Research shows that the main reason that kids don't use alcohol, tobacco, or drugs is because of their parents . . .
Research shows that the main reason that kids don’t use alcohol, tobacco, or drugs is because of their parents -- because of their positive influence and because they know it would disappoint them. That’s why it is so important that parents build a strong relationship with their kids and talk to them about substance abuse -- the earlier the better!
The good news is it’s easy to do! Here are a few ways you can build a positive relationship with your kids and start talking to them about drugs.
Note: “Drugs” refers to alcohol, tobacco, and illegal drugs.
Establish and maintain good communication with your children.
Why? The better you know your children, the easier it will be to guide them towards positive activities and friendships.
Why? Young people are less likely to get involved with drugs when caring adults are a part of their life.
Why? Research shows that when parents set harsh rules or no rules, kids are more likely to try drugs.
Why? Children imitate adults.
Why? When children have friends who don’t engage in risky behaviors, they are likely to resist them too.
Why? When parents talk to their kids early and often about substance abuse, kids are less likely to try drugs.
Mike Robinson Assistant Professor of Psychology, Wesleyan University originally Sep 29, 2017
Why do they do it? This is a question that friends and families often ask of those who are addicted.
It’s difficult to explain how drug addiction develops over time. To many, it looks like the constant search for pleasure. But the pleasure derived from opioids like heroin or stimulants like cocaine declines with repeated use. What’s more, some addictive drugs, like nicotine, fail to produce any noticeable euphoria in regular users.
So what does explain the persistence of addiction? As an addiction researcher for the past 15 years, I look to the brain to understand how recreational use becomes compulsive, prompting people like you and me to make bad choices.
Myths about addiction
There are two popular explanations for addiction, neither of which holds up to scrutiny.
The first is that compulsive drug taking is a bad habit – one that addicts just need to “kick.”
However, to the brain, a habit is nothing more than our ability to carry out repetitive tasks – like tying our shoelaces or brushing our teeth – more and more efficiently. People don’t typically get caught up in an endless and compulsive cycle of shoelace tying.
Another theory claims that overcoming withdrawal is too tough for many addicts. Withdrawal, the highly unpleasant feeling that occurs when the drug leaves your body, can include sweats, chills, anxiety and heart palpitations. For certain drugs, such as alcohol, withdrawal comes with a risk of death if not properly managed.
The painful symptoms of withdrawal are frequently cited as the reason addiction seems inescapable. However, even for heroin, withdrawal symptoms mostly subside after about two weeks. Plus, many addictive drugs produce varying and sometimes only mild withdrawal symptoms.
This is not to say that pleasure, habits or withdrawal are not involved in addiction. But we must ask whether they are necessary components of addiction – or whether addiction would persist even in their absence.
Pleasure versus desire
In the 1980s, researchers made a surprising discovery. Food, sex and drugs all appeared to cause dopamine to be released in certain areas of the brain, such as the nucleus accumbens.
This suggested to many in the scientific community that these areas were the brain’s pleasure centers and that dopamine was our own internal pleasure neurotransmitter. However, this idea has since been debunked. The brain does have pleasure centers, but they are not modulated by dopamine.
So what’s going on? It turns out that, in the brain, “liking” something and “wanting” something are two separate psychological experiences. “Liking” refers to the spontaneous delight one might experience eating a chocolate chip cookie. “Wanting” is our grumbling desire when we eye the plate of cookies in the center of the table during a meeting.
Dopamine is responsible for “wanting” – not for “liking.” For example, in one study, researchers observed rats that could not produce dopamine in their brains. These rats lost the urge to eat but still had pleasurable facial reactions when food was placed in their mouths.
All drugs of abuse trigger a surge of dopamine – a rush of “wanting” – in the brain. This makes us crave more drugs. With repeated drug use, the “wanting” grows, while our “liking” of the drug appears to stagnate or even decrease, a phenomenon known as tolerance.
In my own research, we looked at a small subregion of the amygdala, an almond-shaped brain structure best known for its role in fear and emotion. We found that activating this area makes rats more likely to show addictive-like behaviors: narrowing their focus, rapidly escalating their cocaine intake and even compulsively nibbling at a cocaine port. This subregion may be involved in excessive “wanting,” in humans, too, influencing us to make risky choices.
The recent opioid epidemic has produced what we might call “involuntary” addicts. Opioids – such as oxycodone, percocet, vicodin or fentanyl – are very effective at managing otherwise intractable pain. Yet they also produce surges in dopamine release.
Most individuals begin taking prescription opioids not for pleasure but rather from a need to manage their pain, often on the recommendation of a doctor. Any pleasure they may experience is rooted in the relief from pain.
However, over time, users tend to develop a tolerance. The drug becomes less and less effective, and they need larger doses of the drug to control pain. This exposes people to large surges of dopamine in the brain. As the pain subsides, they find themselves inexplicably hooked on a drug and compelled to take more.
The result of this regular intake of large amounts of drug is a hyperreactive “wanting” system. A sensitized “wanting” system triggers intense bouts of craving whenever in the presence of the drug or exposed to drug cues. These cues can include drug paraphernalia, negative emotions such as stress or even specific people and places. Drug cues are one of an addict’s biggest challenges.
These changes in the brain can be long-lasting, if not permanent. Some individuals seem to be more likely to undergo these changes. Research suggests that genetic factors may predispose certain individuals, which explains why a family history of addiction leads to increased risk. Early life stressors, such as childhood adversity or physical abuse, also seem to put people at more risk.
Addiction and choice
Many of us regularly indulge in drugs of abuse, such as alcohol or nicotine. We may even occasionally overindulge. But, in most cases, this doesn’t qualify as addiction. This is, in part, because we manage to regain balance and choose alternative rewards like spending time with family or enjoyable drug-free hobbies.
However, for those susceptible to excessive “wanting,” it may be difficult to maintain that balance. Once researchers figure out what makes an individual susceptible to developing a hyperreactive “wanting” system, we can help doctors better manage the risk of exposing a patient to drugs with such potent addictive potential.
In the meantime, many of us should reframe how we think about addiction. Our lack of understanding of what predicts the risk of addiction means that it could just as easily have affected you or me. In many cases, the individual suffering from addiction doesn’t lack the willpower to quit drugs. They know and see the pain and suffering that it creates around them. Addiction simply creates a craving that’s often stronger than any one person could overcome alone.
That’s why people battling addiction deserve our support and compassion, rather than the distrust and exclusion that our society too often provides.
From the UMass media release:
Using a computational model of addiction, a literature review and an in silico experiment, theoretical computer scientist Yariv Levy and colleagues suggest in a new paper this week that rehabilitation strategies coupling meditation-like practices with drug and behavior therapies are more helpful than drug-plus-talk therapy alone when helping people overcome addiction.
Levy reports results of his survey of animal and human studies and a computational experiment in a special section on addictive disorders in the current issue of the open access journal Frontiers in Psychiatry. He conducted this investigation while a doctoral student at the University of Massachusetts Amherst with neuroscience researcher Jerrold Meyer, an expert in the neurochemistry of human psychiatric disorders, and computer scientist Andrew Barto, an expert in mathematical theory of learning and planning.
Levy says the goal is to translate what has been learned from animal and human studies to better understand addiction and explore new approaches to treatment. Another member of the research team was neuroeconomist Dino Levy of Tel Aviv University, an expert in decision-making processes who developed the core of the theoretical model. He is no relation to lead author Yariv Levy.
Levy says, “Our higher-level conclusion is that a treatment based on meditation-like techniques can be helpful as a supplement to help someone get out of addiction. We give scientific and mathematical arguments for this.”
His theoretical research approach using virtual subjects is rather unusual, Levy acknowledges, but it’s now gaining significant trust because it offers some strengths. In particular, because it relies on the increasing amount of available data and knowledge, in silico research offers quick preliminary tests of “rationally supported speculations,” he says, before full-scale experiments are launched with human patients or animals.
“I am a theoretician, so I use other peoples’ studies and try to see how they work together and how experiments fit in,” Levy points out. “This work follows a knowledge repository (KR) model, where the knowledge comes from other peoples’ theories and experiments. By consolidating them, we propose some hypotheses that we hope will subsequently be tested by experts in the field.” The KR model used in his current work incorporates pharmacokinetic, pharmacodynamic, neuropsychological, cognitive and behavioral components, the researcher notes.
The researchers explored the allostatic theory of addiction by combining two existing computational models, one pharmacological and the other a more behavioral-cognitive model. The allostatic theory describes changes in the brain’s reward and anti-reward systems and reward set points as substance misuse progresses. “Neural adaptations arising from the reward system itself and from the anti-reward system provide the subject with functional stability, while affecting the person’s mood. We propose a computational hypothesis describing how a virtual subject’s drug consumption, cognitive substrate and mood interface with reward and anti-reward systems,” they write.
Put more simply, the allostatic theory says that when someone takes a drug he or she stresses the reward system and it loses its homeostatic or equilibrium state. “We smoke one cigarette and go out, come back in again, and out with another cigarette, always trying to return to equilibrium,” Levy says.”The reward system tries to change its structure with neural adaptations to get back to equilibrium. But if I continue to smoke, even with such adaptations, I can’t make it back. Equilibrium is broken as long as I continue to smoke.”
Here a second mechanism kicks in. “The reward system is so stressed, one can’t come back to equilibrium,” Levy explains. “So the anti-reward system says, ‘I’ll try to help.’ The person or animal enters an allostatic state.” Other brain structures are affected by the addictive substance, impairing the addict’s evaluation of drug use compared to other reinforcers, he adds.
To bind the two theories and test how they could work together in silico, the authors follow three virtual case studies, each representing a different trajectory of allostatic state during escalation of cigarette smoking. Case Study 1 shows a virtual subject consuming drugs for the first time, relapsing after a period of abstinence with a concomitant negative shift in mood, a baseline situation with no therapeutic intervention. In Case Study 2, among other variations, the virtual subject uses a nicotine patch for 25 days while the same variables including mood are evaluated as for Case Study 1. In Case Study 3, the virtual subject undergoes treatment intended to emulate healing therapy periods that include meditation.
Among other outcomes, Levy says, “We try to describe what could be the cognitive effect of using a nicotine patch. What does it imply at the cognitive level, when people are willing to use one? Others have showed changes in prefrontal cortex where decisions are made, in executive function, as drug use progresses. Also, we did a small simulation of a couple of weeks with a patch, then tried to simulate the cognitive effect of using meditation for a few weeks.”
Overall, “This investigation provides formal arguments encouraging current rehabilitation therapies to include meditation-like practices along with pharmaceutical drugs and behavioral counseling,” the authors write.