of muscle control
• Panic attacks
• Psychotic and violent behavior

Barbiturates, benzodiazepines and hypnotics

Barbiturates, benzodiazepines and hypnotics are prescription central nervous system depressants. They're often used and misused in search for a sense of relaxation or a desire to "switch off" or forget stress-related thoughts or feelings.

• Barbiturates. An example is phenobarbital.
• Benzodiazepines. Examples include sedatives, such as diazepam (Valium), alprazolam (Xanax), lorazepam (Ativan), clonazepam (Klonopin) and chlordiazepoxide (Librium).
• Hypnotics. Examples include prescription sleeping medicines such as zolpidem (Ambien) and zaleplon (Sonata).
• Slurred speech
• Lack of coordination
• Irritability or changes in mood
• Problems concentrating or thinking clearly
• Memory problems
• Involuntary eye movements
• Lack of inhibition
• Slowed breathing and reduced blood pressure
• Falls or accidents

Meth, cocaine and other stimulants

Stimulants include amphetamines, meth (methamphetamine), cocaine, methylphenidate (Ritalin, Concerta, others) and amphetamine-dextroamphetamine (Adderall XR, Mydayis). They're often used and misused in search of a "high," or to boost energy, to improve performance at work or school, or to lose weight or control appetite.

• Feeling of happy excitement and too much confidence
• Increased alertness
• Increased energy and restlessness
• Behavior changes or aggression
• Rapid or rambling speech
• Larger than usual pupils, the black circles in the middle of the eyes
• Confusion, delusions and hallucinations
• Irritability, anxiety or paranoia
• Changes in heart rate, blood pressure and body temperature
• Nausea or vomiting with weight loss
• Poor judgment
• Nasal congestion and damage to the mucous membrane of the nose (if snorting drugs)
• Mouth sores, gum disease and tooth decay from smoking drugs ("meth mouth")
• Depression as the drug wears off

Club drugs are commonly used at clubs, concerts and parties. Examples include methylenedioxymethamphetamine, also called MDMA, ecstasy or molly, and gamma-hydroxybutyric acid, known as GHB. Other examples include ketamine and flunitrazepam or Rohypnol — a brand used outside the U.S. — also called roofie. These drugs are not all in the same category, but they share some similar effects and dangers, including long-term harmful effects.

Because GHB and flunitrazepam can cause sedation, muscle relaxation, confusion and memory loss, the potential for sexual misconduct or sexual assault is associated with the use of these drugs.

Signs and symptoms of use of club drugs can include:

• Larger than usual pupils
• Chills and sweating
• Involuntary shaking (tremors)
• Behavior changes
• Muscle cramping and teeth clenching
• Muscle relaxation, poor coordination or problems moving
• Reduced inhibitions
• Heightened or altered sense of sight, sound and taste
• Memory problems or loss of memory
• Reduced consciousness
• Increased or decreased heart rate and blood pressure

Hallucinogens

Use of hallucinogens can produce different signs and symptoms, depending on the drug. The most common hallucinogens are lysergic acid diethylamide (LSD) and phencyclidine (PCP).

LSD use may cause:

• Greatly reduced perception of reality, for example, interpreting input from one of your senses as another, such as hearing colors
• Impulsive behavior
• Rapid shifts in emotions
• Permanent mental changes in perception
• Rapid heart rate and high blood pressure
• Flashbacks, a reexperience of the hallucinations — even years later

PCP use may cause:

• A feeling of being separated from your body and surroundings
• Problems with coordination and movement
• Aggressive, possibly violent behavior
• Lack of pain sensation
• Increase in blood pressure and heart rate
• Problems with thinking and memory
• Problems speaking
• Intolerance to loud noise
• Sometimes seizures or coma

Signs and symptoms of inhalant use vary, depending on the substance. Some commonly inhaled substances include glue, paint thinners, correction fluid, felt tip marker fluid, gasoline, cleaning fluids and household aerosol products. Due to the toxic nature of these substances, users may develop brain damage or sudden death.

Signs and symptoms of use can include:

• Possessing an inhalant substance without a reasonable explanation
• Brief happy excitement
• Behaving as if drunk
• Reduced ability to keep impulses under control
• Aggressive behavior or eagerness to fight
• Nausea or vomiting
• Appearing under the influence of drugs, with slurred speech, slow movements and poor coordination
• Irregular heartbeats
• Lingering odor of inhalant material
• Rash around the nose and mouth

Opioid painkillers

Opioids are narcotic, painkilling drugs produced from opium or made synthetically. This class of drugs includes, among others, heroin, morphine, codeine, methadone, fentanyl and oxycodone.

Sometimes called the "opioid epidemic," addiction to opioid prescription pain medicines has reached an alarming rate across the United States. Some people who've been using opioids over a long period of time may need physician-prescribed temporary or long-term drug substitution during treatment.

Signs and symptoms of narcotic use and dependence can include:

• A sense of feeling "high"
• Reduced sense of pain
• Agitation, drowsiness or sedation
• Problems with attention and memory
• Pupils that are smaller than usual
• Lack of awareness or inattention to surrounding people and things
• Problems with coordination
• Constipation
• Runny nose or nose sores (if snorting drugs)
• Needle marks (if injecting drugs)

When to see a doctor

If your drug use is out of control or causing problems, get help. The sooner you seek help, the greater your chances for a long-term recovery. Talk with your health care provider or see a mental health provider, such as a doctor who specializes in addiction medicine or addiction psychiatry, or a licensed alcohol and drug counselor.

Make an appointment to see a provider if:

• You can't stop using a drug
• You continue using the drug despite the harm it causes
• Your drug use has led to unsafe behavior, such as sharing needles or unprotected sex
• You think you may be having withdrawal symptoms after stopping drug use

If you're not ready to approach a health care provider or mental health professional, help lines or hotlines may be a good place to learn about treatment. You can find these lines listed on the internet or in the phone book.

When to seek emergency help

Seek emergency help if you or someone you know has taken a drug and:

• May have overdosed
• Shows changes in consciousness
• Has trouble breathing
• Has seizures or convulsions
• Has signs of a possible heart attack, such as chest pain or pressure
• Has any other troublesome physical or psychological reaction to use of the drug

Staging an intervention

People struggling with addiction usually deny they have a problem and hesitate to seek treatment. An intervention presents a loved one with a structured opportunity to make changes before things get even worse and can motivate someone to seek or accept help.

It's important to plan an intervention carefully. It may be done by family and friends in consultation with a health care provider or mental health professional such as a licensed alcohol and drug counselor, or directed by an intervention professional. It involves family and friends and sometimes co-workers, clergy or others who care about the person struggling with addiction.

During the intervention, these people gather together to have a direct, heart-to-heart conversation with the person about the consequences of addiction. Then they ask the person to accept treatment.

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Like many mental health disorders, several factors may contribute to development of drug addiction. The main factors are:

• Environment. Environmental factors, including your family's beliefs and attitudes and exposure to a peer group that encourages drug use, seem to play a role in initial drug use.
• Genetics. Once you've started using a drug, the development into addiction may be influenced by inherited (genetic) traits, which may delay or speed up the disease progression.

Changes in the brain

Physical addiction appears to occur when repeated use of a drug changes the way your brain feels pleasure. The addicting drug causes physical changes to some nerve cells (neurons) in your brain. Neurons use chemicals called neurotransmitters to communicate. These changes can remain long after you stop using the drug.

Risk factors

People of any age, sex or economic status can become addicted to a drug. Certain factors can affect the likelihood and speed of developing an addiction:

• Family history of addiction. Drug addiction is more common in some families and likely involves an increased risk based on genes. If you have a blood relative, such as a parent or sibling, with alcohol or drug addiction, you're at greater risk of developing a drug addiction.
• Mental health disorder. If you have a mental health disorder such as depression, attention-deficit/hyperactivity disorder (ADHD) or post-traumatic stress disorder, you're more likely to become addicted to drugs. Using drugs can become a way of coping with painful feelings, such as anxiety, depression and loneliness, and can make these problems even worse.
• Peer pressure. Peer pressure is a strong factor in starting to use and misuse drugs, particularly for young people.
• Lack of family involvement. Difficult family situations or lack of a bond with your parents or siblings may increase the risk of addiction, as can a lack of parental supervision.
• Early use. Using drugs at an early age can cause changes in the developing brain and increase the likelihood of progressing to drug addiction.
• Taking a highly addictive drug. Some drugs, such as stimulants, cocaine or opioid painkillers, may result in faster development of addiction than other drugs. Smoking or injecting drugs can increase the potential for addiction. Taking drugs considered less addicting — so-called "light drugs" — can start you on a pathway of drug use and addiction.

Complications

Drug use can have significant and damaging short-term and long-term effects. Taking some drugs can be particularly risky, especially if you take high doses or combine them with other drugs or alcohol. Here are some examples.

• Methamphetamine, opiates and cocaine are highly addictive and cause multiple short-term and long-term health consequences, including psychotic behavior, seizures or death due to overdose. Opioid drugs affect the part of the brain that controls breathing, and overdose can result in death. Taking opioids with alcohol increases this risk.
• GHB and flunitrazepam may cause sedation, confusion and memory loss. These so-called "date rape drugs" are known to impair the ability to resist unwanted contact and recollection of the event. At high doses, they can cause seizures, coma and death. The danger increases when these drugs are taken with alcohol.
• MDMA — also known as molly or ecstasy — can interfere with the body's ability to regulate temperature. A severe spike in body temperature can result in liver, kidney or heart failure and death. Other complications can include severe dehydration, leading to seizures. Long-term, MDMA can damage the brain.
• One particular danger of club drugs is that the liquid, pill or powder forms of these drugs available on the street often contain unknown substances that can be harmful, including other illegally manufactured or pharmaceutical drugs.
• Due to the toxic nature of inhalants, users may develop brain damage of different levels of severity. Sudden death can occur even after a single exposure.

Other life-changing complications

Dependence on drugs can create a number of dangerous and damaging complications, including:

• Getting an infectious disease. People who are addicted to a drug are more likely to get an infectious disease, such as HIV , either through unsafe sex or by sharing needles with others.
• Other health problems. Drug addiction can lead to a range of both short-term and long-term mental and physical health problems. These depend on what drug is taken.
• Accidents. People who are addicted to drugs are more likely to drive or do other dangerous activities while under the influence.
• Suicide. People who are addicted to drugs die by suicide more often than people who aren't addicted.
• Family problems. Behavioral changes may cause relationship or family conflict and custody issues.
• Work issues. Drug use can cause declining performance at work, absenteeism and eventual loss of employment.
• Problems at school. Drug use can negatively affect academic performance and motivation to excel in school.
• Legal issues. Legal problems are common for drug users and can stem from buying or possessing illegal drugs, stealing to support the drug addiction, driving while under the influence of drugs or alcohol, or disputes over child custody.
• Financial problems. Spending money to support drug use takes away money from other needs, could lead to debt, and can lead to illegal or unethical behaviors.

The best way to prevent an addiction to a drug is not to take the drug at all. If your health care provider prescribes a drug with the potential for addiction, use care when taking the drug and follow instructions.

Health care providers should prescribe these medicines at safe doses and amounts and monitor their use so that you're not given too great a dose or for too long a time. If you feel you need to take more than the prescribed dose of a medicine, talk to your health care provider.

Preventing drug misuse in children and teenagers

Take these steps to help prevent drug misuse in your children and teenagers:

• Communicate. Talk to your children about the risks of drug use and misuse.
• Listen. Be a good listener when your children talk about peer pressure and be supportive of their efforts to resist it.
• Set a good example. Don't misuse alcohol or addictive drugs. Children of parents who misuse drugs are at greater risk of drug addiction.
• Strengthen the bond. Work on your relationship with your children. A strong, stable bond between you and your child will reduce your child's risk of using or misusing drugs.

Preventing a relapse

Once you've been addicted to a drug, you're at high risk of falling back into a pattern of addiction. If you do start using the drug, it's likely you'll lose control over its use again — even if you've had treatment and you haven't used the drug for some time.

• Follow your treatment plan. Monitor your cravings. It may seem like you've recovered and you don't need to keep taking steps to stay drug-free. But your chances of staying drug-free will be much higher if you continue seeing your therapist or counselor, going to support group meetings and taking prescribed medicine.
• Avoid high-risk situations. Don't go back to the neighborhood where you used to get your drugs. And stay away from your old drug crowd.
• Get help immediately if you use the drug again. If you start using the drug again, talk to your health care provider, your mental health provider or someone else who can help you right away.

Drug addiction (substance use disorder) care at Mayo Clinic

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• Poppy seed tea: Beneficial or dangerous?

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• Published: 22 February 2021

Addiction as a brain disease revised: why it still matters, and the need for consilience

• Markus Heilig 1 ,
• James MacKillop   ORCID: orcid.org/0000-0003-4118-9500 2 , 3 ,
• Diana Martinez 4 ,
• Jürgen Rehm   ORCID: orcid.org/0000-0001-5665-0385 5 , 6 , 7 , 8 ,
• Lorenzo Leggio   ORCID: orcid.org/0000-0001-7284-8754 9 &
• Louk J. M. J. Vanderschuren   ORCID: orcid.org/0000-0002-5379-0363 10  

Neuropsychopharmacology volume  46 ,  pages 1715–1723 ( 2021 ) Cite this article

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A Correspondence to this article was published on 03 May 2021

The view that substance addiction is a brain disease, although widely accepted in the neuroscience community, has become subject to acerbic criticism in recent years. These criticisms state that the brain disease view is deterministic, fails to account for heterogeneity in remission and recovery, places too much emphasis on a compulsive dimension of addiction, and that a specific neural signature of addiction has not been identified. We acknowledge that some of these criticisms have merit, but assert that the foundational premise that addiction has a neurobiological basis is fundamentally sound. We also emphasize that denying that addiction is a brain disease is a harmful standpoint since it contributes to reducing access to healthcare and treatment, the consequences of which are catastrophic. Here, we therefore address these criticisms, and in doing so provide a contemporary update of the brain disease view of addiction. We provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, we argue that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, we propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.

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The neurobiology of drug addiction: cross-species insights into the dysfunction and recovery of the prefrontal cortex

Introduction.

Close to a quarter of a century ago, then director of the US National Institute on Drug Abuse Alan Leshner famously asserted that “addiction is a brain disease”, articulated a set of implications of this position, and outlined an agenda for realizing its promise [ 1 ]. The paper, now cited almost 2000 times, put forward a position that has been highly influential in guiding the efforts of researchers, and resource allocation by funding agencies. A subsequent 2000 paper by McLellan et al. [ 2 ] examined whether data justify distinguishing addiction from other conditions for which a disease label is rarely questioned, such as diabetes, hypertension or asthma. It concluded that neither genetic risk, the role of personal choices, nor the influence of environmental factors differentiated addiction in a manner that would warrant viewing it differently; neither did relapse rates, nor compliance with treatment. The authors outlined an agenda closely related to that put forward by Leshner, but with a more clinical focus. Their conclusion was that addiction should be insured, treated, and evaluated like other diseases. This paper, too, has been exceptionally influential by academic standards, as witnessed by its ~3000 citations to date. What may be less appreciated among scientists is that its impact in the real world of addiction treatment has remained more limited, with large numbers of patients still not receiving evidence-based treatments.

In recent years, the conceptualization of addiction as a brain disease has come under increasing criticism. When first put forward, the brain disease view was mainly an attempt to articulate an effective response to prevailing nonscientific, moralizing, and stigmatizing attitudes to addiction. According to these attitudes, addiction was simply the result of a person’s moral failing or weakness of character, rather than a “real” disease [ 3 ]. These attitudes created barriers for people with substance use problems to access evidence-based treatments, both those available at the time, such as opioid agonist maintenance, cognitive behavioral therapy-based relapse prevention, community reinforcement or contingency management, and those that could result from research. To promote patient access to treatments, scientists needed to argue that there is a biological basis beneath the challenging behaviors of individuals suffering from addiction. This argument was particularly targeted to the public, policymakers and health care professionals, many of whom held that since addiction was a misery people brought upon themselves, it fell beyond the scope of medicine, and was neither amenable to treatment, nor warranted the use of taxpayer money.

Present-day criticism directed at the conceptualization of addiction as a brain disease is of a very different nature. It originates from within the scientific community itself, and asserts that this conceptualization is neither supported by data, nor helpful for people with substance use problems [ 4 , 5 , 6 , 7 , 8 ]. Addressing these critiques requires a very different perspective, and is the objective of our paper. We readily acknowledge that in some cases, recent critiques of the notion of addiction as a brain disease as postulated originally have merit, and that those critiques require the postulates to be re-assessed and refined. In other cases, we believe the arguments have less validity, but still provide an opportunity to update the position of addiction as a brain disease. Our overarching concern is that questionable arguments against the notion of addiction as a brain disease may harm patients, by impeding access to care, and slowing development of novel treatments.

A premise of our argument is that any useful conceptualization of addiction requires an understanding both of the brains involved, and of environmental factors that interact with those brains [ 9 ]. These environmental factors critically include availability of drugs, but also of healthy alternative rewards and opportunities. As we will show, stating that brain mechanisms are critical for understanding and treating addiction in no way negates the role of psychological, social and socioeconomic processes as both causes and consequences of substance use. To reflect this complex nature of addiction, we have assembled a team with expertise that spans from molecular neuroscience, through animal models of addiction, human brain imaging, clinical addiction medicine, to epidemiology. What brings us together is a passionate commitment to improving the lives of people with substance use problems through science and science-based treatments, with empirical evidence as the guiding principle.

To achieve this goal, we first discuss the nature of the disease concept itself, and why we believe it is important for the science and treatment of addiction. This is followed by a discussion of the main points raised when the notion of addiction as a brain disease has come under criticism. Key among those are claims that spontaneous remission rates are high; that a specific brain pathology is lacking; and that people suffering from addiction, rather than behaving “compulsively”, in fact show a preserved ability to make informed and advantageous choices. In the process of discussing these issues, we also address the common criticism that viewing addiction as a brain disease is a fully deterministic theory of addiction. For our argument, we use the term “addiction” as originally used by Leshner [ 1 ]; in Box  1 , we map out and discuss how this construct may relate to the current diagnostic categories, such as Substance Use Disorder (SUD) and its different levels of severity (Fig.  1) .

Risky (hazardous) substance use refers to quantity/frequency indicators of consumption; SUD refers to individuals who meet criteria for a DSM-5 diagnosis (mild, moderate, or severe); and addiction refers to individuals who exhibit persistent difficulties with self-regulation of drug consumption. Among high-risk individuals, a subgroup will meet criteria for SUD and, among those who have an SUD, a further subgroup would be considered to be addicted to the drug. However, the boundary for addiction is intentionally blurred to reflect that the dividing line for defining addiction within the category of SUD remains an open empirical question.

Box 1 What’s in a name? Differentiating hazardous use, substance use disorder, and addiction

Although our principal focus is on the brain disease model of addiction, the definition of addiction itself is a source of ambiguity. Here, we provide a perspective on the major forms of terminology in the field.

Hazardous Substance Use

Hazardous (risky) substance use refers to quantitative levels of consumption that increase an individual’s risk for adverse health consequences. In practice, this pertains to alcohol use [ 110 , 111 ]. Clinically, alcohol consumption that exceeds guidelines for moderate drinking has been used to prompt brief interventions or referral for specialist care [ 112 ]. More recently, a reduction in these quantitative levels has been validated as treatment endpoints [ 113 ].

Substance Use Disorder

SUD refers to the DSM-5 diagnosis category that encompasses significant impairment or distress resulting from specific categories of psychoactive drug use. The diagnosis of SUD is operationalized as 2 or more of 11 symptoms over the past year. As a result, the diagnosis is heterogenous, with more than 1100 symptom permutations possible. The diagnosis in DSM-5 is the result of combining two diagnoses from the DSM-IV, abuse and dependence, which proved to be less valid than a single dimensional approach [ 114 ]. Critically, SUD includes three levels of severity: mild (2–3 symptoms), moderate (4–5 symptoms), and severe (6+ symptoms). The International Classification of Diseases (ICD) system retains two diagnoses, harmful use (lower severity) and substance dependence (higher severity).

Addiction is a natural language concept, etymologically meaning enslavement, with the contemporary meaning traceable to the Middle and Late Roman Republic periods [ 115 ]. As a scientific construct, drug addiction can be defined as a state in which an individual exhibits an inability to self-regulate consumption of a substance, although it does not have an operational definition. Regarding clinical diagnosis, as it is typically used in scientific and clinical parlance, addiction is not synonymous with the simple presence of SUD. Nowhere in DSM-5 is it articulated that the diagnostic threshold (or any specific number/type of symptoms) should be interpreted as reflecting addiction, which inherently connotes a high degree of severity. Indeed, concerns were raised about setting the diagnostic standard too low because of the issue of potentially conflating a low-severity SUD with addiction [ 116 ]. In scientific and clinical usage, addiction typically refers to individuals at a moderate or high severity of SUD. This is consistent with the fact that moderate-to-severe SUD has the closest correspondence with the more severe diagnosis in ICD [ 117 , 118 , 119 ]. Nonetheless, akin to the undefined overlap between hazardous use and SUD, the field has not identified the exact thresholds of SUD symptoms above which addiction would be definitively present.

Integration

The ambiguous relationships among these terms contribute to misunderstandings and disagreements. Figure 1 provides a simple working model of how these terms overlap. Fundamentally, we consider that these terms represent successive dimensions of severity, clinical “nesting dolls”. Not all individuals consuming substances at hazardous levels have an SUD, but a subgroup do. Not all individuals with a SUD are addicted to the drug in question, but a subgroup are. At the severe end of the spectrum, these domains converge (heavy consumption, numerous symptoms, the unambiguous presence of addiction), but at low severity, the overlap is more modest. The exact mapping of addiction onto SUD is an open empirical question, warranting systematic study among scientists, clinicians, and patients with lived experience. No less important will be future research situating our definition of SUD using more objective indicators (e.g., [ 55 , 120 ]), brain-based and otherwise, and more precisely in relation to clinical needs [ 121 ]. Finally, such work should ultimately be codified in both the DSM and ICD systems to demarcate clearly where the attribution of addiction belongs within the clinical nosology, and to foster greater clarity and specificity in scientific discourse.

What is a disease?

In his classic 1960 book “The Disease Concept of Alcoholism”, Jellinek noted that in the alcohol field, the debate over the disease concept was plagued by too many definitions of “alcoholism” and too few definitions of “disease” [ 10 ]. He suggested that the addiction field needed to follow the rest of medicine in moving away from viewing disease as an “entity”, i.e., something that has “its own independent existence, apart from other things” [ 11 ]. To modern medicine, he pointed out, a disease is simply a label that is agreed upon to describe a cluster of substantial, deteriorating changes in the structure or function of the human body, and the accompanying deterioration in biopsychosocial functioning. Thus, he concluded that alcoholism can simply be defined as changes in structure or function of the body due to drinking that cause disability or death. A disease label is useful to identify groups of people with commonly co-occurring constellations of problems—syndromes—that significantly impair function, and that lead to clinically significant distress, harm, or both. This convention allows a systematic study of the condition, and of whether group members benefit from a specific intervention.

It is not trivial to delineate the exact category of harmful substance use for which a label such as addiction is warranted (See Box  1 ). Challenges to diagnostic categorization are not unique to addiction, however. Throughout clinical medicine, diagnostic cut-offs are set by consensus, commonly based on an evolving understanding of thresholds above which people tend to benefit from available interventions. Because assessing benefits in large patient groups over time is difficult, diagnostic thresholds are always subject to debate and adjustments. It can be debated whether diagnostic thresholds “merely” capture the extreme of a single underlying population, or actually identify a subpopulation that is at some level distinct. Resolving this issue remains challenging in addiction, but once again, this is not different from other areas of medicine [see e.g., [ 12 ] for type 2 diabetes]. Longitudinal studies that track patient trajectories over time may have a better ability to identify subpopulations than cross-sectional assessments [ 13 ].

By this pragmatic, clinical understanding of the disease concept, it is difficult to argue that “addiction” is unjustified as a disease label. Among people who use drugs or alcohol, some progress to using with a quantity and frequency that results in impaired function and often death, making substance use a major cause of global disease burden [ 14 ]. In these people, use occurs with a pattern that in milder forms may be challenging to capture by current diagnostic criteria (See Box  1 ), but is readily recognized by patients, their families and treatment providers when it reaches a severity that is clinically significant [see [ 15 ] for a classical discussion]. In some cases, such as opioid addiction, those who receive the diagnosis stand to obtain some of the greatest benefits from medical treatments in all of clinical medicine [ 16 , 17 ]. Although effect sizes of available treatments are more modest in nicotine [ 18 ] and alcohol addiction [ 19 ], the evidence supporting their efficacy is also indisputable. A view of addiction as a disease is justified, because it is beneficial: a failure to diagnose addiction drastically increases the risk of a failure to treat it [ 20 ].

Of course, establishing a diagnosis is not a requirement for interventions to be meaningful. People with hazardous or harmful substance use who have not (yet) developed addiction should also be identified, and interventions should be initiated to address their substance-related risks. This is particularly relevant for alcohol, where even in the absence of addiction, use is frequently associated with risks or harm to self, e.g., through cardiovascular disease, liver disease or cancer, and to others, e.g., through accidents or violence [ 21 ]. Interventions to reduce hazardous or harmful substance use in people who have not developed addiction are in fact particularly appealing. In these individuals, limited interventions are able to achieve robust and meaningful benefits [ 22 ], presumably because patterns of misuse have not yet become entrenched.

Thus, as originally pointed out by McLellan and colleagues, most of the criticisms of addiction as a disease could equally be applied to other medical conditions [ 2 ]. This type of criticism could also be applied to other psychiatric disorders, and that has indeed been the case historically [ 23 , 24 ]. Today, there is broad consensus that those criticisms were misguided. Few, if any healthcare professionals continue to maintain that schizophrenia, rather than being a disease, is a normal response to societal conditions. Why, then, do people continue to question if addiction is a disease, but not whether schizophrenia, major depressive disorder or post-traumatic stress disorder are diseases? This is particularly troubling given the decades of data showing high co-morbidity of addiction with these conditions [ 25 , 26 ]. We argue that it comes down to stigma. Dysregulated substance use continues to be perceived as a self-inflicted condition characterized by a lack of willpower, thus falling outside the scope of medicine and into that of morality [ 3 ].

Chronic and relapsing, developmentally-limited, or spontaneously remitting?

Much of the critique targeted at the conceptualization of addiction as a brain disease focuses on its original assertion that addiction is a chronic and relapsing condition. Epidemiological data are cited in support of the notion that large proportions of individuals achieve remission [ 27 ], frequently without any formal treatment [ 28 , 29 ] and in some cases resuming low risk substance use [ 30 ]. For instance, based on data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) study [ 27 ], it has been pointed out that a significant proportion of people with an addictive disorder quit each year, and that most afflicted individuals ultimately remit. These spontaneous remission rates are argued to invalidate the concept of a chronic, relapsing disease [ 4 ].

Interpreting these and similar data is complicated by several methodological and conceptual issues. First, people may appear to remit spontaneously because they actually do, but also because of limited test–retest reliability of the diagnosis [ 31 ]. For instance, using a validated diagnostic interview and trained interviewers, the Collaborative Studies on Genetics of Alcoholism examined the likelihood that an individual diagnosed with a lifetime history of substance dependence would retain this classification after 5 years. This is obviously a diagnosis that, once met, by definition cannot truly remit. Lifetime alcohol dependence was indeed stable in individuals recruited from addiction treatment units, ~90% for women, and 95% for men. In contrast, in a community-based sample similar to that used in the NESARC [ 27 ], stability was only ~30% and 65% for women and men, respectively. The most important characteristic that determined diagnostic stability was severity. Diagnosis was stable in severe, treatment-seeking cases, but not in general population cases of alcohol dependence.

These data suggest that commonly used diagnostic criteria alone are simply over-inclusive for a reliable, clinically meaningful diagnosis of addiction. They do identify a core group of treatment seeking individuals with a reliable diagnosis, but, if applied to nonclinical populations, also flag as “cases” a considerable halo of individuals for whom the diagnostic categorization is unreliable. Any meaningful discussion of remission rates needs to take this into account, and specify which of these two populations that is being discussed. Unfortunately, the DSM-5 has not made this task easier. With only 2 out of 11 symptoms being sufficient for a diagnosis of SUD, it captures under a single diagnostic label individuals in a “mild” category, whose diagnosis is likely to have very low test–retest reliability, and who are unlikely to exhibit a chronic relapsing course, together with people at the severe end of the spectrum, whose diagnosis is reliable, many of whom do show a chronic relapsing course.

The NESARC data nevertheless show that close to 10% of people in the general population who are diagnosed with alcohol addiction (here equated with DSM-IV “dependence” used in the NESARC study) never remitted throughout their participation in the survey. The base life-time prevalence of alcohol dependence in NESARC was 12.5% [ 32 ]. Thus, the data cited against the concept of addiction as a chronic relapsing disease in fact indicate that over 1% of the US population develops an alcohol-related condition that is associated with high morbidity and mortality, and whose chronic and/or relapsing nature cannot be disputed, since it does not remit.

Secondly, the analysis of NESARC data [ 4 , 27 ] omits opioid addiction, which, together with alcohol and tobacco, is the largest addiction-related public health problem in the US [ 33 ]. This is probably the addictive condition where an analysis of cumulative evidence most strikingly supports the notion of a chronic disorder with frequent relapses in a large proportion of people affected [ 34 ]. Of course, a large number of people with opioid addiction are unable to express the chronic, relapsing course of their disease, because over the long term, their mortality rate is about 15 times greater than that of the general population [ 35 ]. However, even among those who remain alive, the prevalence of stable abstinence from opioid use after 10–30 years of observation is <30%. Remission may not always require abstinence, for instance in the case of alcohol addiction, but is a reasonable proxy for remission with opioids, where return to controlled use is rare. Embedded in these data is a message of literally vital importance: when opioid addiction is diagnosed and treated as a chronic relapsing disease, outcomes are markedly improved, and retention in treatment is associated with a greater likelihood of abstinence.

The fact that significant numbers of individuals exhibit a chronic relapsing course does not negate that even larger numbers of individuals with SUD according to current diagnostic criteria do not. For instance, in many countries, the highest prevalence of substance use problems is found among young adults, aged 18–25 [ 36 ], and a majority of these ‘age out’ of excessive substance use [ 37 ]. It is also well documented that many individuals with SUD achieve longstanding remission, in many cases without any formal treatment (see e.g., [ 27 , 30 , 38 ]).

Collectively, the data show that the course of SUD, as defined by current diagnostic criteria, is highly heterogeneous. Accordingly, we do not maintain that a chronic relapsing course is a defining feature of SUD. When present in a patient, however, such as course is of clinical significance, because it identifies a need for long-term disease management [ 2 ], rather than expectations of a recovery that may not be within the individual’s reach [ 39 ]. From a conceptual standpoint, however, a chronic relapsing course is neither necessary nor implied in a view that addiction is a brain disease. This view also does not mean that it is irreversible and hopeless. Human neuroscience documents restoration of functioning after abstinence [ 40 , 41 ] and reveals predictors of clinical success [ 42 ]. If anything, this evidence suggests a need to increase efforts devoted to neuroscientific research on addiction recovery [ 40 , 43 ].

Lessons from genetics

For alcohol addiction, meta-analysis of twin and adoption studies has estimated heritability at ~50%, while estimates for opioid addiction are even higher [ 44 , 45 ]. Genetic risk factors are to a large extent shared across substances [ 46 ]. It has been argued that a genetic contribution cannot support a disease view of a behavior, because most behavioral traits, including religious and political inclinations, have a genetic contribution [ 4 ]. This statement, while correct in pointing out broad heritability of behavioral traits, misses a fundamental point. Genetic architecture is much like organ structure. The fact that normal anatomy shapes healthy organ function does not negate that an altered structure can contribute to pathophysiology of disease. The structure of the genetic landscape is no different. Critics further state that a “genetic predisposition is not a recipe for compulsion”, but no neuroscientist or geneticist would claim that genetic risk is “a recipe for compulsion”. Genetic risk is probabilistic, not deterministic. However, as we will see below, in the case of addiction, it contributes to large, consistent probability shifts towards maladaptive behavior.

In dismissing the relevance of genetic risk for addiction, Hall writes that “a large number of alleles are involved in the genetic susceptibility to addiction and individually these alleles might very weakly predict a risk of addiction”. He goes on to conclude that “generally, genetic prediction of the risk of disease (even with whole-genome sequencing data) is unlikely to be informative for most people who have a so-called average risk of developing an addiction disorder” [ 7 ]. This reflects a fundamental misunderstanding of polygenic risk. It is true that a large number of risk alleles are involved, and that the explanatory power of currently available polygenic risk scores for addictive disorders lags behind those for e.g., schizophrenia or major depression [ 47 , 48 ]. The only implication of this, however, is that low average effect sizes of risk alleles in addiction necessitate larger study samples to construct polygenic scores that account for a large proportion of the known heritability.

However, a heritability of addiction of ~50% indicates that DNA sequence variation accounts for 50% of the risk for this condition. Once whole genome sequencing is readily available, it is likely that it will be possible to identify most of that DNA variation. For clinical purposes, those polygenic scores will of course not replace an understanding of the intricate web of biological and social factors that promote or prevent expression of addiction in an individual case; rather, they will add to it [ 49 ]. Meanwhile, however, genome-wide association studies in addiction have already provided important information. For instance, they have established that the genetic underpinnings of alcohol addiction only partially overlap with those for alcohol consumption, underscoring the genetic distinction between pathological and nonpathological drinking behaviors [ 50 ].

It thus seems that, rather than negating a rationale for a disease view of addiction, the important implication of the polygenic nature of addiction risk is a very different one. Genome-wide association studies of complex traits have largely confirmed the century old “infinitisemal model” in which Fisher reconciled Mendelian and polygenic traits [ 51 ]. A key implication of this model is that genetic susceptibility for a complex, polygenic trait is continuously distributed in the population. This may seem antithetical to a view of addiction as a distinct disease category, but the contradiction is only apparent, and one that has long been familiar to quantitative genetics. Viewing addiction susceptibility as a polygenic quantitative trait, and addiction as a disease category is entirely in line with Falconer’s theorem, according to which, in a given set of environmental conditions, a certain level of genetic susceptibility will determine a threshold above which disease will arise.

A brain disease? Then show me the brain lesion!

The notion of addiction as a brain disease is commonly criticized with the argument that a specific pathognomonic brain lesion has not been identified. Indeed, brain imaging findings in addiction (perhaps with the exception of extensive neurotoxic gray matter loss in advanced alcohol addiction) are nowhere near the level of specificity and sensitivity required of clinical diagnostic tests. However, this criticism neglects the fact that neuroimaging is not used to diagnose many neurologic and psychiatric disorders, including epilepsy, ALS, migraine, Huntington’s disease, bipolar disorder, or schizophrenia. Even among conditions where signs of disease can be detected using brain imaging, such as Alzheimer’s and Parkinson’s disease, a scan is best used in conjunction with clinical acumen when making the diagnosis. Thus, the requirement that addiction be detectable with a brain scan in order to be classified as a disease does not recognize the role of neuroimaging in the clinic.

For the foreseeable future, the main objective of imaging in addiction research is not to diagnose addiction, but rather to improve our understanding of mechanisms that underlie it. The hope is that mechanistic insights will help bring forward new treatments, by identifying candidate targets for them, by pointing to treatment-responsive biomarkers, or both [ 52 ]. Developing innovative treatments is essential to address unmet treatment needs, in particular in stimulant and cannabis addiction, where no approved medications are currently available. Although the task to develop novel treatments is challenging, promising candidates await evaluation [ 53 ]. A particular opportunity for imaging-based research is related to the complex and heterogeneous nature of addictive disorders. Imaging-based biomarkers hold the promise of allowing this complexity to be deconstructed into specific functional domains, as proposed by the RDoC initiative [ 54 ] and its application to addiction [ 55 , 56 ]. This can ultimately guide the development of personalized medicine strategies to addiction treatment.

Countless imaging studies have reported differences in brain structure and function between people with addictive disorders and those without them. Meta-analyses of structural data show that alcohol addiction is associated with gray matter losses in the prefrontal cortex, dorsal striatum, insula, and posterior cingulate cortex [ 57 ], and similar results have been obtained in stimulant-addicted individuals [ 58 ]. Meta-analysis of functional imaging studies has demonstrated common alterations in dorsal striatal, and frontal circuits engaged in reward and salience processing, habit formation, and executive control, across different substances and task-paradigms [ 59 ]. Molecular imaging studies have shown that large and fast increases in dopamine are associated with the reinforcing effects of drugs of abuse, but that after chronic drug use and during withdrawal, brain dopamine function is markedly decreased and that these decreases are associated with dysfunction of prefrontal regions [ 60 ]. Collectively, these findings have given rise to a widely held view of addiction as a disorder of fronto-striatal circuitry that mediates top-down regulation of behavior [ 61 ].

Critics reply that none of the brain imaging findings are sufficiently specific to distinguish between addiction and its absence, and that they are typically obtained in cross-sectional studies that can at best establish correlative rather than causal links. In this, they are largely right, and an updated version of a conceptualization of addiction as a brain disease needs to acknowledge this. Many of the structural brain findings reported are not specific for addiction, but rather shared across psychiatric disorders [ 62 ]. Also, for now, the most sophisticated tools of human brain imaging remain crude in face of complex neural circuit function. Importantly however, a vast literature from animal studies also documents functional changes in fronto-striatal circuits, as well their limbic and midbrain inputs, associated with addictive behaviors [ 63 , 64 , 65 , 66 , 67 , 68 ]. These are circuits akin to those identified by neuroimaging studies in humans, implicated in positive and negative emotions, learning processes and executive functions, altered function of which is thought to underlie addiction. These animal studies, by virtue of their cellular and molecular level resolution, and their ability to establish causality under experimental control, are therefore an important complement to human neuroimaging work.

Nevertheless, factors that seem remote from the activity of brain circuits, such as policies, substance availability and cost, as well as socioeconomic factors, also are critically important determinants of substance use. In this complex landscape, is the brain really a defensible focal point for research and treatment? The answer is “yes”. As powerfully articulated by Francis Crick [ 69 ], “You, your joys and your sorrows, your memories and your ambitions, your sense of personal identity and free will, are in fact no more than the behavior of a vast assembly of nerve cells and their associated molecules”. Social and interpersonal factors are critically important in addiction, but they can only exert their influences by impacting neural processes. They must be encoded as sensory data, represented together with memories of the past and predictions about the future, and combined with representations of interoceptive and other influences to provide inputs to the valuation machinery of the brain. Collectively, these inputs drive action selection and execution of behavior—say, to drink or not to drink, and then, within an episode, to stop drinking or keep drinking. Stating that the pathophysiology of addiction is largely about the brain does not ignore the role of other influences. It is just the opposite: it is attempting to understand how those important influences contribute to drug seeking and taking in the context of the brain, and vice versa.

But if the criticism is one of emphasis rather than of principle—i.e., too much brain, too little social and environmental factors – then neuroscientists need to acknowledge that they are in part guilty as charged. Brain-centric accounts of addiction have for a long time failed to pay enough attention to the inputs that social factors provide to neural processing behind drug seeking and taking [ 9 ]. This landscape is, however, rapidly changing. For instance, using animal models, scientists are finding that lack of social play early in life increases the motivation to take addictive substances in adulthood [ 70 ]. Others find that the opportunity to interact with a fellow rat is protective against addiction-like behaviors [ 71 ]. In humans, a relationship has been found between perceived social support, socioeconomic status, and the availability of dopamine D2 receptors [ 72 , 73 ], a biological marker of addiction vulnerability. Those findings in turn provided translation of data from nonhuman primates, which showed that D2 receptor availability can be altered by changes in social hierarchy, and that these changes are associated with the motivation to obtain cocaine [ 74 ].

Epidemiologically, it is well established that social determinants of health, including major racial and ethnic disparities, play a significant role in the risk for addiction [ 75 , 76 ]. Contemporary neuroscience is illuminating how those factors penetrate the brain [ 77 ] and, in some cases, reveals pathways of resilience [ 78 ] and how evidence-based prevention can interrupt those adverse consequences [ 79 , 80 ]. In other words, from our perspective, viewing addiction as a brain disease in no way negates the importance of social determinants of health or societal inequalities as critical influences. In fact, as shown by the studies correlating dopamine receptors with social experience, imaging is capable of capturing the impact of the social environment on brain function. This provides a platform for understanding how those influences become embedded in the biology of the brain, which provides a biological roadmap for prevention and intervention.

We therefore argue that a contemporary view of addiction as a brain disease does not deny the influence of social, environmental, developmental, or socioeconomic processes, but rather proposes that the brain is the underlying material substrate upon which those factors impinge and from which the responses originate. Because of this, neurobiology is a critical level of analysis for understanding addiction, although certainly not the only one. It is recognized throughout modern medicine that a host of biological and non-biological factors give rise to disease; understanding the biological pathophysiology is critical for understanding etiology and informing treatment.

Is a view of addiction as a brain disease deterministic?

A common criticism of the notion that addiction is a brain disease is that it is reductionist and in the end therefore deterministic [ 81 , 82 ]. This is a fundamental misrepresentation. As indicated above, viewing addiction as a brain disease simply states that neurobiology is an undeniable component of addiction. A reason for deterministic interpretations may be that modern neuroscience emphasizes an understanding of proximal causality within research designs (e.g., whether an observed link between biological processes is mediated by a specific mechanism). That does not in any way reflect a superordinate assumption that neuroscience will achieve global causality. On the contrary, since we realize that addiction involves interactions between biology, environment and society, ultimate (complete) prediction of behavior based on an understanding of neural processes alone is neither expected, nor a goal.

A fairer representation of a contemporary neuroscience view is that it believes insights from neurobiology allow useful probabilistic models to be developed of the inherently stochastic processes involved in behavior [see [ 83 ] for an elegant recent example]. Changes in brain function and structure in addiction exert a powerful probabilistic influence over a person’s behavior, but one that is highly multifactorial, variable, and thus stochastic. Philosophically, this is best understood as being aligned with indeterminism, a perspective that has a deep history in philosophy and psychology [ 84 ]. In modern neuroscience, it refers to the position that the dynamic complexity of the brain, given the probabilistic threshold-gated nature of its biology (e.g., action potential depolarization, ion channel gating), means that behavior cannot be definitively predicted in any individual instance [ 85 , 86 ].

Driven by compulsion, or free to choose?

A major criticism of the brain disease view of addiction, and one that is related to the issue of determinism vs indeterminism, centers around the term “compulsivity” [ 6 , 87 , 88 , 89 , 90 ] and the different meanings it is given. Prominent addiction theories state that addiction is characterized by a transition from controlled to “compulsive” drug seeking and taking [ 91 , 92 , 93 , 94 , 95 ], but allocate somewhat different meanings to “compulsivity”. By some accounts, compulsive substance use is habitual and insensitive to its outcomes [ 92 , 94 , 96 ]. Others refer to compulsive use as a result of increasing incentive value of drug associated cues [ 97 ], while others view it as driven by a recruitment of systems that encode negative affective states [ 95 , 98 ].

The prototype for compulsive behavior is provided by obsessive-compulsive disorder (OCD), where compulsion refers to repeatedly and stereotypically carrying out actions that in themselves may be meaningful, but lose their purpose and become harmful when performed in excess, such as persistent handwashing until skin injuries result. Crucially, this happens despite a conscious desire to do otherwise. Attempts to resist these compulsions result in increasing and ultimately intractable anxiety [ 99 ]. This is in important ways different from the meaning of compulsivity as commonly used in addiction theories. In the addiction field, compulsive drug use typically refers to inflexible, drug-centered behavior in which substance use is insensitive to adverse consequences [ 100 ]. Although this phenomenon is not necessarily present in every patient, it reflects important symptoms of clinical addiction, and is captured by several DSM-5 criteria for SUD [ 101 ]. Examples are needle-sharing despite knowledge of a risk to contract HIV or Hepatitis C, drinking despite a knowledge of having liver cirrhosis, but also the neglect of social and professional activities that previously were more important than substance use. While these behaviors do show similarities with the compulsions of OCD, there are also important differences. For example, “compulsive” substance use is not necessarily accompanied by a conscious desire to withhold the behavior, nor is addictive behavior consistently impervious to change.

Critics question the existence of compulsivity in addiction altogether [ 5 , 6 , 7 , 89 ], typically using a literal interpretation, i.e., that a person who uses alcohol or drugs simply can not do otherwise. Were that the intended meaning in theories of addiction—which it is not—it would clearly be invalidated by observations of preserved sensitivity of behavior to contingencies in addiction. Indeed, substance use is influenced both by the availability of alternative reinforcers, and the state of the organism. The roots of this insight date back to 1940, when Spragg found that chimpanzees would normally choose a banana over morphine. However, when physically dependent and in a state of withdrawal, their choice preference would reverse [ 102 ]. The critical role of alternative reinforcers was elegantly brought into modern neuroscience by Ahmed et al., who showed that rats extensively trained to self-administer cocaine would readily forego the drug if offered a sweet solution as an alternative [ 103 ]. This was later also found to be the case for heroin [ 103 ], methamphetamine [ 104 ] and alcohol [ 105 ]. Early residential laboratory studies on alcohol use disorder indeed revealed orderly operant control over alcohol consumption [ 106 ]. Furthermore, efficacy of treatment approaches such as contingency management, which provides systematic incentives for abstinence [ 107 ], supports the notion that behavioral choices in patients with addictions remain sensitive to reward contingencies.

Evidence that a capacity for choosing advantageously is preserved in addiction provides a valid argument against a narrow concept of “compulsivity” as rigid, immutable behavior that applies to all patients. It does not, however, provide an argument against addiction as a brain disease. If not from the brain, from where do the healthy and unhealthy choices people make originate? The critical question is whether addictive behaviors—for the most part—result from healthy brains responding normally to externally determined contingencies; or rather from a pathology of brain circuits that, through probabilistic shifts, promotes the likelihood of maladaptive choices even when reward contingencies are within a normal range. To resolve this question, it is critical to understand that the ability to choose advantageously is not an all-or-nothing phenomenon, but rather is about probabilities and their shifts, multiple faculties within human cognition, and their interaction. Yes, it is clear that most people whom we would consider to suffer from addiction remain able to choose advantageously much, if not most, of the time. However, it is also clear that the probability of them choosing to their own disadvantage, even when more salutary options are available and sometimes at the expense of losing their life, is systematically and quantifiably increased. There is a freedom of choice, yet there is a shift of prevailing choices that nevertheless can kill.

Synthesized, the notion of addiction as a disease of choice and addiction as a brain disease can be understood as two sides of the same coin. Both of these perspectives are informative, and they are complementary. Viewed this way, addiction is a brain disease in which a person’s choice faculties become profoundly compromised. To articulate it more specifically, embedded in and principally executed by the central nervous system, addiction can be understood as a disorder of choice preferences, preferences that overvalue immediate reinforcement (both positive and negative), preferences for drug-reinforcement in spite of costs, and preferences that are unstable ( “I’ll never drink like that again;” “this will be my last cigarette” ), prone to reversals in the form of lapses and relapse. From a contemporary neuroscience perspective, pre-existing vulnerabilities and persistent drug use lead to a vicious circle of substantive disruptions in the brain that impair and undermine choice capacities for adaptive behavior, but do not annihilate them. Evidence of generally intact decision making does not fundamentally contradict addiction as a brain disease.

Conclusions

The present paper is a response to the increasing number of criticisms of the view that addiction is a chronic relapsing brain disease. In many cases, we show that those criticisms target tenets that are neither needed nor held by a contemporary version of this view. Common themes are that viewing addiction as a brain disease is criticized for being both too narrow (addiction is only a brain disease; no other perspectives or factors are important) or too far reaching (it purports to discover the final causes of addiction). With regard to disease course, we propose that viewing addiction as a chronic relapsing disease is appropriate for some populations, and much less so for others, simply necessitating better ways of delineating the populations being discussed. We argue that when considering addiction as a disease, the lens of neurobiology is valuable to use. It is not the only lens, and it does not have supremacy over other scientific approaches. We agree that critiques of neuroscience are warranted [ 108 ] and that critical thinking is essential to avoid deterministic language and scientific overreach.

Beyond making the case for a view of addiction as a brain disease, perhaps the more important question is when a specific level of analysis is most useful. For understanding the biology of addiction and designing biological interventions, a neurobiological view is almost certainly the most appropriate level of analysis, in particular when informed by an understanding of the behavioral manifestations. In contrast, for understanding the psychology of addiction and designing psychological interventions, behavioral science is the natural realm, but one that can often benefit from an understanding of the underlying neurobiology. For designing policies, such as taxation and regulation of access, economics and public administration provide the most pertinent perspectives, but these also benefit from biological and behavioral science insights.

Finally, we argue that progress would come from integration of these scientific perspectives and traditions. E.O. Wilson has argued more broadly for greater consilience [ 109 ], unity of knowledge, in science. We believe that addiction is among the areas where consilience is most needed. A plurality of disciplines brings important and trenchant insights to bear on this condition; it is the exclusive remit of no single perspective or field. Addiction inherently and necessarily requires multidisciplinary examination. Moreover, those who suffer from addiction will benefit most from the application of the full armamentarium of scientific perspectives.

Funding and disclosures

Supported by the Swedish Research Council grants 2013-07434, 2019-01138 (MH); Netherlands Organisation for Health Research and Development (ZonMw) under project number 912.14.093 (LJMJV); NIDA and NIAAA intramural research programs (LL; the content is solely the responsibility of the author and does not necessarily represent the official views of the National Institutes of Health); the Peter Boris Chair in Addictions Research, Homewood Research Institute, and the National Institute on Alcohol Abuse and Alcoholism grants AA025911, AA024930, AA025849, AA027679 (JM; the content is solely the responsibility of the author and does not necessarily represent the official views of the National Institutes of Health).

MH has received consulting fees, research support or other compensation from Indivior, Camurus, BrainsWay, Aelis Farma, and Janssen Pharmaceuticals. JM is a Principal and Senior Scientist at BEAM Diagnostics, Inc. DM, JR, LL, and LJMJV declare no conflict of interest.

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Heilig, M., MacKillop, J., Martinez, D. et al. Addiction as a brain disease revised: why it still matters, and the need for consilience. Neuropsychopharmacol. 46 , 1715–1723 (2021). https://doi.org/10.1038/s41386-020-00950-y

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Received : 10 November 2020

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Accepted : 14 December 2020

Published : 22 February 2021

Issue Date : September 2021

DOI : https://doi.org/10.1038/s41386-020-00950-y

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Drug Addiction: Understanding the Patterns, Effects, and Treatment Options

• Signs of Addiction
• Causes and Risks

Living With Drug Addiction

Drug addiction, or substance use disorder, is a mental health condition that can have lifelong impacts. Though it's a treatable illness, substance use disorder recovery often involves a lifelong cycle of relapse (recurrence of use), withdrawal, and abstinence.

This article will define drug addiction, outline signs and symptoms, present possible causes, and provide treatment options.

FatCamera / Getty Images

Support Resources

If you or a loved one are struggling with substance use or addiction, contact the Substance Abuse and Mental Health Services Administration (SAMHSA) National Helpline at 1-800-662-4357 for information on support and treatment facilities in your area.

For more mental health resources, see our National Helpline Database .

How Is Drug Addiction Defined?

Drug addiction is a brain disease that falls into the category of substance use disorders . Generally, substance use disorders are defined as having no control over substance use or an inability to quit due to tolerance , dependence, and withdrawal symptoms .

According to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) , substance use disorders are defined as exhibiting:

• One or more abuse criteria within a 12-month period  and  no dependence diagnosis. (This does not include nicotine.)
• Three or more dependence criteria within a 12-month period.
• Two or more substance use disorder criteria within a 12-month period.

People with substance use disorder struggle to stop using the substance and often experience painful physical or psychological symptoms when they try to.

Why Does Addiction Happen?

Biological, psychological, environmental, and socio-cultural factors can play a role in a person developing a substance use disorder.

Experiencing Drug Addiction Symptoms

Substance use disorder symptoms are categorized into addiction and withdrawal symptoms. Addiction symptoms are those that indicate a person may be addicted to a substance. Withdrawal symptoms are those that occur when a person tries to stop using a substance.

Addiction Symptoms

According to the DSM-5 , addiction symptoms include the following:

• An intense craving for the substance.
• Continued use of the substance despite knowing its adverse effects.
• Difficulty controlling substance use.
• Increased tolerance of the substance over time.
• Losing interest in other activities.
• Losing interest in social, family, and work-related activities.
• Unsuccessful attempts to stop using the substance.
• Withdrawal symptoms after stopping usage of the substance.

Withdrawal Symptoms

People with substance use disorder usually experience several withdrawal symptoms when trying to stop their substance use. These might include:

• Feelings of discomfort
• Irritability
• Lack of interest in activities and relationships
• Sleep problems
• Stomach cramping

Severe withdrawal can lead to dangerous and life-threatening health issues. If you experience withdrawal symptoms, seek medical attention for support with withdrawal management.

While increased tolerance and dependence must be present for a formal substance use disorder diagnosis, many people become addicted to substances before developing physical dependence and withdrawal symptoms.

Signs of Drug Addiction in Others

Substance use disorder usually occurs in a cycle with three stages:

• Intoxication : The period when a person has taken a substance and experiences its effects.
• Withdrawal : The period after substance use has stopped. Uncomfortable physical and emotional symptoms usually accompany this stage.
• Preoccupation : The period when a person is not actively using a substance or experiencing withdrawal symptoms when thoughts about the substance consume them and they anticipate their next use.

Over time, a person with an addiction will start to experience these stages more frequently and more intensely. Additional signs that may indicate a person is using or addicted to a substance include:

• Changes in appearance, such as bloodshot eyes, weight changes, or changes in clothing
• Changes in social activities or interests
• Getting defensive when asked about substance use
• Spending or needing money
• Spending time with new people or spending time alone

Prevalence of Addiction

Addiction affects millions of people each year, causing over 11 million deaths from smoking, alcohol abuse, and illegal drugs.

Drug Addiction Treatment Options

Substance use disorder treatment can include various interventions, such as:

• Clinical support groups : Support groups run by mental health providers. Speak to a mental health provider for local or online support group recommendations.
• Inpatient rehabilitation : A person stays at a rehabilitation center for a period—often 30 days or more—to encourage and support recovery. Inpatient treatment can include individual, group, or family therapy, medication, and other treatment approaches.
• Individual therapy : Involves working directly with a licensed mental health professional, such as a certified substance abuse counselor, to identify recovery goals, learn coping tools, and develop a treatment plan.
• Medication : Healthcare providers can prescribe certain medications to help reduce withdrawal symptoms. These medications will differ depending on the type of substance.
• Outpatient rehabilitation : A treatment facility where the person does not live or stay overnight but attends appointments for medical needs, individual therapy, or group support.
• Peer-support meetings : Supportive sessions that are run by others facing addiction. These include groups like Cocaine Anonymous , Crystal Meth Anonymous , Heroine Anonymous , and Narcotics Anonymous .

Regardless of the treatment approach, each method offers education about addiction and recovery. This may include topics like making life changes to support recovery, being honest, seeking help when needed, and practicing self-care.

Steps to Finding Treatment

To locate treatment facilities in your area, try calling the Substance Abuse and Mental Health Services Administration (SAMHSA) for a list of options. You can also visit SAMHSA's treatment locator website , the American Addiction Centers location finder , or, if you have health insurance, call your insurance company for in-network services. For questions about medical detoxification, talk with your healthcare provider.

To locate a substance abuse mental health provider, you can use a therapist-finder tool, such as the NIAA Alcohol Treatment Navigator , or contact your health insurance for a list of in-network providers.

Effects of Drug Addiction

Substance use disorder is dangerous and can be fatal for those who do not seek treatment. Other health risks from substance use include:

• Diseases that result from sharing needles used for injection, such as HIV and hepatitis C
• Heart problems
• Lung disease
• Skin infections

Substance use disorder can negatively affect a person's relationships, finances, employment, and other aspects of their life.

Addiction Causes and Risk Groups

Though anyone can develop substance use disorder, certain people may be at higher risk of addiction. This includes those who:

• Are experiencing significant stress or distress.
• Are from lower socioeconomic households.
• Had behavioral problems as a child, especially with anger.
• Had minimal adult supervision as children.
• Have access to substances.
• Have tried substances before.
• Struggle with low self-esteem or self-worth and find it challenging to say no to peer pressure.

Most people who develop substance use disorder do so for a combination of reasons, including genetics and environmental factors.

Gateway Drugs

Many people develop substance use disorder after first using a gateway drug, which is often a drug that is more widely available and socially acceptable.

Substance use disorder is a lifelong battle. Most people relapse even after stopping substance use for extended periods. There is a risk for recurrence of use at every phase of recovery. The phases of recovery include:

• Abstinence stage : The person is not using the substance. This stage usually lasts one to two years.
• Post-acute withdrawal stage : The person has already experienced physical withdrawal symptoms and starts to have mainly emotional and psychological withdrawal symptoms. This stage often lasts up to two years.
• Repair stage : The person works on repairing any negative experiences from addiction. This stage usually lasts two to three years.
• Growth stage : The person begins working on skills to help them move forward and hopefully avoid a future relapse. This stage often starts between three and five years after initially stopping the substance use.

Relapse Is Common

The relapse or recurrence of use process begins weeks or months before a person actually takes the substance. Early intervention increases the chances of returning to sobriety. About 85% of adults living with substance use disorder will relapse within a year of quitting their substance use.

A person who is recovering from substance use disorder is always at risk of relapse. The stages of relapse include:

• Emotional : The person does not think about using the substance and may experience denial, isolation, and treatment avoidance, such as no longer attending substance use disorder groups or meetings and poor self-care.
• Mental : The person starts to think about using the substance again but may not want to. They may experience cravings, think about the past when they were using the substance, and start to plan their use. It's also common for people to substitute another substance for the one they had been taking in the past.
• Physical : The person takes the substance again.

Drug addiction, or substance use disorder, is a serious mental illness that affects a person's health, relationships, finances, and well-being. People with substance use disorder usually struggle with relapse for their entire lives and often go through continuous cycles of intoxication, withdrawal, and preoccupation with the substance. Though there are risk factors for developing substance use disorder, anyone can develop it. Treatment is available for people struggling with substance use disorder.

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By Melissa Porrey LPC, NCC Porrey is a licensed professional counselor and writer based in DC. She is a nationally board-certified counselor.

Drugs, Brains, and Behavior: The Science of Addiction Preventing Drug Misuse and Addiction: The Best Strategy

Why is adolescence a critical time for preventing drug addiction.

As noted previously, early use of drugs increases a person's chances of becoming addicted. Remember, drugs change the brain—and this can lead to addiction and other serious problems. So, preventing early use of drugs or alcohol may go a long way in reducing these risks.

Risk of drug use increases greatly during times of transition. For an adult, a divorce or loss of a job may increase the risk of drug use. For a teenager, risky times include moving, family divorce, or changing schools. 35  When children advance from elementary through middle school, they face new and challenging social, family, and academic situations. Often during this period, children are exposed to substances such as cigarettes and alcohol for the first time. When they enter high school, teens may encounter greater availability of drugs, drug use by older teens, and social activities where drugs are used. When individuals leave high school and live more independently, either in college or as an employed adult, they may find themselves exposed to drug use while separated from the protective structure provided by family and school.

A certain amount of risk-taking is a normal part of adolescent development. The desire to try new things and become more independent is healthy, but it may also increase teens’ tendencies to experiment with drugs. The parts of the brain that control judgment and decision-making do not fully develop until people are in their early or mid-20s. This limits a teen’s ability to accurately assess the risks of drug experimentation and makes young people more vulnerable to peer pressure. 36

Because the brain is still developing, using drugs at this age has more potential to disrupt brain function in areas critical to motivation, memory, learning, judgment, and behavior control. 12  

Can research-based programs prevent drug addiction in youth?

Yes.  The term research-based or evidence-based means that these programs have been designed based on current scientific evidence, thoroughly tested, and shown to produce positive results. Scientists have developed a broad range of programs that positively alter the balance between risk and protective factors for drug use in families, schools, and communities. Studies have shown that research-based programs, such as described in NIDA’s  Principles of Substance Abuse Prevention for Early Childhood: A Research-Based Guide   and  Preventing Drug Use among Children and Adolescents: A Research-Based Guide for Parents, Educators, and Community Leaders , can significantly reduce early use of tobacco, alcohol, and other drugs. 37  Also, while many social and cultural factors affect drug use trends, when young people perceive drug use as harmful, they often reduce their level of use. 38

How do research-based prevention programs work?

These prevention programs work to boost protective factors and eliminate or reduce risk factors for drug use. The programs are designed for various ages and can be used in individual or group settings, such as the school and home. There are three types of programs:

• Universal programs address risk and protective factors common to all children in a given setting, such as a school or community.
• Selective programs are for groups of children and teens who have specific factors that put them at increased risk of drug use.
• Indicated programs are designed for youth who have already started using drugs.

Young Brains Under Study

Using cutting-edge imaging technology, scientists from the NIDA’s Adolescent Brain Cognitive Development (ABCD) Study will look at how childhood experiences, including use of any drugs, interact with each other and with a child’s changing biology to affect brain development and social, behavioral, academic, health, and other outcomes. As the only study of its kind, the ABCD study will yield critical insights into the foundational aspects of adolescence that shape a person’s future.

Economics of Prevention

Evidence-based interventions for substance use can save society money in medical costs and help individuals remain productive members of society. Such programs can return anywhere from very little to $65 per every dollar invested in prevention. 39

Every product was carefully curated by an Esquire editor. We may earn a commission from these links.

Is It Time to Quit Coffee for Good?

A growing chorus of concerned former “addicts” are trying to wake people up to caffeine's negative effects.

Petty Officer Second Class Marcus Bivens stood before a panel of U.S. Navy officers, hands cuffed behind his back, facing charges of an unauthorized absence.

For his first fifteen years of service, Bivens had been considered a “squared-away sailor”—orderly, competent, conscientious. A sailor officers could rely on. But he had been missing work lately, sometimes for weeks at a time, and now he was standing in front of an ad hoc disciplinary tribunal investigating his rapid and seemingly inexplicable decline in job performance. Bivens could no longer physically complete his work tasks, even though it was an administrative job.

Several weeks prior, Bivens was driving home on I-15 from the Coronado naval base in San Diego when his eyesight suddenly went double. “It was terrifying,” he recalls. “I literally drove home with one eye closed.” Bivens made it to his house safely but immediately collapsed into bed, clothes still on, and slept for eleven hours. When he woke up, the double vision was worse.

He went to the hospital, where he was subjected to a battery of tests. Doctors examined his eyes, his ear canal, his blood pressure. He was administered an EKG and had blood drawn. All the test results were normal, flummoxing a team of ophthalmologists and neurologists. “Every doctor took out their phone and Googled my symptoms, trying to figure out what was going on with me,” Bivens says. He was eventually diagnosed with myasthenia gravis , a rare neuromuscular disorder that typically affects women between the ages of twenty and thirty.

Bivens’s condition worsened over the next four months. He suffered tremors, sensitivity to light, aches throughout his body, and twitchy eyes. He slept just three to five hours a night. A self-described gym rat, Bivens lost his strength; he couldn’t do a single push-up. Doctors performed MRIs and MRAs and conducted more blood work. They wondered if Bivens had lesions on his brain. They prescribed him Ambien, Zoloft, Xanax, and Cafergot, a caffeine stimulant used to treat headaches. He was given an eye patch to alleviate the double vision. None of the tests revealed any abnormalities, and none of the doctors he saw could give him a satisfactory explanation for his bizarre array of symptoms.

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At his lowest point, Bivens suffered intrusive thoughts. A disembodied voice whispered to him, “You’re gonna die.” He would hide in his closet, away from any overwhelming stimuli, praying for God to spare him. “It was hell on earth,” he says.

In front of the disciplinary review board, Bivens admitted he was having suicidal ideations and was placed on psychiatric hold for a week. A year later, he was medically retired from the Navy. The condition would plague him past that.

Bivens now believes the source of his medical issues was neither a disease nor a mental illness. Rather, he attributes his health decline to caffeine, the most commonly used, socially acceptable psychoactive substance in the world. For years, Bivens had been consuming close to 1,000 milligrams of caffeine per day, two and a half times the daily recommended limit and the equivalent of more than ten cups of coffee. The habit had wreaked havoc on his central nervous system and in turn caused myriad physical and psychological problems.

“People don’t understand that caffeine is an actual drug,” says Bivens. “It’s not Kool-Aid.”

There is perhaps no mind-altering substance as tightly woven into the fabric of daily life than caffeine. Nearly 80 percent of adults in the U.S. consume caffeine , in some form, every day. Coffee is the primary caffeine-delivery mechanism for many people— two thirds of American adults drink it every day —and many consider it an indispensable part of daily life. T-shirts and, naturally, coffee mugs exclaim, “Not before I’ve had my coffee” or “But first, coffee,” as if the travails of everyday living are impossible without a morning cup of joe. For some, coffee even serves as a handy substitute for having a personality. Whether it’s new mothers who think they should have a priority line at Starbucks ; snobs who traffic exclusively in organic, sustainably grown fair-trade beans; or Zoomers sharing their insane coffee concoctions on TikTok , conspicuous coffee consumption is a cultural signifier. Entire human interactions—the coffee date, the coffee break at work, the post-dinner mug—revolve around its ingestion.

(Coffee alone cannot quench our cultural thirst for caffeine. Energy drinks are a fraction the size of the coffee market, but Americans still spend almost $14 billion a year on them , and the category is rapidly growing.)

So ubiquitous is caffeine in our culture that it doesn’t even register to people as a drug. Step out of the office for a midafternoon cigarette and people might look at you askance. Get caught doing a bump of coke in the office bathroom as a midday pick-me-up and it’s grounds for immediate termination. But slam a Monster or a quad-shot Americano at work and people will think you’re a go-getter.

That perception is increasingly being challenged by a small but growing choir of laypeople and experts making a concerted effort to raise awareness about the potential downsides of caffeine dependence. “Caffeine is wildly misunderstood, especially with primarily anxiety-prone people,” says Mark Johnson, a thirty-four-year-old video producer in Greenville, South Carolina.

Johnson’s recovery from caffeine started three years ago, when he began to suspect coffee was the source of his personal and professional problems. A commercial videographer, he creates TV spots and YouTube videos for major brands. The hours are long and, at the time, Johnson was creatively unfulfilled and felt he was burning out. He used caffeine to power through his work, drinking multiple Bang energy drinks a day on top of his morning cup of coffee. “I felt terrible all the time,” he says. During particularly acute periods of anxiety, Johnson would experience derealization, a sense of detachment from one’s surroundings—or the dreadful feeling that the physical world, as you perceive it, is not in fact actually there. He investigated the causes of his anxiety and eventually discovered r/decaf , a Reddit forum for people struggling with caffeine.

Thus began cycles of quitting, withdrawal, and relapse whenever he needed to crank out a project at work. The first time he suffered withdrawal from caffeine, Johnson slept more than fourteen hours a day for a week and felt suicidal. “I’m not a naturally depressed person, but I laid around all day,” he says. “You feel like there is no point to life.”

Many people quitting caffeine say the physical withdrawal symptoms are the biggest obstacle. Some report headaches so severe it’s impossible to function. (One of the strangest aspects of caffeine is that it is both a common cause of and, at other times, an effective treatment for headaches.) More than anything, they report feeling really fucking tired. After years of relying on caffeine to fuel them through school, work, and social life, people often don’t have energy for their everyday lives when they quit cold turkey, finding they’ve been under-rested for years. “Caffeine just masks fatigue,” says Johnson.

Members of r/decaf use the language of addiction (e.g., “sobriety,” “relapse”) to describe their relationships with caffeine, which is controversial because caffeine addiction is not a formally recognized diagnosis (perhaps not yet ). The latest edition of the Diagnostic and Statistical Manual, the official reference guide for defining and diagnosing psychiatric disorders, lists caffeine withdrawal as a condition, but it doesn’t include caffeine use disorder. The American Psychiatric Association, the organization that oversees the manual, says it’s considering caffeine use disorder for inclusion in the next edition.

“Since non-problematic caffeine use is so common and widespread, it may be difficult for some health professionals to accept that caffeine use can result in the same types of pathological behaviors caused by alcohol, cocaine, opiates, or other drugs of abuse,” Merideth A. Addicott wrote in her 2014 study on the subject while she was a psychiatry researcher at the Duke-UNC Brain Imaging and Analysis Center. “Yet there is evidence that some individuals are psychologically and physiologically dependent on caffeine, although the prevalence and severity of these problems is unknown.”

Caffeine might not meet the strict medical definition of addictive, but it does meet more general criteria, according to self-professed caffeine addicts: 1) Addicts continue using caffeine despite its negative effect on their lives, and 2) they want to quit but they have trouble doing so. “It’s one of the only things it’s acceptable to be addicted to,” Johnson says.

Perhaps no one has done more to bring attention to the physical and psychological effects of caffeine than Michael Pollan , arguably the most respected food-science writer in the world—ironic given that Pollan both openly identifies as an addict and ardently defends the positive effects of caffeine. “Yeah, I’m addicted to caffeine,” he admits to me. “So what?”

Pollan investigated his relationship with caffeine in This Is Your Mind on Plants , his 2021 book about the psychoactive properties of various flora. A lifelong coffee and tea drinker, he quit caffeine for three months as research for his chapter on the substance. The effects were drastic. “I felt out of my body,” Pollan says about his caffeine withdrawal. “I felt like I had contracted ADD. I couldn’t wait to get back on it.” A YouTube clip of him recounting his caffeine withdrawal on The Joe Rogan Experience has been viewed nearly ten million times.

The experiment left Pollan with a newfound appreciation for the powers of caffeine—that first cup of coffee after withdrawal was “psychedelic,” he says—but he quickly returned to his usual morning coffee habit after his months off.

Pollan points to studies showing that caffeine may have protective benefits against some types of cancer , dementia , and Parkinson’s . Caffeine can boost athletic and work performance, and coffee is the leading source of antioxidants in the American diet , a troubling sign of just how few vegetables the average American eats. (This applies only to coffee specifically, not caffeine generally. Red Bull won’t neutralize free radicals in your body.) Pollan isn’t dismissive of the potential negative side effects of too much caffeine; he acknowledges that it can disrupt sleep and that it can make people jittery, especially if they’re already prone to anxiety. Generally speaking, he recommends no caffeine after noon.

But the benefits of caffeine far outweigh the risks, he says. Caffeine gave us the Enlightenment, the Age of Reason, and the Industrial Revolution, Pollan writes in his book. Prior to the spread of coffee throughout Europe, people mostly drank beer, a beverage that isn’t conducive to intellectual exchange. Coffee, however, was the catalyst for all kinds of scientific, political, and artistic breakthroughs. Without caffeine, we might still be living in a perpetual drunken stupor, dirt poor, toiling the fields for the benefits of feudal lords. “On balance, the story is very much in favor of drinking coffee and tea,” Pollan says.

“People blanch at this word addiction because they assume that it means unhealthy. And I don’t think that’s a good enough reason to give up caffeine,” he adds. “People love this idea of complete control over their lives, and addiction fights against that. It suggests something else is running me. For people who crave autonomy, that’s difficult. But I like ritual behavior.”

Lisa Axelrad, a nutritionist in Los Angeles , has a more negative view of the substance. She advises her clients to drink no more than one cup of coffee a day and to cut out all other forms of caffeine. “Caffeine is addictive,” she says. “Coffee leads to an afternoon crash and stains our teeth, and that’s from just one cup a day. If you’re drinking more, you are likely to suffer from headaches, disrupted sleep, irritability, high blood pressure, jitters, insulin resistance, and hormone disruption.”

Recovering caffeine addicts and Pollan do agree on one thing: The prevalence of caffeine allows people to never question their relationship with it. (Part of the reason Johnson agreed to moderate r/decaf, an unpaid position, was to combat the widespread social acceptance of coffee and make more people aware of its potential ills.)

“I would lie down to sleep at night, and my brain would run at a mile a minute,” says Bianca Zaklikowski, a forty-one-year-old self-described recovering caffeine addict. “My heart was beating too fast. My blood pressure was too high.” Zaklikowski consulted her physician about her health problems, and it took one conversation about her diet for him to recommend she drink less caffeine. On a typical day, she would drink sixty-four ounces of Diet Coke in addition to as many as three double-shot skinny vanilla lattes from Starbucks. That this was, simply, too much had never occured to Zaklikowski. Her blood pressure and resting heart rate are at healthy levels since cutting it from her diet, and she finally feels rested when she wakes up.

“Caffeine,” she says now, six years since she last consumed the substance, “is a lifestyle.” For Zaklikowski, a single mother of two, that lifestyle included going on the occasional coffee date and bonding with other mothers over their shared love of the drink. Her infatuation with coffee culture began when she was a teenager and would visit the one hip coffee shop in her small Indiana town. “I felt like an adult,” she remembers, “like one of the characters on Friends .”

The sophistication we associate with drinking coffee is also what drew comedian Nikki Glaser to the substance. (With comedy specials on Netflix and HBO, a sold-out international comedy tour, and millions of social media followers, it’s fair to assume Glaser is, by far, the most famous member of r/decaf.) Glaser’s intake is remarkably similar to Zaklikowski’s—two to three Starbucks lattes a day, plus Diet Coke—but unlike Zaklikowski, she hasn’t fully kicked the habit.

“There’s something about drinking coffee that says, ‘I’m a part of the world. I have a big day ahead of me. I’m schlepping from meeting to meeting. I’m hitting deadlines.’ It’s a go-getter’s drink. It’s like carrying a briefcase,” Glaser says.

The seeds of caffeine addiction are planted in early childhood, she adds. Getting “hyper” on a Surge cola is the preadolescent version of getting twisted on booze. For her, acquiring a taste for coffee, a drink most children abhor, was a rite of passage akin to losing her virginity.

Stats on the number of people quitting caffeine are hard to come by, but there are signals that the anti-caffeine crowd is growing. “I hear from readers all the time that they stopped using caffeine, as if I recommended that,” Pollan says. R/decaf membership has increased 25 percent over the past year, to 34,000 subscribers, and there has been a boom the past several years in the number of low-caf or caffeine-free coffee alternatives on the market—Huel, MUD\WTR, Teeccino, matcha, as well as “coffees” made from mushroom, chaga, chicory, and dandelion.

Generationally, coffee consumption appears to be in decline. Less than a third (31 percent) of Zoomers say they can’t live without coffee, compared with half of Millennials and Gen Xers and nearly two thirds (61 percent) of Baby Boomers, according to a new study from the market-research firm NCSolutions. Zoomers are also less likely to keep coffee on hand at home. “Gen Z is more willing to go without coffee,” says NCSolutions CEO Alan Miles. “And while that might have something to do with age, there’s also a sense they may be gravitating towards healthier, more natural and environmentally sustainable foods and beverages.”

People love to debate the relative merits of different dietary philosophies (high carb, low carb, no carb, keto, carnivore, vegan, pescatarian, Mediterranean) and the health benefits of so-called “superfoods” (e.g., blueberries, chia seeds, kale, almonds, salmon), but suggesting that people should curb their caffeine intake might be the most contentious fight in all of food discourse—especially because it seems like every other week, a new study is published claiming that coffee is either the fountain of youth or certain to send you to an early grave.

If your response to this trend is “I’ll give up my coffee when you pry this mug from my cold dead hands,” you’ll be happy to know that Stephen Cherniske, the nutritionist who literally wrote the book on caffeine addiction, says that for most people, coffee in moderation is just fine. “Starting your day with a cup of coffee is not a problem,” he says. “But stringing yourself along with caffeine hit after caffeine hit as the day goes on is problematic. It’s like whipping a tired horse.”

Cherniske is a research biochemist and the author of Caffeine Blues , a book about the perils of caffeine overconsumption and a popular title among members of r/decaf. Years ago, during his clinical practice as a nutritionist, he realized that many of his patients were alarmingly overcaffeinated. Patients would report drinking just a few cups of coffee a day, only to reveal that their idea of one cup was a forty-ounce thermos. “At three of those a day, they were drinking more than 1,000 milligrams of caffeine,” Cherniske says. That amount of caffeine overstimulates a person’s nervous system, causing agitation, elevated heart rate, and high blood pressure.

Caffeine is water soluble, so its effects on the human body occur rapidly, Cherniske says. Almost all (99 percent) of a caffeine dose is absorbed in the bloodstream within forty-five minutes of ingestion. And because caffeine is also fat soluble, it easily passes through cell membranes, including the blood-brain barrier, providing a jolt of energy and alertness. In skeletal muscles, caffeine increases the mobilization of calcium ions, boosting strength and lowering reaction time. (Caffeine is a well-known performance-enhancing drug among athletes , albeit a legal and largely unregulated one.)

In high doses, however, the mental buzz from caffeine can tip from increased focus and mental energy to irritability and panic. “Stimulants, like caffeine, activate the same response humans had thousands of years ago face-to-face with a saber-tooth tiger,” Cherniske says. That fight-or-flight response was integral to our survival as a species in prehistoric times, but it’s unnecessary, and possibly counterproductive, for your nine-to-five desk job. People who consume too much caffeine are in that heightened state of awareness. Their bodies pump adrenaline for too long, and that causes anxiety, trouble sleeping, and extreme swings in energy level and mood.

Problems with caffeine are often genetic, Cherniske says. In 2006, nutrition scientists at the University of Toronto discovered an enzyme , CYP1A2, that accounts for at least 90 percent of caffeine metabolization . People with the CYP1A2-1F variant metabolize caffeine more slowly, which explains why some people can be wired from one cup of coffee while others can take a shot of espresso at 9:00 p.m. and still have no trouble falling asleep.

Even so, Cherniske doesn’t want to take your coffee away. He drinks three cups a day himself. Others, though, advocate for drastic measures. “More people need to know that caffeine is a neurotoxin and it’s hurting you,” Bivens says. “I would like people to treat caffeine the way we treat cigarettes. There should be a warning.”

Bivens didn’t discover that caffeine was at the root of his problems until a year and a half after he left the Navy, when he was in the throes of another mental health crisis. Researching online, he found that caffeine can exacerbate anxiety, especially in large amounts. Bivens was drinking a pot of coffee a day at the time.

This launched a vicious cycle in which Bivens would quit caffeine, go through withdrawal, and see his health improve, only to inexplicably start drinking caffeine again and suffer another spell of panic attacks and intrusive thoughts. Caffeine had been a staple of Bivens’s diet since growing up in Mobile, Alabama, and giving it up proved hard. He drank at least two cans of soda a day as a kid. “That’s just what everybody did,” he recalls. “You go to McDonald’s, and your burger comes with a Coke.” (He now blames caffeine for the chronic headaches he’s suffered since childhood.) In the Navy, Bivens and his fellow sailors drank a sludgy, homemade energy-drink concoction called “Ricky Rockets,” equal parts coffee and sugar, to get through boot camp. “A typical day for me was a cup of coffee in the morning, two to three energy drinks at work, another energy drink or soda on the way home, and then another soda for dinner,” he says.

Bivens’s last relapse, his sixth, occurred three years ago and ended with him staying up until 3:00 a.m. researching conspiracy theories about 9/11 and Prince’s death and getting into heated exchanges in YouTube comments sections. He hasn’t had a drop of the hard stuff since, and he says his health has improved dramatically. The headaches are gone, his vision is steady, his energy level is stable throughout the day, he sleeps through the night, and his anxiety and impulsiveness have ebbed. Bivens now counsels other people on the dangers of caffeine and how to kick their own habits.

“I’ve talked to many people who are a year off of caffeine and they’re still dealing with crazy symptoms, everything from neuropathy to psychosis,” Bivens says. These people have suffered a “caffeine injury,” as he calls it, and he’s certain there are untold numbers of others out there also suffering needlessly. If they only knew the reality of caffeine, he argues, their pain might ease. “Caffeine injures your central nervous system,” he says. “A lot of people are walking around being affected by caffeine and they don’t even know it.”

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Home — Essay Samples — Nursing & Health — Drugs — Drugs: Effects and Solutions Explored in Research

Drugs: Effects and Solutions Explored in Research

• Categories: Drug Addiction Drugs

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Published: Dec 3, 2020

Words: 1959 | Pages: 4 | 10 min read

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Introduction, drugs in general, drugs and society, drug abuse solutions.

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