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49 pages 1 hour read

Gabor Maté

In the Realm of Hungry Ghosts

Nonfiction | Book | Adult | Published in 2008

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Part 3Chapter Summaries & Analyses

Part 3: “A Different State of the Brain”

Part 3, Chapter 11 Summary: “What is Addiction?”

Maté defines addiction scientifically as the recurring use of a substance despite undesired consequences. He warns against defining addiction too simplistically, because it has so many facets. Then he makes the distinction between compulsive and addictive behaviors. An addiction begins in the pursuit of pleasure. But compulsive urges are unpleasant: Someone who acts compulsively does so in order to make the feeling of abstinence stop.

 

In his definition of dependence, “The addict comes to depend on the substance or behavior in order to make himself feel momentarily calmer or more excited or less dissatisfied with his life” (139).

Part 3, Chapter 12 Summary: “From Vietnam to Rat Park: Do Drugs Cause Addiction?”

Maté addresses the misconception that using a drug will always lead to addiction. Addiction is a human problem not easily reduced solely to chemicals. Exposure does not create risk. A person who becomes an addict is already at risk when encountering the drug.

 

His primary example is that of soldiers who used heroin during the Vietnam War. When they returned from Vietnam, the remission rate was “95 percent, unheard of among narcotics addicts treated in the U.S.” (142).

 

Based on animal experiments, and in particular an experiment with rats an addiction known as Rat Park, Maté believes that the roots of addiction are environmental. In a normal environment, rats did not become addicts. Rats in cages—which he reads as rats subjected to unusual stressors—were more susceptible to addiction.

 

In order to increase the probability of addiction, Maté cites three factors that must be present: “A susceptible organism; a drug with addictive potential; and stress” (147). 

Part 3, Chapter 13 Summary: “A Different State of the Brain”

Maté cites research purportedly showing that addiction represents a different brain state. The brains of cocaine addicts show less white matter. There’s also a reduction in grey matter density, and the ratios damaged brain tissue vary across drugs.

 

The remainder of the chapter discusses the function of dopamine in addiction. Dopamine is “a key brain chemical messenger that played a central role in all forms of addiction” (151). Dopamine spikes in relation to actions and habits that the brain interprets as being pleasurable or rewarding. There is research suggesting that the brains of addicts have fewer dopamine receptors, and those brains are more likely to interpret external forms of dopamine stimulus as inordinately rewarding.

 

Any activity that promotes dopamine rises can be addictive. As the brain changes its biology in relation to the dopamine spikes caused by drug use, it begins to encode altered behaviors as normal: “It is in this sense that medical language refers to addiction as a chronic disease” (154). 

Part 3, Chapter 14 Summary: “Through a Needle, a Warm, Soft Hug”

Today’s drugs have their origins in plants that have been known for thousands of years. Maté gives a brief history of heroin, cocaine, and alcohol. The drugs make use of the brain’s natural apparatuses that are already present. He believes that, “Addiction may not be a natural state, but the brain regions in which its powers arise are central to our survival” (158).

 

The brain does not contain circuits that exist solely to facilitate addiction. Rather, “The brain systems involved in addiction are among the key organizers and motivators of human emotional life and behavior—hence addiction’s powerful hold on human beings” (158).

 

Maté spends the rest of the chapter on the network of the Opioid Apparatus, which is responsible for the production of endorphins. Endorphins ease pain and have a soothing effect on stress of all kinds. Endorphins also play a role in emotions that help bond mothers to children, and which produce the intense pleasures and rewards of sex. When endorphins lock into opiate receptors, they create attachments. If a mother became desensitized to the effects of her own endorphins—produced by her own opiate apparatus—the well-being of her infant would be at risk.

 

Opiates do not remove pain, but make it bearable. A structure called the Anterior Cingulate Cortex (ACC) is what interprets pain subjectively and emotionally. Opiates reduce the emotional impact of pain in the ACC. 

Part 3, Chapter 15 Summary: “Cocaine, Dopamine, and Candy Bars: The Incentive System in Addiction”

Maté describes a 24-year-old addict named Lisa, who is suffering from syphilis. She does not know who her sexual partner was when she contracted the disease, because she was prostituting herself with multiple men for cocaine money.

 

To describe an area of the brain known as the Ventral tegmental apparatus (VTA), Maté examines the neurological process of cocaine use. The VTA gives rise to elation and desire. With continual VTA activation, due to cocaine use, the system responds by conditioning itself to want more. Nerve fibers in the VTA release dopamine. Through this process,

 

The VTA thus forms the neurological basis of another major brain system involved in the addiction process: the incentive-motivation apparatus. This system responds to reinforcement, and the reinforcements all have the effect of increasing dopamine levels in the NA (168).

 

The NA is the brain’s pleasure center.

 

Maté gives an example of this process involving a candy bar. If you see a candy bar and want to eat it, this is likely the result of a reinforced behavior. Seeing the candy bar reminds your brain of candy bars that you have enjoyed in the past, and releases dopamine to positively reinforce your desire to eat this one. Environmental cues—including past experience—release dopamine. For instance, Maté feels an increased excitement, brought on by rising dopamine, when he drives towards Sikora’s music store on the way to work. He compares the feeling to the statements of addicts who claim that “obtaining and preparing the substance gives them a rush quite apart from the pharmaceutical effects that follow drug injection” (170).

 

The dopamine released by behaviors such as CD shopping reinforce the urge to shop compulsively in the future, creating an addictive loop. 

Part 3, Chapter 16 Summary: “Like a Child Not Released”

Claire is one of the most challenging personalities at PHS. When under the influence, she has an abusive history with the entire staff, which has specific rules to govern her behavior. When she shouts curses at Maté, he tells her that her behavior is unacceptable. Claire blames her addiction. Maté believes that “her explanation that she is addicted—and that therefore her drug use is not the result of thoughtful deliberation—fits with the research evidence. It sounds like a cop-out, but in neurological terms, it’s not” (174).

 

Much of chapter 16 involves the self-regulation circuits, which an addict needs in order to resist addiction. Disrupted self-regulation circuits are less likely to help an addict resist drug use.

 

Maté gives an evolutionary history of the brain, focusing on the Prefrontal cortex, or PFC, and the orbitofrontal cortex, or OFC. The PFC plays a role in governing (and restraining) impulsive choices. The OFC “is the apex of the emotional brain and serves as its mission control room” (178). If Claire’s OFC is damaged, it makes sense that her self-control is impaired. But at that point, Maté wonders whether a person can actually choose whether to take a drug or not.  

Part 3 Analysis

Maté’s definition of dependence is the foundation for Part 3: “The addict comes to depend on the substance or behavior in order to make himself feel momentarily calmer or more excited or less dissatisfied with his life” (139). This is a more expansive and more useful definition than the myopic view that an addict is someone who needs to use drugs, and who is unwilling to quit. Because he is trying to reach as broad an audience as possible to change society’s perception of addicts, Maté’s framing of dependence is clever: Everyone knows what it is to desire periods of greater calm and less dissatisfaction.

 

If every behavior that results in a dopamine spike is potentially addictive, then the prospect of avoiding anything with addictive potential dwindles. This fact is critical to Maté’s hypothesis that exposure to a substance—or to a potentially addictive behavior—does not create risk. Maté believes that the risk of increased susceptibility to drugs, or addictive behaviors, is already present at the time the future addict encounters the addictive subject.

 

Maté advances the discussion of risk and accountability by citing three factors that must be present for addiction to occur: “A susceptible organism; a drug with addictive potential; and stress” (147). These three conditions are present in the experiments with the laboratory rats, and to some degree, with the soldiers in Vietnam, although there is no way to verify how many of the men suffered from childhood trauma, a later cornerstone of Maté’s criteria for higher risk of addiction.

 

When the three conditions are present, drugs and behaviors can encode new pathways in the brain. The brain of a long-term cocaine user has less grey matter than that of a non-user, suggestion an alteration in the brain of an addict. It has additional properties and neural channels than it did prior to the introduction of drugs into the system.

 

The discussion of dopamine and its role in changing a brain’s neurology addresses how “medical language refers to addiction as a chronic disease” (154). However, calling addiction a disease (as it’s typically understood), does not lead to treatments that Maté considers ideal. Diseases and ailments tend to have tidy prescriptions purporting to alleviate obvious symptoms. It is easier for a doctor to prescribe a pill, or to encourage a cessation of damaging behavior, than it is to ponder the many factors that may lead to addiction.

 

On the side of the addict, claiming that an addiction is a disease can also be a way to abdicate responsibility. If an addict believes that addiction is a disease, in the same way that cancer is a disease, then they may be less inclined to work proactively against their own behaviors.

 

Maté’s story about Claire is a distillation of Maté’s questions about addiction, free will, and accountability. Claire uses her addiction as the reason for all of her undesirable behaviors. She blames her abusive speech and her defiance on her addiction. However, if she has damaged her brain to the point where her OFC can no longer govern her impulsive behaviors, her lashing out is understandable despite the staff frowning upon it.  

 

Part of the stigma surrounding addicts arises from the idea that they are making bad choices and do not want to change. If, in some cases, the addicts cannot change, whether due to brain damage or disproportionate dopamine levels, how should medical professionals, or even the justice system, view their actions?

 

With regards to Claire, Maté writes, “her explanation that she is addicted—and that therefore her drug use is not the result of thoughtful deliberation—fits with the research evidence. It sounds like a cop-out, but in neurological terms, it’s not (174).

 

It is to these neurological terms that Maté turns his attention in Part 4. 

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