Let's get started. I'm Michael Van Ameringen. I'm a professor of psychiatry at McMaster University. Our program today is on ADHD, new and novel therapeutics and technology. There are three speakers today. Is this any better? Okay. Is this any better? Okay. So I'm Michael Van Ameringen, professor of psychiatry at McMaster University. And we have a program on ADHD today, new and novel therapeutics and technology. The first speaker is Dr. Carole Kemp. She's going to be talking about diet, vitamins, exercise, and ADHD. Does it matter? Then I'm going to be talking about ADHD online from screen time to problematic Internet use. And then Dr. Barbara Santos, who was unable to get a visa to come to the U.S. We have her talk, and hers is on new and novel therapeutics and technology. So why don't we get started with Dr. Bergman's talk. Dr. Bergman is an assistant professor in the Department of Psychiatry at McMaster University. Thank you, Dr. Van Ameringen. Thank you, Dr. Van Ameringen. Thank you. Okay. Can you guys hear me? So today we're going to talk about diet, vitamins and exercise for ADHD. I have no conflicts of interest to disclose for this talk. And the objective today is to understand the fact of the dietary changes, exercise, vitamins and minerals on ADHD symptoms. The idea is to review the existing evidence for natural treatments for ADHD. So the complementary and alternative medicine is the use of diets and vitamins and minerals as the main or complementary treatment for any kind of disorder. In psychiatry, we see that 50% of the patients with any mental health disorder try some kind of complementary or alternative medicine intervention during their treatment. And the frequency of that use for ADHD, especially in children, range from 12 to 64%. The role of diets and dietary supplements in the treatment is very controversial. And the topic continues to be an interest for the patients, parents and physicians who prefer to use alternative to the stimulant medication and are seeking complementary treatment. So the idea is, as everyone knows, the treatment with stimulants is the main treatment for ADHD as the first line treatment. But there is also known stimulants and behavioral treatment that can be used and well established. The problem is that all of these treatments have side effects. There is a cost and there is some lack of response. So the dietary changes research came to investigate if there is other ways to reduce the symptoms without that side effect especially and with a different cost. The research for ADHD with these minerals, diets and vitamins is very old. As you can see in the image, this study started in the 70s and are still going on. We're going to talk about all of these options that were researched over time. So when we talk about diets, diet intervention can be done in two different ways. One is to remove elements from a diet that we call the elimination diet. And there is a dietary intervention that is to increase intake of certain specific nutrients. The first study that happened about diets and ADHD was with the artificial food colorants and other additives. The idea was that this one can be done in these two ways or improve the diet of the kid completely taking off any artificial stimulants to see if the symptoms got better or adding additives and artificial colorants to the food, to the diet, to see if the symptoms would get worse. But overall, these studies did not provide any clear or convincing results. And there is four meta-analyses around this specific diet. And there is no significant adverse effect but there is very limited quality of the results. There is two big studies that show that people without ADHD, especially children, would present ADHD-similar symptoms, so ADHD-like behaviors, with the use of azodiacs. And European Union ended putting this as a law that makes every product that has this component to have to be shown as a problem, as a behavior that could cause adverse effect in behaviors in children. And then we go to a different kind of diet. And the idea that sugar and artificial sweeteners would be the cause of hyperactivity. That idea came from parents reporting that kids would get much more hyperactive when they consume more sugar. The problem is that they didn't talk about the idea of when do kids really eat more sugar. And usually it would be in birthday parties and holidays. And it's not clear if it's the sugar that is causing more hyperactivity or if it's the behavior and the stimulation that they are having in the environment. When thinking about adults, one of the sources of sugars for adults is sugar-sweetened beverages. And most of them also have caffeine that, as we know, is a stimulant and could be a way that adults are looking for more self-medication rather than causing a behavior problem itself. The studies did not find any kind of changes in core ADHD symptoms when stopping consuming of sugar or aspartame. And the majority of the control studies failed to demonstrate any significant adverse effect on the ADHD symptoms. The overall idea of the fuel-food diet is to find a specific food that causes to each patient the symptoms. So to do that, it's important to restrict the amount of food and the different types of food that children would get. And start adding foods to see if the symptoms would get worse when the foods are added. The problem with this diet is that it's very complex, very restrictive, and very time-challenging because the whole family has to change the behavior to be able to do. There is two open RCTs that found an improvement in these ADHD symptoms with a response of 64 to 73%. The problem is that there are four uncontrolled studies comparing these gendered behaviors during the fuel-food diets before the introduction of the new diets for them. So the big limitation about these studies is that they have to be uncontrolled. There is no way to do a controlled study about this specific kind of diet. There is lack of blighting in that studies. The parents that would agree to go to these studies are parents that are very into the idea that diets would change the behaviors in the children. The biological explanation is that these diets not themselves would change, and there is no specific kind of allergenic that early suggests that would cause that to the children. The diagnosis of food sensitivity is very complex, time-consuming, and very expensive and burdensome for patients and parents. So there are some benefits, but they are very restrictive and very costly for the families. When we go to the vitamins and minerals, we're going to start talking about the PUFAs, that is the omega-3s and omega-6s. The increase of the polysaccharide fatty acids concentrations in the cell membranes can affect serotonin, dopamine, especially in the frontal cortex. And they can decrease the oxidative stress in the same areas. Some studies show that children with ADHD, compared to controls, they had lower levels in the plasmas and red cells of the polysaccharide fatty acids. So some meta-analyses demonstrate significant benefits of using supplementation with omega-3 compared to the placebo, and can improve inattentive, hyperactive, and impulsive symptoms in children and young adults when compared to the placebo. There is no indication that these PUFAs would help with emotional liability, conduct problems, or aggression in young people with ADHD. And the most important part is how to prescribe this. Because it's not any kind of omega-3 that would help, but specifically the ratio about high doses of EPA and a comparison of 9 to 3 of EPA to 1 of GLA. GLA is the omega-6 that should be in the compound. So the results only happen when you have the correct ratio and really high doses of EPA. Vitamin D is another vitamin that was well studied. And vitamin deficient can cause cerebral dysfunction related to neuropsychiatric diseases in children and adults. And the idea is that the vitamin deficient results is the imbalance of the neurotransmitters in the pulmonary pathway responsible for the pathophysiology of ADHD. The prevalence of vitamin deficient in children is high all over the world. And the serum vitamin D concentrations in children and adolescents with ADHD is much lower than in the healthy population. So there was a few-month analysis about four RCTs that shows that vitamin D supplementation as an adjunctive treatment therapy with metilphenidate would reduce ADHD symptoms without serious adverse effects. And improvements in attention and hyperactive symptoms. And there was no difference in the oppositional and impulsive symptoms. Looking for the melatonin, melatonin seems to be well studied too. Patients with ADHD and sleep problems might benefit from melatonin. And the idea is to decrease the sleep onset latency in these patients in the use of stimulants and decrease the times of sleep onset and increase the total sleep time in these patients. So the evidence suggests that melatonin really reduces the sleep onset latency in children. But there is no benefit specifically for the ADHD symptoms. There is a recommendation of use of three to six milligrams 30 minutes before bed for the kids that have a sleep issue caused by the stimulants or even that were present before of the use of the stimulants. And then there was a few other substances that were researched. There is no big meta-analysis about them. Carnitine is one of them. It's a very small molecule necessary to the producer of energy, specifically involved in oxidation and transport of fatty acids. And the idea of the carnitine appeared when it was found that omega-3 was helpful. So the idea is this would help to absorb better omega-3 and it was not really a good result. There was one randomized double-blind study and completely failed to show any improvement in the symptoms. So there is no evidence for use for carnitine for ADHD. Saffron was the other one studied. Most studies came from places that production of saffron is very prevalent. And the idea is that the parts of saffron would help the reuptake inhibition of dopamine and norepinephrine and GABA-alpha agonists. So there is one study, it was a pilot study, that compared Ritalin to saffron. The problem of this study, there is no comparison to placebo. Ritalin, again, is a pilot study, needs more further investigation for that. And the results were quite good, that compared very similar results to both, to Ritalin. The groups with Ritalin and the groups with placebo had very similar responses. But there is no placebo comparison here and this would be our suggestion, that would be further investigation with bigger group studies. When we talk about iron, the idea here, it was to see the iron deficiency in the children with ADHD. Recent meta-analysis showed that there is, that kids with ADHD would have a lower serine-ferritin levels compared to healthy controls. The same happened with adults too, not only with children. And it showed that these patients with iron deficiency and low ferritin levels might benefit from the use of iron. And but for the trials, didn't show specific improvement in ADHD symptoms, but in the iron deficiency itself. The anemia itself improved, and this is important, remembering that the patients with ADHD tend to have more iron deficiency than the normal population. So the serine-ferritin levels were increasingly correlated with the severity of the ADHD. And the children with the most severe iron deficiency were the most inattentive, impulsive and hyperactive. Zinc was also studied. And the idea, the studies of zinc, was there is places, especially Turkey, Iran, and other Middle Eastern countries, that there is a suspect endemic zinc deficiency that we don't see that much in North America. And the group showed the children that have low zinc levels compared to the normal controls, and zinc as a co-factor of the metabolism, as the neurotransmitters and fattic acid again, that would regulate the dopamine and metabolism involving the ADHD. So the zinc supplementation is the hypothesis that would improve the ADHD. And the meta-analysis really showed that there is association that the symptoms would improve, again, for patients that have low zinc levels, not to everyone. So the results were inconsistent to show that zinc would be something that we would prescribe to everyone, but showed that we should look for that as a deficiency specialist in areas that this is needed to be, that are more common low levels of zinc. Magnesoid was also well-studied, and was also studied, not well-studied. There was no randomized placebo-controlled trial. The rationale about magnesium is to use the magnesium as supplementation. There was a few case-controlled trials that demonstrated that reduced levels of magnesium in ADHD patients, but there is no randomized trial showing, and doesn't seem to be beneficial for everyone. And we have to remember that magnesium can be very toxic, too, if the levels, if you use too much. Zincoglobulin studies came from the idea that would be, that zincoglobulin would be helpful for dementia and memory impairment. So the idea was to use for the cognitive functions in ADHD patients. There is only one, a single sequent randomized trial with methamphetamide. And there was no improvement of using zincoglobulin in patients with ADHD. And again, zincoglobulin can be also dangerous in a way that can increase the risk of bleeding. Sanjohn's wharf was also studied without no evidence for the placebo, versus the placebo. And Sanjohn's wharf can be, can interact with the medication, especially if the stimulants, when you use it together. So it's not something that we should use together, if stimulants at all. And there is no evidence using for ADHD. Then we go to pycnogenol, is a pinus minus, is a extract from the bart of the French marine pine. And the potential came here, but it was, it's unclear, and there was some case reports related to the use as a monotherapy and also in combination with stimulants. That showed that there was some case reports showing that there would be an improvement in the ADHD symptoms. But the randomized placebo and methamphetamide control study didn't show, really failed to demonstrate any improvement for the ADHD symptoms. There is one more study related across ovary, and that also failed to demonstrate any improvement. Then we go to physical activity. So when we go to the studies related to physical activity, they are very different from each other. So we have studies relating yoga, there are studies for cardiovascular kind of physical activities, more aerobic exercise. Physical activity can increase dopamine and norepinephrine in the prefrontal cortex, hippocampus, and the striatum. It's safe, low cost, and it should be used as a drug treatment. In the same way that we should indicate physical activity to almost every patient that we see. So it showed that improved. So there is some evidence that more moderate to intense cardio exercise would be more beneficial, and would especially for the inattentive symptoms, not as much for the hyperactivity symptoms in the children. One big study showed that children that engage in regular physical activity cared less ADHD symptoms to adulthood. So the symptoms were less prevalent during adulthood for the children that had regular. So regular was considered three times a week of moderate to intense exercise. So the conclusions today is when should we really indicate diets, vitamins, or exercise to the patients? The idea is patients that have medication failure or cannot tolerate at all medications. When patients or parents are asking for these interventions, and especially for patients that have symptoms or signs of specific deficiencies. So the risk of using these as our primary treatment, using any of these interventions as our primary treatment, would be delaying to start the most effective treatments that we have evidence that work. The diets are difficult to implement and require a lot of family involvement. So it's not fair to a family to say to them that we should start with diet right away as our first choice. The exclusion of artificial coloring may be useful as an adjunctive treatment, but societies around the world are not. Like the American Academy of Pediatrics, the American Academy of Allergy, Asthma and Immunology, and the NIS in the UK, do not recommend using a restriction diet as a routine treatment for ADHD. Regular physical activity is well tolerated and might be recommended for people with ADHD, especially in combination with the traditional treatments. Overall about the supplements that really can have some improvement is that omega-3 can be reserved for mild cases or as an adjunctive treatment for more severe cases. Melatonin seems to be our first choice for patients that have sleep disturbance caused by the stimulants or even not caused by the stimulants. And investigating iron deficiency is very important and supplementing iron when present deficiency. Zinc should be something that we should look into populations that have a more common zinc deficiency. Saffron should be more studied. There is limited data showing some improvement and should be more studied to see it could be alternative treatment. And vitamin D also can be used as an adjunctive treatment, especially in areas that there is deficiency. Thank you. Why don't we take a few questions while we switch over? No questions? I completely agree with you, there is a huge debate. The meta-analysis that show evidence uses doses between three to six, and this is why I put in this slide. But there is a debate, and I think it should be very personalized to each patient, starting a low dose, like even 0.5 to one milligram, and then increasing slowly as needed and personalizing to each patient. Hi I'm a child psychiatrist practicing in Mexico City, and I remember a good friend of ACAP, who says that anything you do treating patients with ADHD would improve symptoms, anything. And he says, anything. So I wonder if you see, for instance, results comparing placebo versus, I don't know, Tamoxetine, Medilfinidate, at the beginning the results are quite similar. The decrease of ADHD rate and scale, or something like that, with lowering at the beginning. So I wonder how many of these kind of studies, maybe they don't last enough to see the difference and results could be more placebo, or something like that. I completely agree. The studies were not long enough, is a big concern about these studies, and should be longer. This is why they should not be used as a substitute to the stimulants at all. I would love that every patient would respond to anything, it's not what we see in practice. But my suggestion here would be looking for the deficiencies that the patient has, and treat the deficiencies that the patient has, individualizing the treatment. Hi, I just want to make sure I understood the part about iron, and it seemed like even in non-anemic kids who had low iron, that iron was beneficial. And I just wanted to point out, I think that in practice, people are usually doing CBCs, and then if they're anemic, they'll do the ferritin. And so I'm wondering, and as someone who, full disclosure, I get iron infusions because they get so low, but I'm not always anemic, I'm just getting ferritins on everybody. Would it be beneficial, especially in ADHD kids, if you're going to be getting a CBC to also get the ferritin? Completely off-note, I learned to look at ferritin too, I completely agree with you in that. I don't think that CBC would look for the iron deficiency itself. My partner is a hematologist, and who showed me, like, stop ordering CBC, order ferritin, and refer the patients to us. And I joke that he cured some of my patients' depressive symptoms, or even some ADHD symptoms that are not real, they were iron deficiency. And we should be looking more for ferritin than CBC only. One last question, sir? Maybe I'm looking for some of your thoughts or practical guidance on maybe supplements in general. The regulatory framework in the United States for dietary supplements doesn't seem to be sufficient for ensuring accuracy in the labels, and including adulterants that could be quite toxic. And I'm wondering, I typically tell that to patients, and I don't know, I tell them maybe find a brand you trust and just stick with it, but I don't really know, I don't have any better advice than that, and I'm wondering if you have any thoughts about that. I agree with you. I usually tell patients that to be sure about what they are taking, I like to do a good review of all vitamins that they take, all supplements that they take. And there is high risk of intoxication with many of these supplements when they are not taking correctly. I have a quick question. How frequent does it happen that in this patient population, caffeine helps with the sleep? Sorry, I couldn't understand. How frequent does it happen with this patient population that helps for sleep, caffeine? Caffeine? Yeah. So, again, there is no studies that I found for that, but in practice, we see that stimulants can help for some patients with helpful sleep, the same way that some caffeine helps with sleep. And I prescribe the odd stimulant at evening to these patients that feel calmer and tired or need to help with sleep, but it's completely off-label. There is no approval for that. What dose? Depends. Personalized dose. Okay. Thank you for your questions. We're going to move on to the next presentation. I'm going to be speaking on ADHD online from screen time to problematic internet use. This is a list of my disclosures over the last 24 months. So the objectives of my talk today are to understand the relationship of ADHD with problematic internet use and internet addiction, to understand the prevalence and impact of ADHD and problematic internet use comorbidity, to review the treatments for problematic internet use, and then more specifically for this comorbidity of ADHD and problematic internet use, and to understand the potential relationship between media screen time and ADHD. So according to the National Comorbidity Survey replication, if you look at individuals with ADHD, about 15% of them will have a substance use disorder. And if you look at a number of meta-analysis of individuals with substance use disorder, about 21% will have ADHD. So one of the things that changed in the DSM-5 is this introduction of this category of substance related and addictive disorders, which included gambling disorder as the first behavioral addiction. And this was due to strong evidence of its overlap with substance use disorders on multiple domains, including phenomenology, co-occurring disorders, genetics, neurobiology, and treatment response. So behavioral addictions, such as gambling, gaming, internet addiction, are similar to substance use disorders in terms of etiology, comorbidity, functional impairment, and treatment. And there's been meta-analysis of 52 studies that looked at resting state functional connectivity in emotional processing and salience networks of patients with substance use disorders and behavioral addictions. And they are quite similar in comparison to controls. And in another study that looked at the hyper-connectivity between the default mode network and the salience network, these were very similar for internet gaming disorder and substance use disorder. So there seems to be a sort of similar neurobiological overlay between the substance use disorders and these so-called behavioral addictions. So internet addiction appears to be marked by an individual's inability to control his or her use of the internet in an impulsive, excessive, or compulsive way. The individual has a strong preoccupation and psychological dependence accompanied by distress and or functional impairment, resulting in psychological, social, occupational, financial, and personal relationship difficulties. So there's got to be some kind of functional impairment. And it features characteristics of drug addictions. You do see tolerance, you do see withdrawal, you can see craving and loss of control as well as relapse. Now another term that's been used in the literature that sort of overlaps with this is this term called problematic internet use. And this is preferred by many experts in the field. And this discusses or covers a broad range of behaviors such as excessive social media use, gaming, gambling, video streaming, pornography viewing, cyber hoarding, cyberchondria. There's been a lack of consensus of the problematic internet use definition, but the one by Shapira is the most widely used. Other definitions of problematic internet use have been based solely on this idea that it is a substance dependence or a pathological gambling. And these definitions have been felt to be too narrow to capture the population of problematic internet users. So Shapira's definition is a maladaptive preoccupation with the internet, with internet use experiences irresistible use for periods of time longer than intended, there's significant distress or impairment resulting from the use, and there's an absence of other access one disorders, things like mania or hypomania. But these are overlapping constructs, internet addiction that one group has sort of discussed as well as problematic internet use. And the whole literature is sort of some of the studies talk about internet addiction and define it in a particular way, and others have talked about it as problematic internet use. But I think we're talking about things that are on a spectrum, but clearly have functional impairment. So internet addiction was strongly debated in the DSM-5, but not included. Internet gaming disorder was mentioned in the DSM-5 as an entity that requires further investigation and is in the appendix, but in ICD-11 it is listed as a disorder, both as an online and an offline version. Many research argue that internet addiction disorder showed enough criteria that it should be grouped as part of the substance use disorder grouping. So what's the prevalence of problematic internet use? Met analyses of 113 studies over 31 countries suggest that the prevalence in eastern countries being focused on Asia is 8.9% versus in western countries 4.6%. So there are health implications of problematic internet use, including low levels of physical activity, increased rates of obesity, back pain, headaches, migraines, and then psychological consequences such as mood and anxiety disorders, ADHD and impulsivity, poor sleep quality, loneliness, low self-esteem, increased suicide risk, and disability. So there's a meta-analysis that looked at Asian studies of internet addictive disorder and they found significantly higher rates of comorbid depression, ADHD, anxiety, and alcohol abuse in individuals with internet addiction disorder as compared to controls. So this association has been examined further. There's a meta-analysis that found higher rates of ADHD among individuals with internet addiction disorder compared to controls. Another meta-analysis found those that have problematic internet use have greater ADHD symptom severity than controls. And yet another meta-analysis that looked at individuals with ADHD, they found that they had greater problematic internet use severity relative to controls. So turning to this issue of screen time use, which is, you know, parents are always really quite interested in, but in terms of screen media technology use. So most of this literature has been in the children and adolescent populations. And they've looked at the relationship between screen media technology use and ADHD symptoms, but not for the diagnosis of ADHD. So there is evidence that screen media technology affects cognition and includes the ability to interfere with sustained attention. So a meta-analysis looked at this relationship between screen media use and ADHD-related behaviors in children and adolescents, and they found inconsistent findings, but there is a small but significant relationship between screen time use and ADHD symptoms, not the disorder per se. The only study that really has had this link of screen time use with ADHD is this longitudinal Brazilian study that looked at over 2011-year-old children without ADHD, and they followed them to age 22 and then assessed them for ADHD. And in that study, they found that ADHD symptoms at 22 years were positively associated with television time at 11 years old, computer time at 18 years old, and total screen time at ages 11, 15, and 18 years. And when they looked at those, the television time at 11 years and the total screen time at 18 years, these were associated with the diagnosis of ADHD at 22 years. So it's really the only study that has made this link between screen time and the ADHD diagnosis. More recently, there have been systematic reviews that found reciprocal associations between digital media use and ADHD symptoms, with the association being more consistent for the problematic use of digital media than screen time. So saying that this association looks like it's more associated with people developing problematic use of the media. And so children with ADHD symptoms seem to have high or more problematic use of digital media. So meta-analysis findings connecting the screen time use with ADHD-related symptoms have been compelling enough to prompt a lot of concern. But they've been too imprecise due to confounder study design limitations to provide more insight into this relationship of screen time use in the development of ADHD. And again, this is a Japanese study that looked at 3,000 10-year-old children, and they looked at children at baseline who had problematic internet use, and at two-year follow-up, this was correlated with a lot of hyperactivity and inattention difficulties. And the kids at baseline that had hyperactivity and inattention, this is correlated with problematic internet use at two years out. But again, interestingly in this study, they were very careful to note that screen time did not predict the hyperactivity and inattention, suggesting that the addictive aspects of the internet use may be what's worsening the hyperactivity and inattention. So there's a number of studies that have looked at ADHD and problematic internet use. As far in elementary school population, 14% of adults diagnosed with ADHD also have problematic internet use. After higher, ADHD symptoms were associated with internet addiction in a large sample of adolescents. So what's the impact of this comorbidity of ADHD and problematic internet use? So there's this Chinese study looking at 18 to 16-year-old children and youth, and they compared ADHD with problematic internet use to ADHD without. And the group with ADHD with problematic internet use, they had more severe symptoms of inattention, oppositional, defiant behavior, conduct problems, emotional problems. They had more executive function deficits. They had greater damage in the family environment. They perceived more pressure from life events, had lower motivation to learn, and spent fewer hours engaged in physical exercise. So what's the treatment for internet addiction and problematic internet use? Well, a whole slew of cognitive behavioral therapy interventions have been used, including solution-focused brief therapy, reality therapy, harm reduction therapy, social skills training, time management, family therapy. And these have been delivered both individually but probably more successfully within the domain of the family. And then there are a bunch of medications from antidepressants to atypical antipsychotics to mementine to methylalanine that have been studied. And I will go through some of these medication studies. So a meta-analysis of all these treatment studies found that groups who received cognitive behavioral therapy, group counseling, a sports intervention, or internet-based interventions experienced a greater reduction in their internet addiction scores. And network meta-analysis showed that if you combine treatments, that you did have a better outcome. So in terms of the pharmacological treatments, there's been open-label studies with bupropion looking at males with video game addiction, and they found decrease in video game craving and total game play time, as well as reduced internet addiction scale scores in a six-week open-label. In a 12-week open-label, looking at a group who had internet gaming disorder, internet-based gambling disorder, versus healthy control subjects. In the internet gaming disorder group, bupropion improved the internet addiction, the ADHD symptoms, and the depressive symptoms. And in the internet-based gambling disorder group, it seemed to improve the pathological gambling, as well as the ADHD symptoms. There's an Italian study with escitalopram that was 10 weeks open-label, and then it was followed by a nine-week double-blind discontinuation phase of escitalopram or placebo. And interestingly, in the open-label study, they had about a 50% reduction in internet use of hours, from 36 down to 16 hours a week, and about 65% were considered responders. However, at the end of the double-blind placebo discontinuation, there was no difference between the groups in terms of hours of internet use. Another study looking at internet gaming disorder with patients treated with either bupropion or escitalopram, compared to an unmedicated control. Both of the drugs improved the internet addiction scale and clinical global improvement, but bupropion was better than escitalopram at improving internet addiction, the ADHD symptoms, and clinical global improvement. There's a meta-analysis of psychological treatments that were used for problematic internet use and problematic smartphone use, and the psychological interventions were found to be effective, and the interventions included things like CBT, family therapy, mindfulness, psychoeducation, or a variety of self-help tools, and these were seen to be beneficial in the meta-analysis. There's a combination study combining CBT with bupropion versus bupropion alone, and this is in a group of adolescents with problematic online gaming play. They were gaming at least four hours a day, and bupropion lowered, the combination treatment was better at lowering the internet addiction scores, but also the mean time that they were spending playing games online. Another study that compared bupropion with psychoeducation versus escitalopram in psychoeducation with excessive internet game play, and both drugs improved the internet addiction scale, but the bupropion was better for impulsivity and the attentional symptoms. So, in terms of treatment of the actual ADHD, problematic internet use, comorbidity, there's really only two studies. There's one eight-week open label study of children who are diagnosed with ADHD and problematic video game play, and they use methylphenidate, and methylphenidate both decreased their internet use as well as their internet addiction scale scores, as well as improved their ADHD symptoms. Another study in adolescents who had ADHD and internet gaming disorder, 12-week single blind study comparing methylphenidate to atomoxetine, and in this study, both of the drugs equally improved the internet addiction scores, but the methylphenidate was superior to atomoxetine. So, there's clearly this sentiment that using these ADHD treatments is helping treat the internet addiction and the amount of time people are gaming or online. So, to conclude, there's increased prevalence of ADHD in problematic internet use and internet addiction. There's increased prevalence of problematic internet use in ADHD, so it seems like it's a bi-directional association. Problematic internet use have greater ADHD symptom severity than controls, and ADHD has greater problematic internet use symptom severity than controls. Open-label trials with methylphenidate and atomoxetine have demonstrated reductions in symptoms of internet addiction and problematic internet use. There are reciprocal associations between digital media use and ADHD symptoms, with the associations being more consistent for problematic internet use of digital media rather than for screen time use itself. So, children with ADHD symptoms appear more vulnerable to develop high or problematic use of digital media. And I will stop there, thank you. Questions? Comments? Good morning. I just have a quick question about whether or not we know if this affects children who are male differently than how it affects children who are female. Whether it affects children who are male or female? Yeah, like in all the studies done, do we see people participating? Yeah, I mean most of them have been done in males, but it looks like there are many, many women who are involved. We just completed a video streaming kind of survey, and you find almost as many women who are spending hours online as men. I don't think we have the treatment studies so far in women, but we'd expect a similar response because I don't think there's a differential response for ADHD treatment between men and women, but there are a lot of women out there who are gaming particularly. Thank you. Thank you for your talk. Regarding problematic internet use and internet addiction, how much is compulsive email checking and the worries about being behind in your inbox and so forth? So your question is how much is compulsive of this behavior? Well, do the criteria include the behavioral and psychological symptoms associated with the need to check our emails and inboxes associated with our work? Yeah, I mean I think that's why the definition of problematic internet use has been broader, because people do believe there is a significant degree of compulsivity in these constructs. It may not be just an addiction construct, but there's a degree of compulsivity, and certainly in a trial that's been designed, a prevention trial, there are treatments that are working on the compulsivity aspect of this. Thank you. I'll get you after. Go ahead, sir. In your studies, did you come across any data on amphetamines like Adderall impacting problematic internet use? There hasn't been any. I mean, this has not been a widely studied area, although really it's quite a problematic area for parents, for sure. Go ahead, ma'am. Yeah, I mean, you know, I think the pandemic was horrible for ADHD children, adolescents, adults kind of thing. I think, you know, these things are on a spectrum and I don't think everyone has ADHD. I think, you know, I think we want to work at limiting screen time, you know, but it's so hard when it's so ingrained in everyday kind of life. And I think we saw during the pandemic, kids were sort of flipping off from supposedly being online at school to playing games and things, and it was very hard for people to deal with. But I think what, you know, I think when you're seeing kids that are having a lot of problematic use of disengaging, you want to, you know, you want to be, you know, it may be a signal that there may be some underlying ADHD issues and it may be, you know, worse assessing. But this is, you know, every parent's kind of nightmare of dealing with kids and online behavior. Hi, my name is Michael Kornberg. I'm a child adolescent psychiatrist in San Diego, La Jolla. I mean, obviously, there are a lot of comorbidities, right, where a lot of these kids are falling asleep with their electronic devices, they're getting up early in the morning, they're not sleeping well, skipping breakfast, skipping lunch, maybe having dinner later. So I think there's a lot of anxiety, there's ADHD. Sometimes there are other, you know, compulsive type behaviors. So it's also what sometimes like I'll have people with, you know, body focused repetitive behaviors, anxiety, insomnia, ADHD, and might even add in like low doses of the 25 milligrams of naltrexone, for example. Any studies with naltrexone for the problematic internet use? There has been in the non-ADHD literature, there's some studies using naltrexone that have shown some benefit. But they're very kind of small, open label studies. And they weren't very, they weren't particular to ADHD, but they were in problematic internet use and did show some benefit. Just thinking on ADHD as a risk factor to develop internet addiction. Is there any information about is more prevalent on inattentive, maybe because of procrastination or impulsivity, symptoms related to internet addiction because of immediate reward or something like that? Yeah. I mean, when you look at the impulsivity symptoms in these people who have inter problematic internet usage, we've done it some of our work, like the Barrett impulsivity scale is through the roof. And surprisingly, there's a good amount when you measure compulsivity, there's a good amount of compulsivity. I think it's not, you know, there's clearly an addictive component, and it fits in an addictive paradigm. But there is compulsivity and impulsivity in a lot of these people who have problematic internet use in the way we're able to measure it now. Okay, thank you. Okay, let's move on to the last presentation. Hello, so my name is Patra Sanders, and I am a Ph.D. scholar at the McMaster University. And today I'm going to talk about ADHD, behavioral problems, therapeutics, and technology. I've been curious to learn more about ADHD. I'm going to give this talk first by wanting to go over some interesting facts about neurodiversity. So, we want to talk about neurodiversity. This is a fascinating area. I think it's a very similar issue to brain plasticity, neurobiology, and how brain networks function. I'm not going to cover all of those concepts today, because they could be a presentation topic by themselves. But I can say this. In recent years, we are learning more about how to study the brain. And we see that the brain adapts and changes over time, even in adults. And we now have evidence of some structural and functional abnormalities that happen in ADHD. And neural coagulation techniques use that knowledge of those brain neurons that are affected by ADHD to try to change a person and improve relationships. And there is also an unconscious function for people who don't like medications or can't tolerate medications. So we want to use them. And also for children who don't want medications or diabetes. So, there are several neural coagulation techniques. And they vary in the way that energy is transmitted to the brain. And what's the benefit? So, we have implants that require surgery. And some techniques that require the implant to be removed. And we have some graduate classes. Usually, when we have a graduate class, we have a group of students. And we have a group of students who are in the same class. I'm not sure how much time we have today. I'm not going to cover all of them. I'm just going to be discussing ADHS. Which is Transpersonal Direct Coagulation. So, I believe that if you decide to watch this properly, you probably want to know the three questions about neural coagulation. How does it work? Is it safe? And is it effective? So, let's get into it and answer the questions regarding ADHS. So, how does it work? This is a small, round device. It's a little colored. It's a poppy. It has a nine volt battery. And this energy is delivered by the direct current. So, there's an emphasis on neural coagulation modalities. So, this is what a session looks like. This is a photo of a patient during the ADHS session at National University. You can see that she's wearing a little hat. So, we have two hats here and here. There's a sponge. The sponge is packed in a string. So, it's absolutely free to flow. The current flows from the right electrode. So, the positive electrode. To the cathode, which is the negative electrode. And a normal session would be about 20 to 30 minutes. I think this image shows how this technology affects the brain and the brain theory. So, when the current is gone, it flows from the anode to the cathode. And in the middle, the epithelium and the lip are stimulated. So, their function can be boosted. And we can use the cathode for areas we want to inhibit. But usually, this is just positioned in a neutral place. So, it doesn't affect the area we're trying to stimulate. This can be in the other part of the head or even in the shoulder. And the majority of treatments are focused in the sphincter area. And that is the torso, the lateral, the frontal cortex. And this area right here. And you can see it's a relationship between the normal control network. So, there are layers of research that show that TDCS increases excitability, so the risk of fibro can be a lower threshold. So this is an increase in the production age of fibro. We also know that TDCS increases the plant-line elasticity and boosts functioning and protective areas. Also, there is relatively new research that shows that you can cover an area, like the one I showed you before, and boost other areas related to the function that you're trying to boost. So, that's kind of the same. Neurons that wire together, wire together. So you can activate one area that is closer to the superficial than to the rest of the body. And it can have a function in all the other areas that you're trying to reach. We also have some interesting findings that TDCS increases blood flow to the brain. And there are some interesting studies being done right now targeting the blood-brain barrier. So, this seems pretty so far. Why are we using this in everyone? All in humans. So, this is a catch. The current is not actually making those fiber, so only stimulating those that are already fiber. So, we can say that this technique modulates the neural activity in TDCS, but it's ineffective when we're talking about generating the fiber hormones, so the neurons that are not fiber. So, is it safe? As I said before, this is a low current. So, it's not enough to make the neurons fire. Sometimes it only takes a few years, and sometimes it's safe. It's very powerful. We have a lot of global motivations. We need to consume a lot of this, because there are sometimes conditions where it develops a low current. That's it. Is it effective? No. We had some advances from Weissberg in 2021 that had some disappointing results. And I could talk about them with you. We found that most of them had a few TDCS sessions, between one session and five sessions, and they had the neural counter-cortex and the virtual reality counter-cortex. There were two studies. The first one was a study that studied the virtual reality counter-cortex. And there were multiple ways to assess the outcome, the predictive outcomes in those studies. And this was the predictive outcome. Only two studies assessed clinical symptoms, and those studies saw improvement in attention, but not in hyperfibrillity or immunosuppression. And the other ten studies evaluated multiple cognitive functions. So we were looking at inhibition, memory, reaction time. With each study, we had different outcomes. And all studies found that some of those cognitive functions were in a really heterogeneous way. Some improved in some functions, not in others, and not everybody was working at the same time. They weren't able to find out how necessarily they were going to do it. I'll write you this. This is interesting. They had 230 TDCS patients, and they found only once where there were likely effects in inhibition, in those assessments, but unfortunately they didn't find any significant effect in attention. So in 2013, we didn't have any promising outcomes for TDCS as a treatment for ADHD, but the author mentions that the diagnosis was hindered by the heterogeneity of this ADHD protocol and the age and how many years were done according to the cognitive outcomes. So we also have a more recent systematic review from 2022. I'm not going to cover all of it, but I want to bring this to your attention. There were 17 studies for ADHD, and most of them had positive findings with low effect sizes, but as you can see here, 70% of them had only a single session of TDCS, and that's disappointing. So I wanted to talk about a trial with you so we can see a different way to study TDCS. So this is the TUM trial. This was a randomized, double-blind, sham-controlled study, and they excluded patients who had other psychiatric disorders but allowed some patients with low anxiety and some depressive symptoms. This sample consisted of 55 adult patients with ADHD that were not on stimulant medication, and about half of those were of the inattentive subtype. They did TDCS sessions at home for four weeks, 30 minutes daily sessions. The intensity of the current was 2 amperes, and they were targeting the right dorsolateral prefrontal cortex. Their main outcome was inattention, and they assessed it with a clinician-administered ADHD self-report scale, and the secondary outcome that they were looking for was hyperactivity. So this is what they found. Eleven patients of the TDCS group achieved a 30% reduction in inattention symptoms, and there was no effect on hyperactivity or impulsivity. And another important finding of this study was that there was no measurable effect after two weeks or 14 sessions, which makes you think about all the findings we just discussed in the systematic reviews and the meta-analysis that they only had one session or five sessions. So in the TUN trial, the patients were followed for four weeks, and we don't know if the response will be sustained after they stop the treatment, but they had significant results. But we have to think about that this was a small study that had 11 patients responding with a 30% reduction of attention symptoms. So it's a positive study, but we still have many things to do. So this is where we are with TDCS. This is a promising technique that offers a cheap, painless treatment, but we still need to study it more. And remember that I mentioned that TDCS stimulates neurons that are already firing. This could mean that we may need to combine specific activities when the patients are training attention and short-term memory while they're using TDCS, so those areas can be improved. And we don't have evidence of how this technique could be used as an add-on to medications with patients that had a partial response, for example, both for medications with stimulants or stratera, for example. And we definitely still need more randomized trials with a longer duration, longer sessions, and with outcomes evaluated in the same way. And we also don't know about other brain lesions. Another important thing that we need to know is we don't have studies that assess the response that people will have with double the dosage, for example, like twice-a-day sessions or longer trials to check if these effects are sustained over time or if the patient has to keep using the device to maintain its effects. I also wanted to discuss two other promising techniques with you, if I still have some time, the trigeminal nerve stimulation and neurobiological feedback. So, trigeminal nerve stimulation was cleared by the FDA to treat children with ADHD in the U.S. You can see in this picture, this device is similar to TDCS. It has an electrode connected to the forehead, and the goal is to stimulate part of the trigeminal nerve that goes on the forehead. By doing this, it stimulates the brainstem, especially the local cerebrum, an area that is related to the arousal system and attention. And this sends norepinephrine to the cortex and to the basal ganglia region. So, objectively, this is a way to stimulate the frontal lobe in a bottom-up way. It increases activity in those areas and influences other neurotransmitters, like glutamate, dopamine, and serotonin. And it has to be used at night because the patient has to use it for about 8 hours. So, each session is about 8 hours. So, is it effective? Let me show you this trial. This is a controlled trial with Shen Treatment. They had 62 ADHD children that had 4 weeks of nightly treatments. 32 of them used TNS. And the treatment group had improvements in ADHD symptoms. And, interestingly, they were able to measure that with EEG. So, the increased activation in mid- and frontal regions of the brain were correlated with clinical improvement. And you can see it's pretty safe. The children in the study had some minimal side effects. And let's talk about neurofeedback for a bit. This is a really interesting technique. It teaches the brain to increase activity in a certain area as making the patient play a game. So, through trial and error, the patient discovers how to make the object on the screen move with their brain. So, there's an interesting way to see it. This study here used a rocket. And the patient is doing an fMRI during the session. And the patient is connected to the machine. And when the fMRI sees that the patient is activating the target area, the rocket on the screen moves up. So, is it effective? This trial here was a randomized controlled trial with 31 ADHD adolescents. And they played the game for sessions of 8.5 minutes during four hours of fMRIs, like multiple 8.5 sessions during those four hours. And this was done 11 times. The active group had 18 participants. And they targeted the right inferior frontal cortex. And the control group was targeting a different area. The sessions increased activity in those areas in both groups after 8 runs. So, this increased activity in the control group. And it was correlated with improvements in ADHD symptoms immediately after the 11 runs. But more interestingly, as time went by, these participants had an even greater symptom reduction. So, they had 26% reduction after 11 months, after they stopped the treatment. This could mean this technique has a sustainable long-term effect, which is really promising. I wanted to leave you with this idea. There's still much work to be done in this field. But these techniques are evolving fast. And they are promising treatments for ADHD. So, thank you. I hope I can answer your questions through online video. Or if you just want to email me, please feel free to email me with questions. Thank you very much. I'd be happy to take any comments. I'm not sure if we'd be able to answer the questions without Barbara here. We did try to have a Zoom link with her. But it was not possible through the APA. And Barbara very much wanted to come to this meeting. But she could not get a visa to come to the US. Thank you. I think it's interesting. There's a good group of people who have ADHD who don't want to be on a stimulant medication or don't do well with it. And the other potential use of this is as an augmentation kind of treatment. I mean, not everyone gets sort of 80 or 90% of their symptoms gone with a stimulant medication and behavioral interventions kind of thing. I mean, I think that we need to investigate it more. I think the Brazilian study was really interesting because the people didn't have to come into the clinic. They showed them how to put on the direct current stimulation device. And the patients did it at home on their own sort of week daily for four weeks. So, you know, one of the problems with neurostimulation is that people typically have to come into the clinic and come into the clinic every day. And that's very onerous where if you had an intervention, even if the effect size isn't as good, you have a treatment that people can do at home. So, you know, there is some promising potential for it. I think in the Brazilian study, they only stimulated people once a day. A lot of the ones that have been done in OCD and depression where people are stimulated twice a day kind of thing. So, I mean, the dose may not have been strong enough in the Brazilian study. So, you know, I do think there needs to be, you know, more work in this area. We need to have other kind of non-stimulant methods available for, you know, some of our patients. So that's sort of my view on things. But I think it was an exciting finding, the Brazilian study, because it was done at home and patients weren't on any stimulants at all. So there's certainly room for optimism and requiring further investigation. All right. Well, we apologize for the audio kinds of problems. They're really not in our control. And thank you for being a great audience and wish you a good rest of your day in San Francisco for the last day of the conference.

ADHD treatment

novel therapeutics

dietary interventions

omega-3 supplements

internet addiction

cognitive behavioral therapy

bupropion

neurostimulation

transcranial direct current stimulation

trigeminal nerve stimulation

pharmacological studies

holistic treatment