Surgeon General’s Report Summary – Chapter 2
Surgeon General’s Report Summary – Chapter 2
Scientific breakthroughs have revolutionized the understanding of substance use disorders. For example, severe substance use disorders, commonly called addictions, were once viewed largely as a moral failing or character flaw, but are now understood to be chronic illnesses characterized by clinically significant impairments in health, social function, and voluntary control over substance use. – Pg. 2-1
Through rigorous scientific studies, addiction to alcohol or drugs has been found to be a chronic brain disease. As stated in this Report, not everyone who uses alcohol or drugs will develop an addiction. There are many factors that contribute to the development of a Substance Use Disorder (SUD), or Alcohol Use Disorder (AUD), also known as addiction.
Those factors include:
These factors can either elevate risk of substance use, misuse, and substance use disorders, or they can act as barriers against these risks.
The three brain regions which are involved in the development and continuation of SUD’s are the basal ganglia, extended amygdala, and the prefrontal cortex. Using MRI’s and PET scans, researchers are better able to understand the long-term effects of substance use, as well as the changes in brain chemistry. Each of these three regions of the brain are responsible for the following:
While these three regions are not solely responsible for addiction, they do play a large part.
Through human and animal research, studies have provided a useful way to understand addiction. The three stages of addiction are:
During the initial, and subsequent use of substances, the following four behaviors are fundamental to the addiction cycle:
Impulsivity occurs when a person takes a drug or a drink, without thinking about the consequences. For example, an adolescent takes a drink because of peer pressure, and does not take into consideration the possible punishment from a parent.
Positive reinforcement occurs when a person experiences a pleasurable experience during use. For example, no consequences occur during or after use, which results in increased likelihood of using again.
Negative reinforcement occurs when a person uses a substance to find relief from negative feelings such as stress, anxiety or depression. For example, a person drinks at a social gathering to relieve themselves of the stressors related to social anxiety. When this feeling is relieved, the likelihood of continued use is increased.
As a person continues using, they build a tolerance to the substance. As their tolerance grows, they continually seek the relief they first experienced upon initial use. Therefore, compulsivity can be described as an attempt to escape the negative feelings associated with withdrawals.
Eventually, the person begins taking the substance not to get “high,” but rather to escape the “low” feelings to which, ironically, chronic drug use has contributed. Compulsive substance seeking is a key characteristic of addiction, as is the loss of control over use. Compulsivity helps to explain why many people with addiction experience relapses after attempting to abstain from or reduce use. – Pg. 2-8
During this stage, substance use heavily affects the basal ganglia, as well as its two sub-regions which are the nucleus accumbens and the dorsal striatum. The nucleus accumbens involves motivation and the experience of reward. The dorsal striatum involves habit forming and routine behaviors.
When using a substance such as alcohol, or drugs, they produce a feeling of pleasure. The rewarding effects produced by a substance activate the brain’s dopamine and opioid signaling system, which reinforces the likelihood of continued use. Stimulants such as nicotine, cocaine, and amphetamines are shown to affect the dopamine releasing neurons.
Studies also show changes in the brain relating to how a person is affected by outside stimuli. When using a substance, the reward centers are not only triggered by the substance itself, but also by people, places, and things associated with using. For example, a bar where one does most of their drinking, drug paraphernalia, or people that a person uses with.
This triggering affect is called incentive salience, and can continue not only after the effects of a substance wears off, but also while a person is in recovery.
Together, these studies indicate that stimuli associated with addictive drugs can, by themselves, produce druglike effects on the brain and trigger drug use. These findings help to explain why individuals with substance use disorders who are trying to maintain abstinence are at increased risk of relapse if they continue to have contact with the people they previously used drugs with or the places where they used drugs. – Pg. 2-12
The dorsal striatum is involved in the habit-forming aspect of addiction. Changes in the dorsal striatum can be triggered by release of dopamine and glutamate. If these changes occur, substance seeking and use strengthen the process of addiction, and can lead to compulsive use.
The withdrawal/ negative affect stage occurs after a person stops using alcohol or other substances. Depending on the frequency of use, the withdrawal symptoms can be mild to severe, and can include physical illness, and/ or negative emotions.
Researchers believe the negative withdrawal affects come from two sources:
Studies of human brain scans have shown decreases in the D2 dopamine receptor. Because of this decrease in dopamine release, studies suggest the brain’s reward system and circuitry are affected, thus promoting the continued use of substances. A person who is addicted continues to attempt to achieve the pleasurable feelings associated with use, but is unable to because of this change in the reward system. This impairment is believed to be a contributing factor to continued substance use in an individual who is addicted.
During the withdrawal stage, a second process occurs in the extended amygdala which is the activation of stress neurotransmitters. Pg. 2-14
The negative feelings associated with stress-triggered substance use, and withdrawal are suggested to be caused by the activation of these neurotransmitters.
This stage of addiction involves a decrease in the function of the brain reward systems and an activation of stress neurotransmitters, such as CRF and dynorphin, in the extended amygdala. Together, these phenomena provide a powerful neurochemical basis for the negative emotional state associated with withdrawal. The drive to alleviate these negative feelings negatively reinforces alcohol or drug use and drives compulsive substance taking. –
In Summary, Pg. 2-15
During the preoccupation/ anticipation stage, a person who is addicted experiences craving, or preoccupation with using again. Human studies have not been able to measure craving, and has not been shown to coincide with relapse.
During this stage, the prefrontal cortex is affected. This region is responsible for:
Because of changes to the prefrontal cortex, a person’s ability to use executive function is diminished. Executive function is the ability to choose whether to use a substance or not, and override urges to use when faced with environmental triggers, or stressful experiences.
Some scientists have divided the roles of this area of the brain into two functions: Stop and Go.
When changes in the prefrontal cortex have occurred, the Go function of this area is overstimulated, resulting in increased habit forming and impulsivity found in substance use. The Stop function of the brain is also affected when the ability to use executive function is diminished.
With continued use of substances, the cycle of binge/ intoxication, withdrawal/ negative affect, and preoccupation/ anticipation worsens over time, and causes changes in the brain. These changes are found to provide the urge to use substances more and more often.
This report goes into further detail how different substances affect the brain. Because of my goal to present the information contained in this report in simple, easy to read information, I will refrain from recapping this section. Please see the chapter link at the end of this post for more information. Beginning on page 2-18, the following substances are reviewed:
Certain stressors experienced in early childhood or adolescence are found by researchers to act similarly to addictive substances by triggering stress circuits in the brain. Those risk factors include:
In addition to these risk factors, research has indicated possible pre-existing differences in the brains of adolescents who go on to develop an SUD vs. those who do not. This difference lies in the frontal cortex, which is part of the prefrontal cortex, and is located in the front part of the brain.
About three quarters (74 percent) of 18- to 30-year-olds admitted to treatment programs began using substances at the age of 17 or younger. – Pg. 2-22
This region of the brain is also a critical at-risk region in adolescents because not only is it the last region to fully develop, that development is not complete until a person reaches their early to mid-20’s. The earlier an adolescent is exposed to drugs or alcohol, the greater the possibility of developing a substance use disorder down the line.
Genetic factors are thought to account for 40 to 70 percent of individual differences in risk for addiction. – Pg. 2-22
Along with environmental factors, a person’s genes can also play a part. Studies have found specific gene variants that can protect against, or predispose, the development of an addiction. Some of these gene variants are linked to metabolism of nicotine and alcohol, while others are linked to key neurotransmitters and molecules in the brain.
According to a study done in 2015 by NSDUH (National Survey on Drug Use and Health), 20.8 million people aged 12 or older had a substance use disorder during the past year. Of those 20.8 million:
Particularly striking is the 3- to 4-fold higher rate of tobacco smoking among patients with schizophrenia and the high prevalence of co-existing alcohol use disorder in those meeting criteria for PTSD. It is estimated that 30-60 percent of patients seeking treatment for alcohol use disorder meet criteria for PTSD, and approximately one third of individuals who have experienced PTSD have also experienced alcohol dependence at some point in their lives. – Pg. 2-22 to 2-23
While the link between substance use disorders and mental disorders is unclear, three possible explanations may help us understand this link:
Because these three possibilities do not affect everyone in the same way, mental and substance use disorders may form from a mixture of the above processes. Also, diagnosis and treatment planning is made difficult because these two disorders commonly have overlapping symptoms. For example, meth users may experience hallucinations, paranoia, and delusions, which are also common symptoms of schizophrenia. Pg. 2-23
Although many factors play a role in the vulnerability of developing a substance misuse or use disorder, studies have shown gender may make one more susceptible than others.
For example, men are at a higher risk for alcohol use disorder because they tend to drink more than women. This trend of men drinking more than women is shown to be declining. They are also more likely to experience other substance use disorders.
However, according to clinical reports, women are shown to progress from initial use to a disorder at a faster rate when they use cocaine, alcohol, or opioids. This progression is called telescoping. Women are also shown to suffer greater symptoms of withdrawal from nicotine. Women’s withdrawal symptoms have been reported to be worse, and they are shown to have higher cortisol levels (stress hormone). Pg. 2-23
Limited research has been done in the area of racial and ethnic groups in terms of substance use and substance use disorders. From the research that has been conducted, the following points have been found:
While addiction to alcohol or other substances has been shown to be a relapsing brain disease, studies have shown that recovery is possible.
To view the PDF file of this chapter, please follow this link: https://addiction.surgeongeneral.gov/chapter-2-neurobiology.pdf