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Attention-deficit/hyperactivity disorder (ADHD) is the most common neurodevelopmental disorder in childhood. Children and adolescents with ADHD are at increased risk for behavioral issues, academic issues, substance abuse issues, and legal problems. Approximately 50% of cases of childhood ADHD will persist into adulthood where it can impact employment, organizational skills, and frustration tolerance. Use of amphetamine and methylphenidate stimulant medications have shown to have the best outcomes, and are considered first line treatments. It is important to monitor stimulant use closely in individuals with substance abuse concerns, however, studies in adolescents with both substance abuse histories and ADHD tend to support their use and benefits. It is important to identify other co-morbid conditions that a patient with ADHD may be struggling with and treat those accordingly. Providers should re-evaluate the symptoms and clinical presentation of patients that show minimal or no improvement with treatment to ensure a proper diagnosis has been made.

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Suicide currently ranks as the second leading cause of death in the U.S. in youth ages 10-24, and in young adults ages 25-34. It is also the third leading cause of death in youth and young adults worldwide. Although there are multiple factors that increase one's risk for suicide, a history of a previous suicide attempt is likely one of the strongest predictors of a future completed suicide. Alcohol use, substance use, bullying, a history of mental illness, a family history of suicide, hopelessness, and many other risk factors exist that may increase one's risk for attempting suicide. Implementation of screening questionnaires such as the PHQ-A, PHQ-9, or the Columbia-Suicide Severity Rating Scale may help clinicians identify those patients who may be struggling with depression or who may be at risk for suicide. Research has shown that approximately 45 percent of patients who die by way of suicide visited their primary care provider within a month before completing suicide, so it is important that clinicians become comfortable with evaluating and talking with their patients about suicide.

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Consuming excessive amounts of alcohol has the potential to modify an individual's brain and lead to alcohol dependence. Alcohol use leads to 88,000 deaths every year in the U.S. alone and can lead to other health issues including cancers, such as colorectal cancer, and mental health problems. While drinking behavior varies due to environmental factors, genetic factors also contribute to the risk of alcoholism. Certain genes affecting alcohol metabolism and neurotransmitters have been found to contribute to or inhibit the risk. Geneenvironment interactions may also play a role in the susceptibility of alcoholism. With a better understanding of the different components that can contribute to alcoholism, more personalized treatment could cater to the individual. This review discusses the major genetic factors and some small variants in other genes that contribute to alcoholism, as well as considers the gene-environmental interactions.

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CASE: A highly anxious and dehydrated adolescent came to a local emergency department with complaints of intractable emesis, weight loss, and abdominal pain. He stated that bathing and "guzzling water" ameliorated symptoms. He admitted to using marijuana socially. Efforts at palliation with benzodiazepines, atypical antipsychotics, and antiemetic medications were unable to soothe the patient. After thorough initial diagnostics and physical exam failed to elucidate etiology, the patient was referred to an inpatient psychiatric facility for further evaluation of potential psychosomatic or affective causes. During psychiatric evaluation and upon obtaining additional information from family and reviewing the work done by primary care providers, the patient was questioned stringently about his marijuana use patterns. Questioning revealed that the patient had previous chemical dependency treatment, legal charges related to drug use, and heavy daily marijuana use including "dabbing," ingestion of THC candy, and smoking up to several grams a day. DISCUSSION: Cannabinoid hyperemesis syndrome (CHS) consists of intractable emesis, abdominal pain, and weight loss. There is often a history of symptom amelioration with bathing and showering. These patients may or may not admit to heavy marijuana use. Cannabis effects vary and are dose dependent. Historically, CHS would require over a year of heavy daily use. In this day and age of higher THC potency marijuana and even higher THC potency "dabs," it is anticipated that more cases of cannabis related syndromes in general, and CHS in particular will be presenting more frequently to ambulatory and emergency room settings. The patients will potentially be younger and have a shorter duration of heavy cannabis use before symptoms start. A high index of suspicion will be required to prevent expensive and potentially invasive workups and thus delaying diagnosis and treatment.

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With the recent legalization of recreational marijuana in Colorado, Washington, Alaska, the District of Columbia and legislation pending for both medical and recreational marijuana in several other states, it is important for the facts regarding its potential for serious mental health consequences to be known. Little has been said about the psychiatric risks of this substance, particularly in youth. Several studies have shown increased rates of depression, anxiety and schizophrenia among those who use marijuana on a regular basis. In addition, permanent loss of IQ and structural changes in the brain have been demonstrated with habitual use. Legalization of marijuana for recreational use can influence an adolescent's perception of this substance as "safe." In states that have legalized marijuana for medical purposes, there is the very real problem of "diversion." As many as 34 percent of 12th-graders who use marijuana in states with legalized marijuana had obtained it from a person who had received it through a prescription.

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Olanzapine is a first line medication for the treatment of schizophrenia, but it is also one of the atypical antipsychotics carrying the highest risk of weight gain. Metformin was reported to produce significant attenuation of antipsychotic-induced weight gain in patients, while the study of preventing olanzapine-induced weight gain in an animal model is absent. Berberine, an herbal alkaloid, was shown in our previous studies to prevent fat accumulation in vitro and in vivo. Utilizing a well-replicated rat model of olanzapine-induced weight gain, here we demonstrated that two weeks of metformin or berberine treatment significantly prevented the olanzapine-induced weight gain and white fat accumulation. Neither metformin nor berberine treatment demonstrated a significant inhibition of olanzapine-increased food intake. But interestingly, a significant loss of brown adipose tissue caused by olanzapine treatment was prevented by the addition of metformin or berberine. Our gene expression analysis also demonstrated that the weight gain prevention efficacy of metformin or berberine treatment was associated with changes in the expression of multiple key genes controlling energy expenditure. This study not only demonstrates a significant preventive efficacy of metformin and berberine treatment on olanzapine-induced weight gain in rats, but also suggests a potential mechanism of action for preventing olanzapine-reduced energy expenditure.

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Due to serious adverse effects and the limited effectiveness of currently available pharmacological therapies for obesity, many research efforts have focused on the development of drugs from natural products. Our previous studies demonstrated that berberine, an alkaloid originally isolated from traditional Chinese herbs, prevented fat accumulation in vitro and in vivo. In this pilot study, obese human subjects (Caucasian) were given 500 mg berberine orally three times a day for twelve weeks. The efficacy and safety of berberine treatment was determined by measurements of body weight, comprehensive metabolic panel, blood lipid and hormone levels, expression levels of inflammatory factors, complete blood count, and electrocardiograph. A Sprague-Dawley rat experiment was also performed to identify the anti-obesity effects of berberine treatment. The results demonstrate that berberine treatment produced a mild weight loss (average 5 lb/subject) in obese human subjects. But more interestingly, the treatment significantly reduced blood lipid levels (23% decrease of triglyceride and 12.2% decrease of cholesterol levels) in human subjects. The lipid-lowering effect of berberine treatment has also been replicated in the rat experiment (34.7% decrease of triglyceride and 9% decrease of cholesterol level). Cortisol, calcitriol, ACTH, TSH, FT4, and SHBG levels were not significantly changed following 12 weeks of berberine treatment. However, there was interestingly, an increase in calcitriol levels seen in all human subjects following berberine treatment (mean 59.5% increase, p=0.11). Blood inflammatory factors (CRP, IL-6, TNFα, COX-2) and erythrocyte sedimentation rate (ESR) were not significantly affected by treatment with berberine. Tests of hematological, cardiovascular, liver, and kidney function following berberine treatment showed no detrimental side effects to this natural compound. Collectively, this study demonstrates that berberine is a potent lipid-lowering compound with a moderate weight loss effect, and may have a possible potential role in osteoporosis treatment/prevention.

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The Affymetrix Drug Metabolism Enzymes and Transporters (DMET) microarray is the first assay to offer a large representation of SNPs conferring genetic diversity across known pharmacokinetic markers. As a convenient and painless alternative to blood, saliva samples have been reported to work well for genotyping on the high density SNP arrays, but no reports to date have examined this application for saliva-derived DNA on the DMET platform. Genomic DNA extractions from saliva samples produced an ample quantity of genomic DNA for DMET arrays, however when human amplifiable DNA was measured, it was determined that a large percentage of this DNA was from bacteria or fungi. A mean of 37.3% human amplifiable DNA was determined for saliva-derived DNAs, which results in a significant decrease in the genotyping call rate (88.8%) when compared with blood-derived DNAs (99.1%). More interestingly, the percentage of human amplifiable DNA correlated with a higher genotyping call rate, and almost all samples with more than 31.3% human DNA produced a genotyping call rate of at least 96%. SNP genotyping results for saliva derived DNA (n = 39) illustrated a 98.7% concordance when compared with blood DNA. In conclusion, when compared with blood DNA and tested on the DMET array, saliva-derived DNA provided adequate genotyping quality with a significant lower number of SNP calls. Saliva-derived DNA does perform very well if it contains greater than 31.3% human amplifiable DNA.

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Globally, tobacco smoking is responsible for the deaths of five million people each year and increases the risk of developing numerous disorders, particularly pulmonary and cardiovascular disease, as well as many cancers. It has long been known that several environmental factors influence the decision to smoke. However, in recent years, we have learned more about the role that genes play in the development of nicotine dependence. Twin and family studies have shown that there is not one specific gene that determines who will develop a smoking addiction but rather several genes that cause an individual to become more susceptible to being addicted to nicotine. These genes are responsible for how certain neurotransmitters are produced and metabolized, the number of receptors that are available to act on and how rapidly nicotine is metabolized by the individual. The more we understand these processes, the better the opportunity will be to formulate effective treatments. This review discusses the role genetics plays in the decision to smoke, the ability to quit and how human genetic variation can influence the success of therapeutics in the treatment of smoking behavior.

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BACKGROUND: Anxiety disorders often coexist with substance use and complicate treatment by causing non-adherence and relapse. Optimal treatment generally involves the treatment of anxiety along with the treatment of substance abuse. Substance-abuse treatment generally involves individual and group therapy, sobriety maintenance interventions, structured living, and attending self-help groups such as Alcoholics Anonymous. Pharmacotherapy options for treating substance abuse are limited, but atypical antipsychotic medications have reportedly reduced substance abuse when used in patients with alcohol and drug problems. However, there are no reports of long-term benefits of these medications. OBJECTIVE: To assess long-term effects of adjunctive quetiapine on substance abuse in patients treated with quetiapine for severe anxiety symptoms. METHOD: In a previous paper, we reported that adjunctive treatment with quetiapine reduced symptoms of anxiety and cravings for alcohol and drugs when used in patients with anxiety disorders or with anxiety due to alcohol/drug dependence/abuse. In this study, we followed up with these patients one year later to assess their current symptoms, cravings and use of alcohol/drugs, and compared these to results of random breathalyzer and urine drug screening tests conducted as part of routine outpatient treatment of their substance abuse. RESULTS: Six of nine patients continued to take adjunctive quetiapine over the previous 12-month period and reported complete sobriety (substantiated by their random breathalyzer and urine drug screens) and significant reduction in anxiety, depression, and cravings for alcohol and drugs. CONCLUSION: Adjunctive quetiapine used for treatment of anxiety symptoms that may occur as part of different psychiatric disorders in patients with alcohol and drug problems might reduce cravings and substance use.

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