Deborah R. Simkin, MD

). Mindfulness falls under the category of focused attention, which has recently received considerable attention.

Since the 1990s, mindfulness meditation has been studied in healthy groups and increasingly in clinical populations in adults. The research is quite robust in adults with depression and anxiety, but research in youths with the same conditions is just starting. Jon Kabat-Zin brought mindfulness into the clinical realm with mindfulness-based stress reduction (MBSR). Defining this state of mind, he shared this awareness that emerges through purposeful attention, in the present moment, and nonjudgmentally to the unfolding of experience moment by moment.

 With the possible exception of sleep, all that we do each day can be done mindfully.

Mindfulness practices have been used primarily to aid in stress reduction and the promotion of health and well-being in various populations, including those with chronic pain, depression, anxiety, or other mental health conditions. Mindfulness practices often include body relaxation, mental imagery, breathing practice, and mind-body awareness.

MBSR is a manualized approach. This 8-week group intervention meets once a week for 2 and a half hours with an all-day session during week 6. Each meeting includes one of the mindful practices along with mindfulness to daily activities.

Neuroscience research has found 3 possible mechanisms through which mindfulness meditation increases self-regulation:

Within attentional control is alerting and orienting as well as conflict monitoring. With the experienced meditation practitioner, there is greater alerting enhancement, whereas the beginner experiences better conflict-monitoring and orienting.

Neuroimaging studies have supported both functional and structural changes in the anterior cingulate cortex and the dorsolateral prefrontal cortex. Specifically, there is a thickening of the gray matter in these specific areas along with activation. In addition, there is a decrease in amygdala activation.

 The research is so compelling that Tang and Leve

 suggest that mindfulness meditation interventions are a possible prevention strategy. However, this needs to be further studied in translational neuroscience.

Mindfulness meditations specific to clinical populations

Research in mindfulness meditation and youth has been primarily in healthy populations with research conducted in community settings such as schools. Two of many such programs are The Hawn Foundation MindUp4 and the Inner Resilience Program by Lantieri and Goleman.

Different interventions have evolved with the perceived need of different clinical populations (

). The 2 most popular are MBSR and mindfulness-based cognitive therapy (MBCT), which was adapted from MBSR.

 Both have a manualized group protocol, but MBCT has an added component of cognitive interventions to disrupt repetitive negative thought patterns. The intent is to identify the intrusive thoughts as “just thoughts,” to practice a nonjudgmental approach; to observe the thoughts, to recognize them rather than avoiding them or returning to habitual thought patterns.

With children and teens, modifications have allowed for developmental differences such as increased repetition and reduced time spent in meditation. The MBCT-C protocol has been tested in children aged 8 to 14 years. Parent training happens as well to further support the child. The MBSR-T protocol is specific for teens aged 14 to 18 years. With children and teens, an all-day workshop is typically not used.

A meta-analysis of mindfulness in children and adolescents

 reviewed the current state of research in youth. They focused on the value of mindfulness meditation, and on which symptoms or sample populations would benefit most. Twenty studies met inclusion criteria. Based on their data, the researchers concluded that mindfulness interventions with youth were helpful; moreover, there was no iatrogenic harm. Effect size was in the small to moderate range (0.23,

 > .001), which indicates mindfulness interventions were better than the active control. Of note, there was a significantly larger effect size for psychological symptoms when compared with other dependent variables as well as for clinical samples compared with non-clinical samples.

Of the 20 studies reviewed, most were conducted in schools and used a variety of intervention types: 3 used MBSR, 3 used MBCT-C, 5 used part of MBSR, and 9 used other mindfulness interventions. The participants were aged 6 to 21 years. Although most comprised nonclinical populations, 4 studies included clinical samples; 12 studies had active controls. Measures included psychological symptoms such as anxiety or depression; general function such as social skills; and measures of mindfulness.

A moderate effect size in the clinical population was 3-fold higher than the effect size of the nonclinical sample. This suggests that mindfulness may be most helpful in clinical populations. Mindfulness appeared to address symptoms of psychopathology quite well when compared with other outcome measures.

undertook one of the largest randomized controlled studies in youths: 102 adolescents in a psychiatric outpatient clinic were randomized to either treatment as usual (TAU) or TAU and an 8-week MBSR program facilitated by trained personnel. Significant improvement in mental health measures were seen in the MBSR group (

 = .0001). Important to this study is the correlation between time spent in mindfulness practice and the improvement in clinician-rated functioning and self-reported depression and anxiety symptoms from baseline to 3-month follow-up (

Teaching parents and children MBSR using either formal home practice with an instructor or informal practice at home can have added benefits. In a study by Saltzman and Goldin,

 informal practice decreased self-reported depressive symptoms in the adults (

 < .05) and increased cognitive control of attention in children (

 < .05), thereby increasing family harmony.

A high theta/beta ratio is associated with some forms of ADHD. Although mindfulness techniques are usually associated with decreases in anxiety, which has an indirect effect on attention, the use of transcendental meditation showed improvements in attention associated with changes in the theta/beta ratio of EEG.

In a pilot study, 18 children were randomized to either transcendental meditation or a control group.

 Significant decreases in theta/beta ratios of EEG were recorded at Cz in the transcendental meditation group (

 = .05) that correlated to improvements in ADHD symptoms. There were significant increases from pretest to 3-month post-test in letter fluency for the transcendental meditation group (

 = .017) on the Delis-Kaplan Executive Function System test. There were also significant improvements on parent rating scales in the ability to focus on schoolwork, organizational abilities, ability to work independently, happiness, and quality of sleep. All of these results were maintained at 6-month follow-up.

Although this is a small trial, it shows that transcendental meditation warrants further study as a possible adjunct treatment, especially for ADHD. These findings correlate with results from a magnetoencephalography study that demonstrated that transcendental meditation increases activity in prefrontal executive circuits and anterior cingulate attention circuits.

A mind-body technique referred to as meditation/relaxation has been used for PTSD by Catani and colleagues

 in a randomized comparative study. This study was conducted within the first 5 months after a tsunami in the northeastern part of Sri Lanka. Thirty-one children were randomized to either 6 sessions of a meditation/relaxation technique or 6 sessions of narrative exposure therapy for children (KIDNET). PTSD symptoms (avoidance, intrusions, and hyperarousal) and impairment in functioning were significantly reduced at 1 month after treatment and remained stable over time at the 6-month follow-up. The effect size for the KIDNET group was 1.76 (confidence interval [CI], 0.9-2.5) at post-test and 1.96 (CI, 1.1-2.8) at the 6-month follow-up. The effect sizes for the meditation/relaxation group were 1.83 (CI, 0.9-2.6) and 2.20 (CI, 1.2-3.0). At the 6-month follow-up, recovery rates were 81% for the children in the KIDNET group and 71% for those in the meditation/relaxation group.

Mind-body techniques may show some promise in children with autism spectrum disorder (ASD). Rosenblatt and colleagues

 designed a program that engaged the unique sensory features of patients with ASD using yoga and music. Twenty-four children (ages 3 to 18) participated; parents were given a CD and guidelines on how to practice at home. Results using BASC-2 (Behavioral Assessment System for Children, Second Edition) demonstrated that the behavior symptom index changed for all participants. The change was greater for the latency-aged group (

 < .05). Unexpectedly, the post-treatment scores on the atypicality scale of the BASC-2, which measures some of the core features of autism, changed significantly (

 = .003). For the latency-aged children, there was a trend toward improvement on the irritability scale of the aberrant behavior checklist (

 = .06). Although small, this study suggests that body-mind techniques may be especially beneficial in latency-aged children with ASD.

Although data on mindfulness specific to youths with mental health problems are limited, it is clear that there is a foundational improvement in psychological function and resilience in the healthy youths studied. In the meta-analysis, there was strong effect size for reduction in psychological symptoms in the clinical population-mindfulness interventions had the strongest outcome measure.

Areas of future study to consider would be attempts to replicate the impact of meditation in areas of the world where trauma is prevalent. These interventions can be taught to health care workers in underserved areas. It can be a safe and effective intervention in high distress zones. Another area of future study is to see whether mindfulness meditation practice affects the dose of or need for medications in ADHD, anxiety, and depression.

Finally, it is important to study which forms of meditation are of most benefit to which disorder. For example, body-mind techniques that utilize music and yoga might be better suited to autistic children than traditional mindfulness techniques.

Dr. Pentz is Assistant Professor, Department of Psychiatry and Behavioral Science, University of New Mexico, Albuquerque, NM; and she has a small private consultation practice. Dr. Simkin is Clinical Assistant Professor at Emory School of Medicine, Atlanta, GA, and is in private practice in Destin, FL. The authors report no conflicts of interest concerning the subject matter of this article.

 Kabat-Zin J. Mindfulness-based interventions in context: past, present, and future. 

 Tang YY, Leve LD. A translational neuroscience perspective on mindfulness meditation as a prevention strategy. 

 Annells S, Kho K, Bridge P. Meditate don’t medicate: how medical imaging evidence supports the role of meditation in the treatment of depression. 

The MindUp Curriculum: Brain-Focused Strategies for Learning and Living

. New York, NY: Scholastic Teaching Resources; 2011.

Building Emotional Intelligence: Techniques to Cultivate Inner Strength in Children

Mindfulness-Based Cognitive Therapy for Depression: A New Approach to Preventing Relapse

Mindfulness-based cognitive therapy for prevention of depressive relapse. In: Baer RA, ed. Mindfulness-Based Treatment Approaches: Clinician’s Guide to Evidence Base and Applications

 Zoogman S, Goldberg SB, Hoyt WT, et al. Mindfulness interventions with youth: a meta-analysis. 

 Biegel GM, Brown KW, Shapiro SL, et al. Mindfulness-based stress reduction for the treatment of adolescent psychiatric outpatients: a randomized clinical trial. 

 Saltzman A, Goldin P. Mindfulness-based stress reduction for school-age children. In: Greco LA, Hayes SC, eds. 

Acceptance and Mindfulness Treatments for Children and Adolescents: A Practitioner’s Guide

. Oakland, CA: New Harbinger Publications, Inc; 2008:139-161.

 Simkin D, Black N. Meditation/mindfulness. In: Simkin D, Popper C, eds. 

Alternative and Complementary Therapies for Child and Adolescent Psychiatric Disorders

. Toronto, Ontario: Elsevier Canada; 2014:487-534.

 Travis F, Grosswald S, Stixruds W. ADHD, brain functioning, and transcendental meditation practice. 

 Yamamoto S, Kitamura Y, Yamada N, et al. Medial prefrontal cortex and anterior cingulate cortex in the generation of alpha activity induced by transcendental meditation: a magnetoencephalographic study. 

 Catani C, Kohiladevy M, Ruf M, et al. Treating children traumatized by war and tsunami: a comparison between exposure therapy and meditation-relaxation in North-East Sri Lanka. 

 Rosenblatt LE, Gorantia S, Torres JA, et al. Relaxation response-based yoga improves functioning in young children with autism: a pilot study. 

Articles

This review provides information to assist clinicians who are considering mindfulness meditation for their patients.

The Use of Meditation in Children With Mental Health Issues

The apparent strong association between bipolar disorder and substance use disorders (SUDs) could be explained in several ways. Bipolar disorder may be causing SUD, SUD may be causing bipolar disorder, or both disorders may share common origins. As discussed by Brown,

 however, it is not likely that any of these explanations is correct.

Since both of these disorders often have their onset in adolescence, it might be important to look at the effects that bipolar disorder and SUD have on the developing brain. Perhaps either or both of these disorders disrupt the normal development of the brain in such a way that the brain never reaches full maturity; this, in turn, could make the brain vulnerable to a more insidious course of illness than if the disorders had occurred after the brain was mature. If this is true, then medical interventions may not be as effective as they would have been had the brain reached full maturity. This article will look at the development of the brain and whether neurobiology of the brain can play a role in predicting risk for future bipolar disorders and SUDs.

 have shown that patients with either manic or euthymic bipolar disorder (aged 17 to 45 years) and healthy controls performed similarly on the delayed response test (which measures spatial working memory and involves the dorsolateral prefrontal cortex [DLPFC]). However, patients with euthymic and manic bipolar disorder performed significantly more poorly than controls on the Object Alternation Test (which measures inhibitory control and involves the orbitofrontal cortex [OFC], the part of the brain that influences inhibition). This suggests that adults with bipolar disorder may have a deficit in the OFC.

Inhibitory control may be involved in inhibiting manic symptoms, such as hypersexuality. Inhibitory control also plays a part in SUD. Since bipolar disorder and SUD may have their onset during adolescence, the question is whether the OFC deficit occurs because these disorders prevent the brain from fully maturing as it normally would (by the end of early adulthood or about age 22) or whether these disorders damage the OFC no matter when they occur. Because earlier onset of these disorders usually results in a poorer prognosis, the first explanation may account for the influence an immature brain has on a disease state compared with the influence a mature brain would have when the disease state occurs later in life.

In order to understand how brain development may be disrupted by the emergence of bipolar disorder or SUD during adolescence, it is important to understand the normal development of the brain during this period. Much research is beginning to emerge on the development of the adolescent brain. Chambers and colleagues

 have summarized some of the findings in terms of 3 important events: (1) pruning neurons, (2) the role of hormones, and (3) maturation of the prefrontal cortex (PFC).

First, the adolescent brain begins the process of pruning. During pruning, adolescents lose 20% to 40% of their total neurons. One of the neurons involved is associated with serotonin. When serotonin neurons are lost, impulsivity increases, which may be the reason adolescents are less able to carry on cognitive processes. In a study of adolescent decision making, Baird and colleagues

 showed that, compared to adults, adolescents took significantly longer to decide whether a presented scenario was not a good idea. The adults were able to quickly elicit mental images of possible outcomes that steered their decision- making process by recruiting greater activation of the insula and the right fusiform face area. Adolescents may impulsively act before they take time to decide whether their choice is a good one, and they are not as likely to use mental images when making a choice.

Second, when hormones come on board, they influence the primary motivational circuitry, cortical-striatal (including the nucleus accumbens)-thalamic-cortical, which increases sensitivity to pleasurable experiences. The seeking out of pleasurable experiences, some of which may be risky, may be caused not only by an increased sensitivity to these experiences but also by the inability to distinguish which events are motivationally relevant or irrelevant.

In a study comparing adolescents to young adults, Bjork and colleagues

 showed that there were no differences in brain activity while performing a task for monetary gain. However, the adolescents had less recruitment of the right amygdala and the right ventral striatum than adults while anticipating response for such gain. 

The amygdala establishes learned associations between motivationally relevant events.

 This inability to anticipate what events are motivationally relevant or irrelevant may be why adolescents seek out risky behaviors more than adults.

Third, the PFC does not mature until about age 22. This means the PFC in adolescents is immature (will not have proper connections to other parts of the brain that would allow inhibition to occur quickly, especially in emotionally charged situations).

The inability to inhibit responses has been elaborated by Casey and colleagues, 

 who studied children aged 7 through 12 years and adults aged 21 through 24 years, and by Tamm and coauthors,

 who studied participants aged 8 through 20 years, on a go/no-go task with corresponding functional MRI studies. These studies showed that children used the DLPFC and had more errors than adults, who used the ventral PFC or the OFC.

Another separate process that occurs during adolescence is myelination. This can influence the speed with which one processes and the speed with which one inhibits responses. In 2006, Luna and Sweeney

 showed that the changes in the brain during adolescence occur in order to move from a brain that requires much more energy to process information to a more efficient brain as an adult. These processes can explain why experimentation may be more likely to occur in adolescence. For instance, if children do not have anything they are passionate about, such as athletics, music, or academics, they may be more likely to seek out other means of feeling pleasure (eg, risky behaviors), which puts them at increased risk for substance abuse. In fact, academic and social failure by age 7 through 9 can predict substance abuse by age 14 through 15.

If the adolescent does not succumb to substance abuse, or other psychiatric disorders that may influence normal development, the brain will continue to undergo these changes. In particular, the PFC and the corresponding inhibitory response will mature.

Therefore, one can assume that if the brain is allowed to develop normally, the mature PFC can help to control or inhibit the disease state more effectively if bipolar disorder emerges after adolescence than it could if the disorder emerges earlier. One might wonder what would occur if bipolar disorder begins in adolescence.

 looked at adolescents who were treated for bipolar disorder and found that they had significantly lower levels of 

-acetylaspartate (which measures neuronal density) in the right DLPFC when compared with controls. Because 

-acetylaspartate serves as a brake control during adolescence, reduced levels may translate into reduced effectiveness in inhibiting mania in subcortical structures.

On the other hand, neither Gallelli and colleagues

-acetylaspartate levels in adolescents with early onset bipolar disorder (most were taking medication) and in healthy controls. This may indicate that the longer the disorder progresses, the greater the effect on the DLPFC. What remains to be understood is whether certain medications or combinations of medications can decrease the effect of bipolar disorder on the DLPFC by indirectly regulating a number of factors involved in cell survival pathways.

What is the effect of SUD in the developing brain? The ventral tegmentumnucleus accumbens (VTA-NA) tract is important to acute drug use disorder. Kalivas and Volkow6 have shown that when substances like cocaine are used, dopamine increases in the shell of the nucleus accumbens. Increased levels of dopamine in the shell direct the brain to experiences that are more salient and pleasurable; because dopamine levels are increased with cocaine, this results in an increase in the magnitude of pleasurable effect. During withdrawal, less dopamine is released and there is a decrease in D2 receptors. When D2 receptors decrease in the shell of the nucleus accumbens, natural reinforcers are no longer salient, but drugs are.6,15 As D2 receptors decline, more drugs are needed to get the same effect.

 have studied the effects of administering adenovirus to mice to increase D2 receptors by 50%. Results showed that the mice decreased alcohol intake by 70%. While the role of the VTA-NA tract and increased dopamine in the shell of the nucleus accumbens is important in acute drug use, dopamine in the PFC and the amygdala, and glutamate release in the core of the nucleus accumbens play a key role in the reinstatement of drug seeking after chronic drug use disorder.

During chronic drug use, dopamine is released between the VTA-PFC tract and the VTA and amygdala. During chronic drug use and withdrawal periods, there is also an increase of G protein binding--protein AGS3--in the PFC. Increased AGS3 levels inhibit D2 receptor signaling and correspondingly increase D1 receptor signaling, which causes increased activity of projections from the PFC (in this case, the anterior cingulate and the OFC) to the core of the nucleus accumbens. When cues or stimuli occur that are associated with drug seeking, increased activation of projections from the PFC occurs, which, in turn, increases release of glutamate in the core of the nucleus accumbens. This increase in glutamate causes an increase in drug seeking and intake. Such stimuli might include a cue previously associated with drug use, a mild stressor, or a single dose of the drug

The release of dopamine in the PFC and the amygdala is necessary for the amygdala to recognize cue-associations with drug use (motivationally relevant events) and for the PFC to exert its effect on the nucleus accumbens (to mediate behavior). In this scenario, the PFC would not be able to restrict the compulsion to seek out stimuli that have cueassociations with drug use. Hence, this process may correlate with addiction or the loss of control, with the addict continuing to use the drug even though there is no longer pleasure in its use.

The changes that occur after chronic drug use are more permanent than changes that occur during acute drug use and may be a reason why relapse occurs in addicts. Since adolescents may not be able to differentiate between motivationally relevant and irrelevant events (as previously discussed), when addiction occurs, the PFC may increase the tendency to seek out risky behaviors whether they are relevant or not. Alternatively, addiction may tune the otherwise less sensitive amygdala found in adolescents into a more sensitive adultlike amygdala that seeks out only drugassociated relevant events.

Although patients may use substances to self-medicate their manic symptoms, it is clear that the use of multiple substances, such as marijuana and alcohol, may, in reality, make the neurobiologic effect even worse. When patients (aged 18 to 65 years) presented with active marijuana and alcohol use in the manic phase, the marijuana did not decrease the level of the manic state.

 Thus, although the sensation of feeling calmer with marijuana may have been experienced by bipolar substance abusers who were manic and using alcohol, the mania symptoms were actually worse in those who presented with bipolar disorder and marijuana and alcohol use than in those with bipolar disorder and alcohol use alone.

Use of multiple substances may be a sign of a more progressive addiction, which would likely decrease the ability to inhibit compulsive behavior and the level of mania. Moreover, the type of treatment used may have greater effect on those who are actively using marijuana during their presentation with mania and alcohol. Those who were treated with lithium and psychosocial therapy in this study (compared with those treated with lithium, valproic acid, or psychosocial treatment alone), had the highest percentage of heavy drinking days.

One might wonder whether valproic acid may have reduced craving and the urge to use drugs because of its antiglutaminergic effect on the projections from the PFC to the nucleus accumbens that occurs with chronic drug use. The individuals who used alcohol and marijuana were younger than the other study participants; because alcohol and marijuana are the most frequent substances of abuse in children and adolescents with bipolar disorder, early onset of bipolar disorder and multiple substance abuse disorders may have a greater neurobiologic effect on the immature brain if the disorders go undetected and untreated.

How else might bipolar disorder and SUD influence each other when they occur during adolescence? As noted, teens are more likely to experiment if they have had little academic or other success before adolescence. If they have a family history of substance abuse, they are also more likely to have a genetic predisposition to tolerance.

 Since a family history of substance abuse is more likely to result in progressing from initiation to dependence, these adolescents may do so without becoming fully aware that they have a problem because their tolerance allows them to use drugs without feeling the effects as strongly as nontolerant adolescents. They may have been born with lower D2 levels or reduced D2 levels may have developed secondary to drug use.

 Whatever the reason, they are more likely to become chronic abusers and hence, become addicted.

If substance abuse occurs before the development of bipolar disorder, there may be a more rapid onset of mania because there is less ability to control or inhibit symptoms of mania (eg, hypersexuality) or mood associated with subcortical structures

 because of the effect of addiction on the OFC, as noted by Goldstein and Volkow.

 If the bipolar disorder occurs before the substance abuse, the effect on the OFC may strengthen the compulsion to use drugs.

 In addition, the addiction process changes the way the OFC normally performs (by forming different connections); thus, the OFC may not function as it normally would have before the addiction.

One may also wonder whether this reorganization of connections prevents the OFC from ever fully developing. If normal functioning or maturation of the OFC does not occur in adolescence, this may lead to less control of symptoms of mania in adulthood. This could explain why early onset of mania has a higher risk for a worse prognosis. On the other hand, if all adolescents must rely more on the less efficient DLPFC for inhibitory control during adolescence, the adolescent with bipolar disorder, who has a less mature DLPFC, may have more difficulty throughout this period. Decreases in 

-acetylaspartate levels in the DLPFC (used primarily during adolescence for inhibition) were found in euthymic bipolar patients and manic patients compared with healthy adolescents. We would hope that earlier detection and treatment of bipolar disorder and SUD (presenting separately or together) would increase the likelihood that the OFC would be able to fully mature.

Early detection and treatment of SUD and bipolar disorder is extremely important to neurobiologic development in adolescents. If the developmental processes discussed above are proved true, not treating adolescents with SUD and bipolar disorder may prevent normal development of the brain and decrease the ability of the child to function at his or her fullest potential as an adult. Just as important, not treating the disorders early may decrease the responsiveness of a mature brain to medication interventions. Neurobiology is in its infancy. More research is needed to more accurately understand the underlying causes of bipolar disorder and SUD on the developing brain. New research should also concentrate on finding treatments that may allow normal development of the brain to occur despite the onset of psychiatric disorders.

Dr Simkin is clinical assistant professor at the Florida State University College of Medicine in Tallahassee, Florida. She reports that she is a speaker for Abbott Laboratories.

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A discussion of the development of the brain and whether neurobiology of the brain can play a role in predicting risk for future bipolar disorders and substance use disorders SUDs.

Author | Deborah R. Simkin, MD

Articles

The Use of Meditation in Children With Mental Health Issues

Developmental Neurobiology of Bipolar Disorder and Substance Use Disorder