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Drugs, in short, do not make anyone into an addict, any more than food makes a person into a compulsive eater. There has to be a preexisting vulnerability. There also has to be significant stress, as on these Vietnam soldiers—but, like drugs, external stressors by themselves, no matter how severe, are not enough.
Thus, we might say that three factors need to coincide for substance addiction to occur: a susceptible organism; a drug with addictive potential; and stress.
Researchers even know how to make some laboratory creatures—rats, mice, monkeys, and apes—more vulnerable to addiction by genetic manipulations or by interference with prenatal and postnatal development.
Electroencephalograms (EEGs) have identified abnormal electrical brain-wave patterns in some young people who are at greater-than-normal risk for alcoholism.
In the brains of cocaine addicts the age-related expansion of white matter is absent.3 Functionally, this means a loss of learning capacity—a diminished ability to make new choices, acquire new information, and adapt to new circumstances.
It gets worse. Other studies have shown that gray matter density, too, is reduced in the cerebral cortex of cocaine addicts—that is, they have smaller or fewer nerve cells than is normal. A diminished volume of gray matter has also been shown in heroin addicts and alcoholics, and this reduction in brain size is correlated with the years of use: the longer the person has been addicted, the greater the loss of volume.4
In animal studies, reduced nerve cell counts, altered electrical activity, and abnormal nerve cell branching in the brain were found after chronic cocaine use.5 Similarly, altered structure and branching of nerve cells has been seen after long-term opiate administration and also with chronic nicotine use.6 Such changes are sometimes reversible but can last for a long time and may even be lifelong, depending on the duration and intensity of drug use.
the brains of chronic cocaine users had fewer than normal dopamine receptors. The fewer such receptors, the more the brain would “welcome” external substances that could help increase its available dopamine supply.
This recent primate study showed for the first time that the monkeys who developed a higher rate of cocaine self-administration—the ones who became more hard-core users—had a lower number of these receptors to begin with, before ever having been exposed to the chemical.
Because dopamine is important for motivation, incentive, and energy, a diminished number of receptors will reduce the addict’s stamina and his incentive and drive for normal activities when not using the drug. It’s a vicious cycle: more cocaine use leads to more loss of dopamine receptors. The fewer receptors, the more the addict needs to supply his brain with an artificial chemical to make up for the lack.
The brain is accustomed to a certain level of dopamine activity. If it is flooded with artificially high dopamine levels, it seeks to restore the equilibrium by reducing the number of receptors where the dopamine can act. This mechanism helps to explain the phenomenon of tolerance,
It can take months or longer for the receptor numbers in the brain to rise back to pre-drug use figures.
Released from a neuron, or nerve cell, a neurotransmitter such as dopamine “floats” across the synaptic space and attaches to receptors on a second neuron. Having carried its message to the target nerve cell, the molecule then falls back into the synaptic cleft, and from there it is taken back up into the originating neuron for later reuse—hence the term reuptake. The greater the reuptake, the less neurotransmitter remains active between the neurons.
Prozac belongs to a family of drugs that increase the levels of the mood-regulating neurotransmitter serotonin between nerve cells by blocking its reuptake. They’re called selective serotonin reuptake inhibitors, or SSRIs. Cocaine, one might say, is a dopamine reuptake inhibitor.
food seeking can increase brain dopamine levels in some key brain centers by 50 percent. Sexual arousal will do so by a factor of 100 percent, as will nicotine and alcohol.
But none of these can compete with cocaine, which more than triples dopamine levels. Yet cocaine is a miser compared with crystal meth, or “speed,” whose dopamine-enhancing effect is an astounding 1,200 percent.
shift. There are also long-term consequences: chronic drug use remodels the brain’s chemical structure, its anatomy, and its physiological functioning. It even alters the way the genes act in the nuclei of brain cells.
When the brain is diseased, the functions that become pathological are the person’s emotional life, thought processes, and behavior. And this creates addiction’s central dilemma: if recovery is to occur, the brain, the impaired organ of decision making, needs to initiate its own healing process.
The very concept of choice appears less clear-cut if we understand that the addict’s ability to choose, if not absent, is certainly impaired.
All the substances that are the main drugs of abuse today originate in natural plant products and have been known to human beings for thousands of years.
In what was probably the first ideological “War on Drugs” in the New World, the Spanish invaders denounced coca’s effects as a “delusion from the devil.”
must “serve some critical purpose other than promoting the vigorous intake of highly purified chemical compounds recently developed by humans.”1 Addiction may not be a natural state, but the brain regions it subverts are part of our central machinery of survival.
In reality, the constellation of behaviors we call addiction is provoked by a complex set of neurological and emotional mechanisms that develop inside a person.
Addiction may not be a natural state, but the brain regions in which its powers arise are central to our survival.
There is no addiction center in the brain, no circuits designated strictly for addictive purposes. The brain systems involved in addiction are among the key organizers and motivators of human emotional life and behavior—hence addiction’s powerful hold
It was in the 1970s that an innate opioid system was first identified in the mammalian brain. The protein molecules that serve as the chemical messengers in this system were named endorphins by the U.S. researcher Eric Simon because they are endogenous—they originate within the organism—and because they bear a resemblance to morphine.
Not surprisingly, endorphins do for us exactly what plant-derived opioids can do: they’re powerful soothers of pain, both physical and emotional.
nervous system—the part that’s not under our conscious control. They affect many organs in the body, from the brain and the heart to the intestines. They influence mood changes, physical activity, and sleep and regulate blood pressure, heart rate, breathing, bowel movements, and body temperature. They even help modulate our immune system.
When the natural opioid receptor systems of infant lab animals have been genetically “knocked out,” they’re unable to experience secure connection with their mothers.
Using a special tracer chemical, the scan highlighted the activity of opioid receptors in the emotional centers of each participant’s brain. While the women were under the spell of sad memories, these receptors were much less active.6
Scientists have observed, for example, that when people expect relief from pain, the activity of opioid receptors will increase. Even the administration of inert medications—substances that do not have direct physical activity—will light up opioid receptors, leading to decreased pain perception.7
This is the so-called placebo effect, which, far from being imaginary, is a genuine physiological event. The medication may be inert, but the brain is soothed by its own painkillers, the endorphins.
role. In the nervous system they are tranquilizers and painkillers, but in, say, the gut, their role is to slow down muscle contractions. In the mouth, they diminish secretions.
As evolution progressed, systems and substances that had a relatively narrow function in simpler organisms found new arenas of activity in the higher, more complex species that emerged.
vasotocin—a primitive version of the protein oxytocin, which triggers labor contractions and breastfeeding in female mammals.
Vasotocin is an ancient brain molecule that controls sexual urges in reptiles. This same molecule … also helps deliver reptilian young in the world. When a sea turtle, after thousands of miles of migration, lands on its ancestral beach and begins to dig its nest, an ancient bonding system comes into action.… Vasotocin levels in the mother turtle’s blood begin to rise as she digs a pit large enough to receive scores of eggs, and reach even higher levels as she deposits one egg after the other. With her labors finished, she covers the eggs, while circulating vasotocin diminishes to insignificant
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And oxytocin—a more sophisticated version of vasotocin—plays a much more diverse role than does its reptilian counterpart. It not only induces labor but also affects a mother’s moods and promotes her physical and emotional nurturing of infants.
Nurturing mothers experience major endorphin surges as they interact lovingly with their babies—endorphin highs can be one of the natural rewards of motherhood. Given the many thankless tasks required in infant and child care, Nature took care to give us something to enjoy about parenting. Tolerance would more than rob of us those pleasures; it would threaten the infant’s very existence.
By making our brain cells more sensitive to opioids, oxytocin allows us to remain “hooked” on our babies.
Opiates, in other words, are the chemical linchpins of the emotional apparatus in the brain that is responsible for protecting and nurturing infant life.
Thus addiction to opiates like morphine and heroin arises in a brain system that governs the most powerful emotional dynamic in human exi...
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When endorphins lock onto opiate receptors, they trigger the chemistry of love and connection, helping us to be the social creatures we are.
Opiates do not “take away” pain. Instead, they reduce our consciousness of it as an unpleasant stimulus.
A child who complains bitterly of the slightest hurt and is often accused of being a “crybaby” is probably low on endorphins and is likely to be less adventurous than his peers.
A recent imaging study showed that the ACC also lights up when people feel the pain of social rejection.11
Children who have not received the attentive presence of the parent are, as we will see, at greater risk for seeking chemical satisfaction from external sources later in life.
Activation of opiate receptors contributes to the pleasures of marijuana use as well.16
the life-foundational opioid love/pleasure/pain relief apparatus provides the entry point for narcotic substances into our brains. The less effective our own internal chemical happiness system is, the more driven we are to seek joy or relief through drug-taking or through other compulsions we perceive as rewarding.
Cocaine increases brain levels of the neurotransmitter dopamine by blocking it from being transported back into the nerve cells that release it.
There is an area in the midbrain that, when triggered, gives rise to intense feelings of elation or desire. It’s called the ventral tegmental apparatus, or VTA.
