Never Enough: The Neuroscience and Experience of Addiction
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The opposite of addiction, I have learned, is not sobriety but choice.
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As James Baldwin put it, “Freedom is hard to bear”; for those who don’t recognize the tenuousness of the situation, just pray that habits, bank accounts, or other props remain securely in place.
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I’d finally reached the dead end where I felt I was incapable of living either with or without mind-altering substances. This bleak situation describes the condition of many, if not all, addicts and illustrates why relatively few recover. Despite being depleted, they think the cost of abstinence seems much too high: Without drugs, what is there to live for anyway?
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Never does nature say one thing and wisdom another. —Juvenal (Roman poet, A.D. 60–130)
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it’s beginning to seem that the brain is more like a stage for our life to be acted out upon than like the director behind a curtain calling shots.
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The brain is no more static than a river as currents constantly form from the flow of our experience. In this way, and in others, we are shaped by our environment.
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The fundamental role of the brain is to be a contrast detector. As experiences are distinguished from monotony, they spark neurochemical changes in specific brain circuits, informing us of all we care to know:
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all addictive drugs are addictive precisely because they share the ability to stimulate the mesolimbic dopamine system.
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We now also understand that the opposite of pleasure is not depression but anhedonia, the inability to experience pleasure.
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In recent years, new evidence has shown that dopamine in the mesolimbic pathway works not exactly by signaling pleasure but by signaling the anticipation of pleasure. This anticipatory state is not the same as the pleasure associated with satisfaction, contentment, or release, but rather the anxious, lip-smacking foretaste of something of import that is just around the corner.
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Parkinson’s sufferers have extreme difficulty enacting their intentions. For instance, people with Parkinson’s describe an incredible mental effort required to do a simple motor task such as buttoning a shirt. Parkinsonian deficits occur between the desire to move and the movement circuitry, which are both intact.
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An addict doesn’t drink coffee because she is tired; she is tired because she drinks coffee.
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“How singular is the thing called pleasure, and how curiously related to pain, which might be thought to be the opposite of it…he who pursues either of them is generally compelled to take the other. They are two, and yet they grow together out of one head or stem.” This philosophical observation, recorded around 350 B.C.E., astutely predicted the experimental insights of the nineteenth-century French physiologist Claude Bernard. Bernard is credited as the first to note that moving between opposite biological states enables our bodies to maintain stability in the face of disruption—anything ...more
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Developing tolerance to selective serotonin reuptake inhibitors (SSRIs) may help to change a pathological affective “set point” so that being depressed is no longer the patient’s normal state.
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Maybe this helps explain why people push themselves to exercise or go to graduate school.
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Cutting-edge treatments take almost the opposite tact from the pastoral setting strategy (unless of course your using primarily took place on the farm). Following detox and some stability in mood and physiology (usually after several weeks of clean time), the addict is purposely exposed to cues that used to coincide with using, but this time within a supportive, therapeutic context. Wads of cash, drawing fluid into a syringe, or experiencing a disappointing day at first is likely to produce profound physiological and psychological effects such as changes in heart rate, body temperature, and ...more
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Not to belabor the point, but in many ways my relationship with the drug was among the purest and most wonderful relationships of my life. From the first time I got high until long after I’d smoked my last bowl, I loved marijuana like a best friend.
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So, if you smoke weed, remember that infrequent and intermittent use is the best way to prevent downregulation and its unfortunate effects: tolerance, dependence, and a loss of interest in the unenhanced world.
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endorphins (endogenous morphine-like substances), the body’s natural painkillers.
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mouth? Anti-opiates are at least partly to blame. Research has demonstrated that anti-opiates contribute to addiction as a major source of sickness and misery in opiate addicts.
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Although the number of opiate receptors isn’t dramatically decreased in a chronic narcotic user (the way CB1 receptors decrease in marijuana smokers), the ability of opiates to affect intracellular signaling is compromised with frequent use, so the receptors are downregulated in effectiveness if not in number.
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This is to say that opiate addiction (like all addiction) is to some degree contextual. Such a point was made most strongly in recent history by a large group of U.S. veterans of the Vietnam War. Up to 20 percent of these troops sought escape by taking narcotics that were readily available in Southeast Asia. Congress had some warning of the pending problem as the troops were scheduled to return home at the end of the war, and national hearings were held by the Nixon administration to figure out what to do. It was decided that soldiers who tested positive would be detoxed overseas and carefully ...more
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The bottom line for opiate users, and the bottom line of this book, is that there can never be enough drug. Because of the brain’s tremendous capacity to adapt, it’s impossible for a regular user to get high, and the best a voracious appetite for more drug can hope to accomplish is to stave off withdrawal. This situation is best recognized as a dead end.
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The bipolar practice of pitying addicts while at the same time greasing virtually every social interaction with an obscene amount and variety of booze seems heartless if not mindless.
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True, at times life can be awful, disappointing, terrifying, or mind-numbingly tedious. But just the same, there is the frequent possibility of being overcome with joy, gratitude, or delight.
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Some of it is metabolized in the stomach, though more for men than for women due to sex differences in the amount of enzyme contained in the gastric fluid.
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My sense of ease was likely due to the drug’s foremost neural consequence: facilitating GABA neurotransmission. GABA is one of the most prevalent neurotransmitters and the primary inhibitory neurotransmitter in the brain. Because GABA-mediated inhibition is enhanced by alcohol, neural activity slows down. At moderate doses this reduces anxiety, but at higher concentrations it produces sedation and eventually sleep (sometimes known as passing out). Enhancing activity at GABA synapses likely made me feel very relaxed.
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Alcohol also reduces activity at glutamate receptors. Glutamate happens to be the primary excitatory neurotransmitter, so this plus GABA inhibition really tamps down the electrical activity of neurons. Glutamate is also critical for forming new memories,
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Because beta-endorphin contributes to a sense of well-being by soothing stress and facilitating social affiliation, those of us with naturally low levels may experience less sense of safety and connection, even as children, on a day-to-day basis.
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A recent study evaluated the effects of drinking in over half a million people around the world and found that even one drink a day is associated with a number of diseases (including cancers and cardiovascular issues) that lead to premature death.
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People who begin drinking in their early teens, as I did, are at least four times more likely to eventually meet the criteria for an alcohol use disorder.
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The dosage difference between the sexes is due to the fact that it takes less alcohol for women to achieve the same blood concentrations as men. This is due to differences in the concentration of the ALDH enzyme found in the gut, mentioned above, as well as sex differences in the proportion of body fat. A male typically has more blood than an equally weighted female because women have a higher proportion of body fat, and fat requires less blood than muscle does. Lower blood volume and slower metabolism may also partly explain the steeper dive in women alcoholics who more quickly progress to ...more
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And in the United States during the period between 2006 and 2010, excessive alcohol use was responsible for close to 90,000 deaths a year, including one in ten deaths among adults aged twenty to sixty-four, translating to 2.5 million years of potential life lost.
Adam
My dad forms part of that statistic!
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Stereotypy is evident as highly dosed or sensitized individuals engage in purposeless, repetitive movement. There can be other causes of stereotypical behavior besides drugs, but it is common enough among speed users to have its own slang: users often refer to stereotypies as punding or tweaking, as they mindlessly sort, clean, or dis- and reassemble objects, for example.
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Some have hypothesized that this quirky and unfortunate adaptation may account for the association between cocaine use and anxiety disorders, which emerge with frequent use and grow worse as the addiction progresses.
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In moderate doses, caffeine may elevate mood and reduce symptoms of depression.
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Adenosine may be familiar in its role in adenosine triphosphate, or ATP, a primary source of energy. But adenosine also serves as a neurotransmitter and is thought to build up over the day, accumulating in synapses where it binds to its receptors, precipitating a state of drowsiness. When caffeine is on board, adenosine signaling is blocked and as a result temporarily prevents or relieves drowsiness and maintains or restores alertness.
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On average, tobacco users lose fifteen years of life.
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A cousin of the GABAA receptor, nAChRs are also made of five subunits that surround a central pore. This receptor permits the flow of sodium, rather than chloride, and because sodium ions carry a positive charge, nAChRs are excitatory. Nicotine activates these receptors by substituting for acetylcholine and thereby increasing neuronal activity. Also reminiscent of the GABAA receptor, much of the structural and functional diversity of nAChRs arises from the many possible subunit combinations; in this case, there are sixteen different subunits. These combine to form different nAChR subtypes, ...more
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the nAChR has three states: closed, open, and desensitized. The open state is responsible for the stimulant properties of the drug, while the desensitized state produces a cigarette’s calming effects.
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Like other addictive substances, nicotine initiates addiction by stimulating mesolimbic dopamine pathways, but cigarette smoking affects multiple processes including thinking and attention, learning and memory, emotion, arousal, and motivation because of the distribution of nAChRs in circuits that contribute to all these behaviors.
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Because nAChRs affect the release of virtually every major transmitter, neuro-adaptations from chronic exposure lead to widespread and general alterations in neurotransmission throughout the brain.
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Despite its action being specific and well known, there are no FDA-approved pharmacotherapies for cocaine addiction.
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A study published by Lynn Taurah and her colleagues in 2014 should be read by everyone thinking of using this drug.10 The aim of their study was to see whether MDMA produces lasting effects on humans, as it does in other animals.
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occasion special. I’ve often been caught in this logical koan: I can do any drug I want, as long as I don’t really want to do it.
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One of my favorite examples from the animal kingdom comes from a particular species of ants (Lasius flavus) that fosters beetles (Lomechusa) in an apparently symbiotic relationship where the ants feed adult beetles and nurture their larvae (at the expense of their own colony) in order to regularly partake of a goo exuded from beetle glands that seemingly serves no purpose other than to make the ants really calm.
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The four are these: an inherited biological disposition, copious drug exposure, particularly during adolescence, and a catalyzing environment. It’s not necessary to have all four, but once some threshold is reached, it’s like breaching a dam—virtually impossible to rebuild.
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For example, Rachel Yehuda and her colleagues have data suggesting that children of Holocaust survivors might carry epigenetic modifications from their parents that make them primed for stress.
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As I confronted my own assumptions, I realized how incredibly convenient a biological explanation for Native addiction rates would be for the rest of us. If we could attribute the epidemic of alcoholism and fetal alcohol effects on reservations to something about “them,” we wouldn’t have to ask about our complicity in the systematic denigration of their cultures, the theft of land and other resources, or realize that being exiled with little hope for personal growth or community prosperity might drive anyone to drink.
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By any account, the “war on drugs” has been a recurrent and dismal failure. I would argue that that is because finger-pointing and violence do nothing to subdue the drive to escape the pain of our existence; if anything, they make it worse.
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