Attention deficit hyperactivity disorder (ADHD) is one of the most commonly diagnosed disorders in childhood. In fact, estimates of the rates of ADHD had found that between 5-10 percent of all children meet diagnostic criteria for the disorder. Children with and without ADHD, at a group level, show several differences, including poorer school performance, more peer rejection, and increased rates of anxiety, depression, and acting out behavior. Following children over time is a common way to study the long term effects associated with psychological problems. Many scientists have used follow-up (longitudinal) studies to examine whether children with ADHD are a greater risk for substance use and abuse/dependence than children without ADHD. Any single study may be imperfect, as studies differ in the way ADHD is measures, substance use or abuse/dependence is measures, the group of children that were followed, or how much time passed between the follow-up assessment. One way to help find clarity in multiple studies of the same question is to conduct a meta-analysis. Meta-analyses run one major analysis using all of the data collected using different groups – more heavily weighting the results from larger studies. Earlier this year, a meta-analysis on the association between a childhood diagnosis of ADHD and trying alcohol, tobacco, marijuana, as well as a substance use disorder (substance abuse or dependence/addiction) was conducted. Continue reading
Do you remember what you did last night? Have you ever not remembered what you did after drinking? Drinking alcohol over a long time period can affect the brain and cause lasting damage including, but not limited to, slips in memory. These memory slips can be due to lack of blood flow to brain areas that are important for memory consolidation and are more commonly known as blackouts. Contrary to what most people seem to believe, blackouts often occur in social drinkers and are don’t seem to be related to age or level of alcohol dependency. Continue reading
Children with attention deficit hyperactivity disorder or ADHD (formerly known also as ADD) are classically seen as the kids in class who have trouble staying in their seats and paying attention during long lessons. Underlying these problematic behaviors is a confluence of factors, with evidence pointing to genetics, neural function, and environmental factors (including parenting and lead exposure), which all can affect ADHD behavior. Many children diagnosed with ADHD seem to simply “grow out” of their symptoms. They may learn particularly effective strategies for managing inattention and disorganization (I myself am a notorious list maker), or learn to control some of the fidgeting and restlessness or channel that energy into sports or other activities.
Scientists who want to find the source of inattention, hyperactivity, and impulsivity try to use measures that more directly approximate brain activity. Therefore, neurocognitive tests, presumably linked to specific functions in the brain, may help to gain insight into the causes of ADHD. These tests vary widely, and measure things like the response speed, planning, memory capacity, and the extent to which someone chooses a smaller reward now or a larger rewards later. Continue reading
Here are some drug use statistics:
- Over 80% of teens engage in some form of deviant behavior (1).
- Over 50% of high-school seniors admit to having used drugs (2).
- Only 10%-15% of the population develop drug addiction problems related to their drug use (1).
The question is:
If the majority of teens experiment with drug use, and so few eventually develop drug addiction problems, should we be focusing on something other than stopping kids from trying drugs? Continue reading
Almost everyone has heard about the placebo effect – the finding that treatment that have no particularly relevant effect (like a sugar or vitamin pill, or a behavioral equivalent) can make patients feel better. The placebo effect is actually the reason that all FDA approved drugs have to go through a double-blind placebo-controlled clinical trial before being approved for use – It has to be shown that using a specific medication is more beneficial than a non-active placebo even when the experimenter (or doctors) and the patient have no idea which treatment the patients are receiving. Otherwise, companies could simply continuously create placebos, show that they produce improvements in patients, and bring in the dollars.
Until now, it’s been assumed that in order for placebos to work, the patients have to be told that they are effective medications, amounting to an unethical lie by the doctors that prescribe them. This is the reason that very few doctors use pure placebos, though in a recent survey more than 50% of doctors reported using mild prescriptions (like over-the-counter pain medications) that they don’t believe are actually relevant to the condition as “impure placebos.” Given the large placebo effect, we can expect that these treatment, even if unethical, resulted in significant improvements in conditions that those same doctors were unable to treat using conventional methods. Still, it doesn’t feel good to know your doctors have to lie to you to make you feel better, right? Well they might not have to. Continue reading
If you’ve been reading A3 for a while, you know that we’re big supporters of scientific progress in addiction treatment. While it may be true that addicts need to want recovery in order to truly turn their lives around, the choice is hardly ever that simple and if we can tip the balance in the favor of treatment, or a better way of life, I say let’s go for it. When it comes to genetics and addiction, I’ve normally talked only about the fact that a person’s genetic code may predispose them to addiction or to other related conditions (like depression, anxiety, and so on). Aside from a single mention of pharmacogenomics, I don’t think I’ve spoke much about the way genetics can help us tailor addiction treatment to individual needs. We’re about to fix that.
In cognitive behavioral therapy they’re a big part of the “Five W’s” = When, Where, Why, With, and What. In the various 12-step programs they’re simply referred to as “People, places, and things.” But no matter how you refer to them, drug-associated cues, or “triggers” as they are more commonly known, obviously play a big role in reminding addicted individuals about their drug-seeking behavior, and they are often enough to restart old behavior, even among those who have been abstinent for a while and especially when unprepared for their effect.
Different triggers to reactivate old behavior
Research on relapse (what researchers call reinstatement) has long shown that there are a number of things that can return a person, or an animal, to drug seeking after they have been abstinent for a while. Stress, small drug doses, and the presentation of triggers are all very capable of doing this, even after months of abstinence and likely even years. It’s probably not surprising that giving drugs to an abstinent person can make them want the drug again. In fact, I would venture to guess that most readers believe that this is the most powerful way to induce a relapse (assuming the initial exposure was out of a person’s control and doesn’t count).
Well, recent research suggests that in actuality, triggers, or those people, places, and things, might be more powerful or at least longer lasting relapse risks than even taking drugs!
Triggers, not drugs, are shown to be longest lasting relapse risk
Researchers in Japan trained mice to press a lever for meth, getting them to poke their nose into a hole 60 times for a total of 30 meth administration per three hour session. Every time they poked their nose in the right hole they got a shot of meth and a little light above their nose-poke hole went on (this will become the trigger in the end). Once they were doing this reliably the researchers took away the meth and the animals learned, within 10-20 days, that pressing the lever no longer got them a drug and reduced their number of presses to less than 15 presses per session.
After all this the researchers gave the mice an injection of meth 30 minutes before putting them back in the box – leading the mice to start pressing again for the drug even though in the previous session they has pretty much stopped pressing knowing that no drug was coming. Obviously, the drug injection caused the mice to relapse back into their drug seeking. But, as you can see from the figure below (on the left side, the right side shows that the mice didn’t poke their nose into a hole that did nothing as a control), this little trick only worked once, and the next time the mice were given a shot of meth before being put in the box (after once again being taken through extinction training teaching them that pressing the lever did nothing), they didn’t press the lever any more and just around not doing much.
For the following part of the study the researchers once again took the animals through extinction training (and once again the mice stopped pressing the lever for meth) and then in a following session reintroduced the little light that used to go on every time the mice originally got meth. Just like they did with the meth the animals immediately went back to pressing the lever like crazy, hoping that now that the light was back, so was their meth. Just like with the drug relapse experiment above, the researchers repeated this whole process over two months later, only this time, the little light managed to re-trigger the lever pressing again, unlike the one-trick-pony meth. Seeing this, the researchers went for broke and tried another run of this with the same animals, now following up five months after the last time the animals received meth when they pressed the lever. Again the little light got the animals to increase their pressing, only this time it was a little less impressive than the first two tries (but still significantly higher). All in all, the little light managed to restart the lever pressing by the mice three times and a full five month after the meth-relapse experiment had failed!!!
Conclusion, thoughts, and implications about triggers, relapse, and addiction
In a completely different article I’d written that researchers found a number of different patterns of relapse among alcoholics who went to rehab and that in fact, the vast majority of those who did relapse never went back to the kind of heavy drinking that characterized their earlier problem (see here for One is too many, a thousand not enough). While this research touches on a different aspect of relapse, it once again challenges our thinking about the crucial factors in relapse prevention among addicts. Everyone knows that triggers are important, but the fact that they are at least as powerful and apparently longer lasting dangers than even being re-exposed to the addictive drug is a novel one. Still, this isn’t very surprising given the very long-lasting impact of drugs of abuse (especially stimulants like crystal meth) on learning mechanisms. In my opinion, and based on my own experience, those changes are essentially permanent and the only thing that makes an ex-user less likely to run back to pressing that drug lever when being re-triggered 10 years later is the life they’ve built, the experience they have, and the training they’ve undergone in reacting to those triggers. As you can see from the graph above, if a person runs back to the drugs and actually starts using again on that first, second, or third exposure to a trigger they are likely to start the whole cycle again, possibly making it ever more difficult to escape the next time.
Obviously preventing trigger-induced relapse should be a major strategy of addiction treatment and indeed, from CBT relapse prevention strategies to groundbreaking medications that have been shown to be effective for relapse rate reduction (like Vivitrol, Buprenorphine, Bupropion, and more), there is quite a bit of effort going exactly that way.
Yijin Yan, Kiyofumi Yamada, Atsumi Nitta and Toshitaka Nabeshima (2007). Transient drug-primed but persistent cue-induced reinstatement of extinguished methamphetamine-seeking behavior in mice. Behavioral Brain Research, 177, 261-268.