When you’re feeling stressed, sometimes there’s nothing like picking up your favorite comfort food — chocolate, chips, fries, ice cream, soda, or an alcoholic drink — to self-soothe. You know the feeling, and you can be sure your patients do, too. The message, then, to help patients is: Although it may feel good in the moment, a repetitive cycle of boosting your cortisol levels and seeking solace in food can make stress worse. Eating too many “treats” regularly can also shift your microbiome, metabolic health, and gut-brain relationship as a result. “Although many people may not realize it, there is a connection between how we feel and our food choices. We make hundreds of choices a day, including the type of foods we choose to eat, whether we order takeout or make a home-cooked meal, or whether we choose to fry a filet of fish or bake it,” said Roxana Ehsani, a registered dietitian nutritionist based in Miami. “How we feel mood-wise can dictate these food choices,” she added. “If we are feeling stressed, we may gravitate toward choosing a meal that provides stress relief or comfort, which may not be the most nutritious food choice.” Feeling and Feeding Our Emotions While it’s natural for people to reach for comfort foods during times of stress, strong emotions, or even boredom, it can become a problem when a pattern of subconscious behavior emerges. “I see people get into these patterns of feeling a negative emotion, reaching for comfort food, and feeling guilty, which creates a negative cycle of guilt and shame,” said Whitney Linsenmeyer, PhD, RD, assistant professor of nutrition and dietetics at Saint Louis University in St. Louis and a spokesperson for the Academy of Nutrition and Dietetics. This isn’t to say physicians should tell their patients to ban this type of comfort-seeking. They just need to know the consequences of too much of a good-tasting thing. “It’s fine to recognize you’re feeling sad and enjoy a food that brings you comfort,” she said. “The key is bringing awareness to it, understanding the reasons why you’re doing it, and maybe thinking about other ways you might comfort yourself, such as calling a friend or going for a walk.” These patterns emerge due to strong relationships across the body. When stressed, for instance, the body releases a hormone called cortisol through the hypothalamic-pituitary-adrenal axis, which increases blood flow, heart rate, breathing, and other factors such as blood clotting. Over time, persistently high levels of cortisol can lead to long-term health issues, such as obesity, insulin resistance, and metabolic syndrome. Comfort foods, in turn, can add to those long-term health issues due to added sugars, sodium, and unhealthy fats. As a result, spikes in blood sugar and blood pressure can then lead to even greater irritability and stress — as well as brain fog, poor memory, and low energy. “The gut-brain connection between your gastrointestinal [GI] tract and central nervous system goes both ways, where you might feel stress in your brain, but it manifests in your GI system as a stomachache or IBS [irritable bowel syndrome] flare,” Linsenmeyer said. “It can go the other way, too, where a disruption in healthy gut microbes through illness or poor diet can affect your cognitive health and well-being.” Chronic inflammation plays a role in the cycle of stress for both mental and physical health, which has become increasingly common in recent years as more people consume ultraprocessed foods that contain dyes, preservatives, and stabilizers but lack the fiber or nutrients of whole foods. “Studies have shown that when there are inflammatory markers in the gut, there are markers of neuroinflammation as well,” said Uma Naidoo, MD, director of nutritional and lifestyle psychiatry at Massachusetts General Hospital in Boston and author of the book, This Is Your Brain on Food. “Neuroinflammation has been linked to a host of mental health and neurological conditions, including anxiety, depression, mood disorders, and cognitive problems,” she said. “In my practice, I’ve seen that adjusting the diet of those with various psychiatric problems can help to calm this inflammation and improve mood, stress, and emotional well-being over time.” Trying Other Coping Strategies Another good message for patients: When you feel stressed and in need of a comforting snack, stop and bring awareness to the moment, Linsenmeyer said. Consider what’s prompting them to eat and identify where in the body the “hunger” is coming from, which could be physically in the stomach or more emotionally in the brain or heart. If a patient realizes they’re simply bored, encourage them to choose another activity to satisfy the craving for action, she said. If you realize your mouth wants to taste flavor or a crunchy texture, try to choose a healthy alternative. If they feel emotional, maybe they can find release through physical activity, journaling, meditation, or connection with a friend. To get started, Linsenmeyer recommends people become familiar with their behavioral patterns by tracking what they eat and drink across 3 days — and record their emotion each time. Consciously stopping and reflecting on both the foods and feelings can reveal when someone may feel stress throughout the day, how they react, and what else they could do instead. After learning the patterns, planning can start by setting up meals or snacks to make healthier choices throughout the week, Ehsani said, adding that it doesn’t have to be an extensive or stressful process. Once per week, she suggests people write down a few meals and snacks that they plan to make, check their inventory, and set themselves up for success. This could include buying healthy snacks, chopping fruits and vegetables for easy access in the fridge, and putting comfort foods in less convenient locations. “Then throughout your busy week, you don’t need to be as mindful about considering what to eat or cook, since you’ve already thought about your food choices ahead of time,” she said. “This can help eliminate making poor food choices when you’re feeling stressed or tired, especially at the end of a workday.” Naidoo also advised using the “SAW Method” to swap out unhealthy options, add in more vegetables and fiber, and walk to reduce stress and boost mood. For instance, swapping ice cream for fruits can help satisfy a sweet tooth, and adding cruciferous vegetables can provide a crunchy texture while cutting down on the sugars and salt in ultraprocessed foods that compound stress. “It’s about adapting these principles to what you need to do to help yourself,” she said. “When you’re making food choices, it’s important to consider how they will affect not only your physical body but your emotional self as well.” Note: This article originally appeared on Medscape .

Canada’s legalization of cannabis has been linked to an increase in schizophrenia cases, new research shows. Over a 16-year time period — spanning before and after legalization of cannabis for medical and recreational use — the number of new cases of schizophrenia associated with cannabis use disorder (CUD) in Ontario nearly tripled after legalization, investigators found. “There has been a lot of research on the association between cannabis use and schizophrenia and one of the main concerns about cannabis legalization is whether it might result in increases in cases of schizophrenia,” study investigator Daniel Myran, MD, MPH, with Ottawa Hospital Research Institute, Ottawa, Ontario, Canada, told Medscape Medical News. “We found that there have been concerning increases over time in the percentage of people with a new schizophrenia diagnosis who had received care for a cannabis use disorder before their diagnosis,” Myran added in a news release. The study was published online on February 4 in JAMA Network Open . A Growing Public Health Challenge The researchers evaluated the electronic medical records of more than 13.5 million residents of Ontario (mean age, 39 years) without a history of schizophrenia and considered three policy time periods between 2006 and 2022 — before legalization (January 2006 to November 2015), after legalization of medical cannabis (December 2015 to September 2018), and after legalization of nonmedical cannabis (October 2018 to December 2022). In total, 118,650 individuals (0.9%) had an emergency department visit or hospital stay for CUD. During the study period, 10,583 (9.0%) of individuals with CUD developed schizophrenia compared with 80,523 (0.6%) of individuals without CUD. After legalization of cannabis, the number of people in Ontario who required hospital care for CUD jumped by 270%, from about 1.3 in every 1000 people before legalization to 4.6 after legalization, results showed. In addition, the proportion of new cases of schizophrenia associated with CUD increased from 3.7% (95% CI, 2.7%-4.7%) before legalization to 10.3% (95% CI, 8.9%-11.7%) after legalization, with young men aged 19-24 years most likely to be affected. “Our study highlights the growing public health challenge posed by the combination of increasingly high-potency cannabis and rising regular cannabis use,” Myran said in the news release. Myran added that “part of the challenge with cannabis is that with all the discussion around medical cannabis, people may think if this is a medicine it can’t possibly be hurting me. I think the conversation has to be — just because cannabis is now legal and the social norms are changing, doesn’t mean that there is not at risk, particularly in younger people.” “Alcohol and tobacco are legal and that doesn’t not mean that those products are safe or without consequences,” he noted. The investigators pointed out that the study does not settle ongoing debate about whether or not heavy cannabis use can cause schizophrenia . However, Myran said, “what is clear from the scientific literature is that people who are going to develop schizophrenia if they use cannabis and they use it regularly, they will develop it earlier in life and their symptoms will be worse.” A Natural Experiment The author of an invited commentary said this study “adds further support for mounting evidence on the association between cannabis use and increased risk for psychosis, and it shows that this association is most robust among young adults who are developmentally vulnerable to both the neurologic effects of cannabis and developing psychosis.” “As legalization of cannabis becomes more widespread, along with a rapidly expanding commercial cannabis market, a natural experiment of population exposure to commercial cannabis markets is occurring,” wrote Jodi Gilman, PhD, with the Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston. “Epidemiologic studies should include long time intervals to account for processes of legalization and the emergence of mental illness, sufficient numbers to identify subpopulations at risk, such as young adults, and information concerning not only the quantity and frequency but also the potency of cannabis used. “Without these critical factors, this research will be skewed toward nonsignificant findings, potentially obscuring important associations between cannabis policy and mental health outcomes,” Gilman said. The study was supported by the Canadian Institutes of Health Research and by ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-Term Care. Myran and Gilman had no relevant disclosures. Note: This article originally appeared on Medscape .

A few years ago, UCLA Health began asking patients if they used cannabis as part of an electronic previsit questionnaire completed before well visits. The question is still an unusual ask for most primary care clinicians, said Lillian Gelberg, MD, a professor of family medicine at the UCLA David Geffen School of Medicine. “Doctors don’t ask, and patients don’t tell,” she said. If a patient’s answers indicate a risk for cannabis use disorder— a complex diagnosis that involves clinically significant impairment or distress linked to the drug over a 12-month period — Gelberg receives a flag before the visit, enabling her to provide a brief intervention. “What I say to them is, ‘I thank you for completing your questionnaire, and I’m concerned about your scores on your cannabis screen,’” Gelberg said. The rate of people older than 12 years in the United States reporting daily or near-daily use of cannabis rose 15-fold between 1992 and 2022 , with an increase in absolute numbers of daily or near-daily users from about 1 million to 17.7 million over that period. And while some clinicians may not think their patients are part of that increase, screening may help identify those who are. A study of nearly 1700 patients found that 38.8% responding to a confidential survey in 2021 reported using cannabis in the previous year, but only 4.8% had that information in their electronic health record. Meanwhile, average levels of tetrahydrocannabinol (THC) in cannabis samples in the United States rose from 3.96% in 1995 to 16.14% in 2022. The drastic increases in potency, combined with inconsistent regulations between states, such as caps on potency or tracking systems verifying product quality, should be of concern, according to Fred Rottnek, MD, a professor and director of community medicine, as well as the program director of the addiction medicine fellowship , at the Saint Louis University School of Medicine in St. Louis. Experts say primary care clinicians need to ask about cannabis use to better counsel their patients about the health risks of the substance. A recent study published in JAMA Network Open reported a nearly threefold risk for death in patients within 5 years following an emergency department visit or a hospitalization due to cannabis use disorder. The causes of death linked to cannabis use included suicide, trauma, poisonings linked to opioids and other drugs, and lung cancer. And complications of cannabis can happen to anyone: Emergency department visits in adults older than 65 years were 19 times higher in 2019 than in 2005 in California. Why Ask? Researchers at UCLA Health identified actionable items — such as the identification of cannabis use disorder, need to discuss interactions with common prescription medications, and safety issues associated with the presence of edibles in the home— after they began screening sent out through their electronic health record in 2021. Overall, 17% of patients reported using cannabis, and 34.7% of those patients had results indicating a moderate to high risk for cannabis use disorder. Marjan Javanbakht, PhD, an adjunct professor in the Department of Epidemiology at the UCLA Fielding School of Public Health and co-lead author of the study, said her team uncovered much more cannabis use than they expected. She was also surprised at the 80% of patients who classified themselves as recreational users who were taking cannabis to manage a symptom. The most common uses were for sleep (56%), mental health symptoms (55.5%), stress (50.2%), worry or anxiety (36.3%), and nonspecific pain (31.7%). “Patients may be using marijuana instead of the medications that we’re prescribing for them,” Gelberg said. “And we need to have a dialogue about that.” Talking with adults older than 65 years is also crucial because this population prefers consuming cannabis through edibles, Rottnek said. “Edibles don’t kick in as quickly because like most drugs taken orally, it takes a while for them to absorb,” Rottnek said. Intoxication increases fall risks in older adults. In addition, clinicians may want to counsel patients on safe storage of their cannabis products if grandchildren or other children are in the home. Unintentional intoxication from edibles is well-documented in children: Between 2017 and 2021, 22% of such episodes in children reported to US poison control centers resulted in hospitalization. Clinicians may also want to talk to patients about interactions between cannabis and other medications, such as commonly prescribed analgesic, psychotropic, and cardiovascular agents. Both THC and cannabidiol (CBD) can alter levels of certain opioids, statins, antidepressants, and anticoagulants. THC also can increase the effects of central nervous system depressants, such as alcohol and benzodiazepines, increasing the risk for memory loss and confusion in older adults. For his younger patients, Rottnek said he worries about those with a family history of schizophrenia. “A lot of young people, teenagers and young adults, are showing up in ERs [emergency rooms] for psychotic breaks that can go for 5-7 days, depending on the potency of what they’re using,” he said. He also noted the risks associated with cannabis use during pregnancy, such as low birthweight in infants and psychopathology later in childhood. How to Ask When Rottnek teaches medical students, residents, and fellows about clinical interviewing, he advises starting with legal substances: Alcohol, tobacco, and cannabis. He advised against using the phrase, “You don’t smoke or drink, do you?” Instead, clinicians should adopt a more open-ended approach, such as, “Tell me about your cannabis use.” If a patient says they do use various substances, he asks about the route of ingestion, frequency of use, and why they use the substance to inform his discussion of how to reduce potential harms. The researchers from UCLA used a more systematic approach, using the World Health Organization’s screening test adapted for tobacco and cannabis. Javanbakht said patients are more truthful on self-administered, computerized questionnaires, which also save time for the clinician. Take Home Messages for Your Patients Many clinicians might associate harm reduction with syringe access or safe injection practices, but Rottnek said harm reduction is about making good day-to-day decisions. “If somebody’s engaging in an inherently risky behavior, how do you mitigate bad things from happening?” he said. He bases his harm reduction approach to counseling on a systematic review of measures to lower health risks for anyone using cannabis. Clinicians should advise patients to: Choose low-potency THC or balanced cannabis products with a balanced ratio of THC to CBD because products high in THC are associated with higher risks for acute and chronic mental health and behavioral problems. Limit use to 1 d/wk or weekends only. Daily use has been linked to mental health problems, cardiovascular disease, motor vehicle accidents, suicidal behavior, and neurocognitive effects. Abstain from using synthetic cannabinoids because more severe health effects have been linked to these products. Avoid combusted cannabis inhalation and instead use nonsmoking use methods. Regular inhalation of cannabis can induce chronic bronchitis. Avoid deep inhalation or breath holding to increase absorption, which can damage the lungs. Do not drive or operate heavy machinery for 6 hours after using cannabis. People with a history of schizophrenia, uncontrolled hypertension or coronary artery disease, or chronic obstructive lung disease or other lung pathology should not use cannabis because of a higher risk for related health problems. Note: This article originally appeared on Medscape .

TOPLINE: Increased loneliness during adolescence is associated with various health and well-being outcomes, including an increased risk for asthma and depression, in adulthood. METHODOLOGY: Researchers conducted a longitudinal study to examine the association between increased loneliness over 1 year during adolescence and its subsequent health and well-being outcomes in adulthood. They utilized data from a nationally representative sample involving 20,745 US adolescents (mean age, 15.04 years; 49.7% girls; 65.98% White) initially surveyed in 1994-1995, of whom 11,040 and 9003 were analyzed over average follow-up periods of 11.37 and 20.64 years, respectively. Loneliness in adolescents was assessed at prebaseline (1994-1995) and baseline (1996) through the self-reported frequency of feeling lonely during the past 7 days, with response options ranging from "never" to "most of the time." The associations between changes in loneliness and 41 health and well-being outcomes, including dimensions of physical health, health behavior, mental health, psychological well-being, social factors, and civic and prosocial behaviors, were evaluated. TAKEAWAY: Increased loneliness during adolescence was associated with an increased likelihood of asthma (relative risk [RR], 1.24; P = .041) and depression (RR, 1.25; P = .010) diagnosis in adulthood. Increased loneliness was also associated with an increased likelihood of posttraumatic stress disorder diagnosis (odds ratio, 1.84; P = .002). Increased loneliness was associated with worse social outcomes, such as reduced quality of romantic relationship and increased perceived discrimination, and worse psychological well-being outcomes, such as decreased happiness, job satisfaction, and optimism. No significant associations were found between increased loneliness and health behaviors or civic and prosocial behaviors. IN PRACTICE: "Our study likely captures early risk indicators for adverse health outcomes, highlighting pathways through which loneliness may gradually influence health outcomes over time," the authors wrote. "Our findings suggest that ongoing development and application of interventions and policies aimed at reducing loneliness is a promising method of reducing the risk of some adverse health/well-being outcomes for our adolescent and emerging adult populations," they added. SOURCE: This study was led by Eric S. Kim, PhD, of the University of British Columbia in Vancouver, British Columbia, Canada, and Renae Wilkinson, PhD, of the Institute for Quantitative Social Science at Harvard University in Cambridge, Massachusetts. It was published online on January 20, 2025, in the Journal of Adolescent Health. LIMITATIONS: This study acknowledged potential confounding by unmeasured variables and reverse causality, though these were considered unlikely. A single-item measure for assessing loneliness limited the ability to differentiate between the types of loneliness. The use of data for some outcomes in two separate waves for analysis potentially introduces a 10-year gap in the measure of some outcomes. DISCLOSURES: This study was supported by grants from the Michael Smith Health Research BC, the Canadian Institutes of Health Research, and the John Templeton Foundation. One author reported receiving licensing fees from Flerish, Inc. and Flourishing Metrics. Note: This article originally appeared on Medscape .

Adding measures of anxiety and depression to the American Heart Association’s Predicting Risk of Cardiovascular Disease Events (PREVENT) model may have little additional effect on predicting the risk for new cases of cardiovascular disease (CVD) at the population level, according to new research. Yet numerous studies have noted the associations between these mental health conditions and an increased risk for CVD, the authors wrote, so other tools, broader mental health conditions, or diagnostic interview data could be useful in future studies. “The additive values of these mental health measures were lower than we expected. New CVD risk factors don’t always improve the existing CVD risk scores meaningfully, as shown by a previous study, which investigated the additive values of apolipoproteins,” said lead author Shinya Nakada, a PhD student at the University of Glasgow, Glasgow, Scotland, who researches mental health and CVD. “However, new predictors with limited additive values may still offer practical advantages when it is reproducible, noninvasive, and less costly,” Nakada said. “The measures used in this study were drawn from real-world settings, such as electronic health records and short self-reports, since they are of lower cost and can be implemented relatively easily.” The study was published online on January 13 in the Canadian Medical Association Journal . Little Additional Effect In 2024, PREVENT model was developed to predict the risk for an initial CVD event among the general adult population aged 30-79 years in the United States. The model incorporates risk predictors relevant to cardiovascular, kidney, and metabolic diseases, including factors related to obesity, diabetes, and antihypertensive and statin medications. Because anxiety and depression are the most common mental health conditions worldwide, increasing in prevalence, and independently associated with CVD, Nakada and colleagues analyzed whether incorporating certain mental health measures into PREVENT model could detect high-risk groups that were previously overlooked. The research team developed and internally validated prediction models of 10-year risk for incident CVD (comprising coronary artery disease, stroke, and heart failure) using cohort data from the UK Biobank. They included mental health predictors such as baseline depressive symptom score, self-reported anxiety and depression, and a record-based history of anxiety and depression diagnoses . After randomly assigning more than 500,000 UK Biobank participants to a derivation set (60%) and a validation set (40%), the research team determined incremental predictive values based on C-indices, sensitivity, specificity, and net reclassification improvement indices, using a threshold of 10-year risk for incident CVD > 5%. The derivation set of 195,000 participants had 15,787 CVD events, whereas the validation set of 130,000 participants had 10,639 CVD events. In both groups, participants with a CVD event were more likely to be older, men, and current smokers. They also were more likely to have higher systolic blood pressure, diabetes, and mental health conditions . In the single-predictor models, all mental health predictors were associated with CVD. In the validation set, including all the mental health measures — except self-reported anxiety — resulted in a modest increase in the C-index and specificity, though sensitivity was unchanged. Among the mental health predictors, the depressive symptom score had the largest, though still modest, improvements in C-index (difference of 0.005) and specificity (difference of 0.89%). As a result, the model including depressive symptom score had the largest overall (1.14) and nonevent (0.89) net reclassification indices. Based on the findings, the models including depressive symptom score were more likely to distinguish those at higher risk for CVD from those at lower risk, the authors wrote. For every 1000 people at lower risk, about nine would no longer be incorrectly classified as high risk, which suggests relatively limited effects on risk classification. “In our study, although the measures of anxiety and depression were associated with CVD, including them in PREVENT had little additional effect on the risk classification of CVD at the population level,” Nakada said. “So it may not be worthwhile, especially when it is costly.” Extremely Debilitating Conditions However, new CVD risk predictors — such as anxiety and depression — could help identify targeted therapeutic pathways or actionable responses in primary care settings, the study authors wrote. For instance, the depressive symptom score may help identify previously undiagnosed depression and could be considered during CVD risk prevention visits, despite its limited contribution in the PREVENT model itself. “Anxiety and depression are extremely debilitating conditions, and in some cases can substantially interfere with treatment for CVD,” said Scott Lear, PhD, professor of health sciences and the Pfizer/Heart and Stroke Foundation chair in cardiovascular prevention research at Simon Fraser University in Burnaby, British Columbia, Canada. “In addition, some CVD risk factors likely to be affected by depression and anxiety, such as smoking and blood pressure, are already included in the PREVENT model, so this may water down the value of assessing anxiety and depression,” he said. Lear, who wasn’t involved with this study, has researched various CVD risk predictors, including by ethnicity. In this study using UK Biobank data, participants were more likely to be White, affluent, and healthy than the general UK population — and the results may not be generalizable to other populations worldwide. Future studies could look at other populations and broader mental health measures, such as anxious feelings and insomnia, and associations with CVD risk prediction, the authors wrote. “I wouldn’t want people to think that anxiety and depression don’t matter when considering CVD risk and treatment,” Lear said. “I’m sure many primary care physicians realize that.” No independent funding for the study was reported. Nakada and Lear reported no relevant financial relationships. Note: This article originally appeared on Medscape .

Key Takeaways Antipsychotics are frequently prescribed off-label for children, despite limited long-term efficacy data and potential adverse effects, including metabolic and neurological issues. Comprehensive assessment and nonpharmacological approaches should precede antipsychotic use, with careful monitoring and consideration of tapering when possible. Short-term antipsychotic use can stabilize symptoms, but long-term use requires regular evaluation of benefits versus risks, with a focus on minimizing dosage. Medication substitution with less toxic alternatives should be considered, especially when adverse effects are present or when tapering is unsuccessful. “Bridget,” a 15-year-old girl, is referred by her foster care case manager for continued aggression. She has diagnoses of attention-deficit/hyperactivity disorder (ADHD), conduct disorder, and posttraumatic stress disorder (PTSD) related to sexual abuse she experienced in a stepfamily setting from 9 to 12 years of age. Her mother is receiving inpatient behavioral health care in an extended stay program. Bridget’s father is not available, and her 2 younger siblings are in different foster care settings. Bridget is currently prescribed risperidone 3 mg daily, methylphenidate extended-release 54 mg daily, and clonidine immediate-release 0.2 mg nightly. Approximately 1% of children aged 7 to 12 years and 1.5% of individuals aged 13 to 18 years are prescribed antipsychotic medications, according to findings from a study. These medications are sometimes US Food and Drug Administration (FDA) approved for conditions such as schizophrenia, bipolar disorder, and irritability associated with autism.2 However, approximately 65% of antipsychotic medications for children and adolescents are prescribed for off-label uses, including managing aggression, agitation, disruptive behaviors, and irritability as well as adjunct treatment for ADHD.3 Although there are limited data on the long-term effectiveness of these medications, research has shown that they can lead to a reduction in neuronal tissue and various neurological and metabolic adverse effects.4 Additionally, high doses of antipsychotics have been linked to increased mortality rates in this age group. This article expands on our previous work and discusses the appropriate duration for antipsychotic use and strategies for safely tapering or discontinuing them. First Things First: Is There a Need? Although frank psychosis and bipolar mania remain clear indications for use or consideration of dopamine receptor 2 (D2)–blocking antipsychotic medications, in these circumstances and in all other cases, a comprehensive assessment is warranted to clarify the diagnoses and options for addressing the symptoms. For example, the differential diagnosis for an agitated teenager with seemingly mixed mania may include malignant catatonia, for which antipsychotic medication is generally contraindicated, as it is likely to exacerbate the condition. This is particularly more common in patients with autism. Another more common concern is aggression associated with ADHD; Blader found that well-crafted trials of stimulant medications (eg, first trying methylphenidate and then trying dextroamphetamine) were effective for managing aggression in approximately 60% to 80% of young patients. Given the potential severity of metabolic and neurologic adverse effects of antipsychotic medications, we wrote treatment algorithms to begin with nonpharmacological approaches and treatment of co-occurring conditions before approaching the use of antipsychotics. We also made recommendations for monitoring patients during their use and, once patients are stable, looking at whether, when, and how these medications might be discontinued. How Well Do Antipsychotics Work? Antipsychotics can be beneficial for short-term stabilization, such as preventing psychiatric hospitalization, helping a student remain in a less restrictive school environment, and reducing aggression or self-harming behaviors. However, the evidence does not strongly support their use in treating severe ADHD or oppositional defiant disorder.13 Even in cases where there is FDA approval, such as for managing irritability in autism, it is important to assess whether the patient meets the criteria for antipsychotic treatment (eg, aggression, self-injury, severe mood instability) and whether other approaches might be effective. This could include addressing sensory or communication challenges or considering medications with a safer adverse effect profile. For How Long Should They Be Used? The use of antipsychotic medications in children has primarily been studied and approved by the FDA for short-term treatment, generally up to 6 months.14 There is limited research on the long-term benefits and adverse effects of antipsychotic use in children.15 Concerns commonly associated with antipsychotic medications include the following: Metabolic effects (such as weight gain, diabetes, and hyperlipidemia) Somnolence Prolonged corrected QT interval Elevated prolactin levels Extrapyramidal symptoms Neuroleptic malignant syndrome How long should you use these medications? It will not always be possible to reduce D2-blocking antipsychotic medications, because some patients have symptoms related to psychosis or affective conditions that do not respond to other approaches and where the benefits of continuing the medication outweigh the risks, perhaps keeping the patient safe and/or functioning. We recommend that you use them with an intent to reduce and discontinue their use whenever and however possible, such as when an episode of mania has passed, when you can build a more robust therapy or community plan to support the patient, or when you can substitute less toxic medications, such as antiepileptic drugs for mood stability or stimulant medications for aggression in ADHD, as noted previously. Given these considerations, how do we minimize the use of D2-blocking antipsychotic medications? Start With Discontinuation in Mind When initiating antipsychotic medication, it is crucial to consider the end goal from the start. As part of the informed consent process, discuss the intended duration of treatment with patients and their families. Important topics to cover include the following: The severity of symptoms The natural progression of the condition The child’s age The response to other psychosocial treatments Since there is no set duration for antipsychotic use in nonpsychotic conditions, it is important to monitor the frequency and severity of specific symptoms. Collaborate with patients and families to determine the desired level and duration of improvement that would justify tapering or discontinuing the medication. As a possible guideline, when we use selective serotonin reuptake inhibitors (SSRIs) for depression, we like to see at least 6 to 12 months of remission before we consider tapering and to look at any seasonal or stress-related aspects such as fall/winter effects, school-related stress, or even loss of school structure. Still, the treatment period should be as brief as possible for most clinical situations in children and adolescents. When to Reduce Antipsychotics? At each appointment, discuss the ongoing treatment plan with the patient and their family, focusing on the following: How much improvement has occurred since the initial symptoms? Are there concerning adverse effects (eg, weight gain, elevated cholesterol level, drowsiness, involuntary movements)? How well is the patient adhering to the medication regimen and required monitoring? Are the patient and family open to the idea of tapering the medication? Tapering may not be feasible for patients with primary psychotic disorders or severe mood instability or those with previous failed tapering attempts. If there are ongoing symptoms, take another look at the differential diagnosis and possible treatment options. You do not want to continue ineffective treatment with potentially severe adverse effects. In any case, if you are continuing the medication, you should document the reasons for doing so and consistently monitor for metabolic and movement-related adverse effects. Refer to the American Academy of Child and Adolescent Psychiatry’s Practice Parameter for the Use of Atypical Antipsychotic Medication in Children and Adolescents for monitoring guidelines.17 When you take over care for patients already taking antipsychotic medications, reassess the decision to continue them during your evaluation. For patients on long-term antipsychotic treatment, revisit this discussion every 6 months to evaluate whether continuing the medication remains the best option, considering its effectiveness and potential adverse effects. Begin these conversations by asking patients and families what they perceive as the benefits and drawbacks of the medication. How Slow Should You Go? Tapering does not necessarily mean discontinuing the medication entirely. Even minor dose reductions can help alleviate adverse effects such as elevated cholesterol level or weight gain and lower the risk of neurological adverse effects, such as tardive dyskinesia.18 Once you and your patient agree to taper, consider the following strategies: This is ideal for straightforward cases without co-occurring conditions or a complicated medication history. Ensure at least 3 to 6 months of stability and choose a time without new stressors. Arrange for additional support (eg, therapeutic interventions, school-based services). Reduce the dose by no more than approximately 25% of the original dose every 3 to 6 months or 5% to 10% every 2 months.19 Although there are no clear data to guide the rate of the dosage reduction in children and teenagers, adult research supports very gradual reduction over many months to 2 or 3 years to reduce relapse rates of psychosis in patients who have been on long-term antipsychotic treatment. Consider gradual weekly reductions toward the new dose (eg, recommending the patient take the current dose daily and then substituting the new lower target dose for 1 of 7 days the first week, 2 of 7 days the second week, etc, until every day is at the new lower dose). Schedule regular follow-ups to monitor for any worsening of target symptoms. Bridget is now receiving therapy for her PTSD, and you have stabilized her aggression by shifting her from methylphenidate to dextroamphetamine. However, she is gradually gaining weight, and you decide to reduce her risperidone to 2.5 mg daily using a gradual weekly reduction over 6 weeks. Is Switching Medication an Option? In many situations, you can effectively substitute the antipsychotic or reduce it substantially by using other less potentially toxic medications, such as in the following suggestions: For ADHD with aggression, consider using different kinds of stimulants or even nonstimulant ADHD medications. If there is cooccurring anxiety or irritability, consider trying SSRIs. For behavioral dysregulation or aggression associated with underlying anxiety or autism, explore options such as α agonists or β-blockers. After 6 months, you have reduced Bridget’s risperidone to 0.5 mg daily. Her aggression is well managed, she is making friends, and she is doing better academically, although her appetite and weight have not stabilized. You attempt to discontinue the risperidone altogether, but Bridget becomes far more agitated. Intraclass Medication Substitution When a patient needs to stay on an antipsychotic due to severe symptoms (such as psychosis, self-injury, or mania), consider switching to a more weight-neutral option such as ziprasidone or lurasidone (keeping in mind that insurance coverage might make these medications challenging to start). This approach is also worth considering if a previous antipsychotic trial was unsuccessful or if the patient presents with psychotic symptoms or mania. Offer this alternative if a patient experiences adverse effects that lead to discontinuation of a medication such as risperidone or aripiprazole. Bridget has stability on ziprasidone 20 mg along with the dextroamphetamine and clonidine. Screening and follow-up ECG results are normal, and her weight gain has stabilized. Bridget’s mother is in a step-down psychiatric placement facility, and the family is beginning therapy aimed at possible reunification. Concluding Thoughts Antipsychotics can be lifesaving, but they should only be used when necessary and when accompanied by continuous discussions about the length of treatment and strategies to minimize dosage and adverse effects. Note: This article originally appeared on Psychiatric Times .

A widely accepted assumption in the addiction field is that neuroanatomical changes observed in young people who use alcohol or other substances are largely the consequence of exposure to these substances. But a new study suggests neuroanatomical features in children, including greater whole brain and cortical volumes, are evident before exposure to any substances. Investigators, led by Alex P. Miller, PhD, assistant professor, Department of Psychiatry, Indiana University, Indianapolis, noted that the findings add to a growing body of work that suggests individual brain structure, along with environmental exposure and genetic risk, may influence risk for substance use disorder. The findings were published online on December 30, 2024, in JAMA Network Open . Neuroanatomy a Predisposing Risk Factor? Earlier research showed that substance use is associated with lower gray matter volume, thinner cortex, and less white matter integrity. While it has been widely thought that these changes were induced by the use of alcohol or illicit drugs, recent longitudinal and genetic studies suggest that the neuroanatomical changes may also be predisposing risk factors for substance use. To better understand the issue, investigators analyzed data on 9804 children (mean baseline age, 9.9 years; 53% men; 76% White) at 22 US sites enrolled in the Adolescent Brain Cognitive Development (ABCD) Study that’s examining brain and behavioral development from middle childhood to young adulthood. Researchers collected information on the use of alcohol, nicotine, cannabis, and other illicit substances from in-person interviews at baseline and years 1, 2, and 3, as well as interim phone interviews at 6, 18, and 30 months. MRI scans provided extensive brain structural data, including global and regional cortical volume, thickness, surface area, sulcal depth, and subcortical volume. Of the total, 3460 participants (35%) initiated substance use before age 15, with 90% reporting alcohol use initiation. There was considerable overlap between initiation of alcohol, nicotine, and cannabis. Researchers tested whether baseline neuroanatomical variability was associated with any substance use initiation before or up to 3 years following initial neuroimaging scans. Study covariates included baseline age, sex, pubertal status, familial relationship (eg, sibling or twin), and prenatal substance exposures. Researchers didn’t control for sociodemographic characteristics as these could influence associations. Significant Brain Differences Compared with no substance use initiation, any substance use initiation was associated with larger global neuroanatomical indices, including whole brain (β = 0.05; P = 2.80 × 10−8), total intracranial (β = 0.04; P = 3.49 × 10−6), cortical (β = 0.05; P = 4.31 × 10−8), and subcortical volumes (β = 0.05; P = 4.39 × 10−8), as well as greater total cortical surface area (β = 0.04; P = 6.05 × 10−7). The direction of associations between cortical thickness and substance use initiation was regionally specific; any substance use initiation was characterized by thinner cortex in all frontal regions (eg, rostral middle frontal gyrus, β = −0.03; P = 6.99 × 10−6), but thicker cortex in all other lobes. It was also associated with larger regional brain volumes, deeper regional sulci, and differences in regional cortical surface area. The authors noted total cortical thickness peaks at age 1.7 years and steadily declines throughout life. By contrast, subcortical volumes peak at 14.4 years of age and generally remain stable before steep later life declines. Secondary analyses compared initiation of the three most commonly used substances in early adolescence (alcohol, nicotine, and cannabis) with no substance use. Findings for alcohol largely mirrored those for any substance use. However, the study uncovered additional significant associations, including greater left lateral occipital volume and bilateral para-hippocampal gyri cortical thickness and less bilateral superior frontal gyri cortical thickness. Nicotine use was associated with lower right superior frontal gyrus volume and deeper left lateral orbitofrontal cortex sulci. And cannabis use was associated with thinner left precentral gyrus and lower right inferior parietal gyrus and right caudate volumes. The authors noted results for nicotine and cannabis may not have had adequate statistical power, and small effects suggest these findings aren’t clinically informative for individuals. However, they wrote, “They do inform and challenge current theoretical models of addiction.” Associations Precede Substance Use A post hoc analysis further challenges current models of addiction. When researchers looked only at the 1203 youth who initiated substance use after the baseline neuroimaging session, they found most associations preceded substance use. “That regional associations may precede substance use initiation, including less cortical thickness in the right rostral middle frontal gyrus, challenges predominant interpretations that these associations arise largely due to neurotoxic consequences of exposure and increases the plausibility that these features may, at least partially, reflect markers of predispositional risk,” wrote the authors. A study limitation was that unmeasured confounders and undetected systemic differences in missing data may have influenced associations. Sociodemographic, environmental, and genetic variables that were not included as covariates are likely associated with both neuroanatomical variability and substance use initiation and may moderate associations between them, said the authors. The ABCD Study provides “a robust and large database of longitudinal data” that goes beyond previous neuroimaging research “to understand the bidirectional relationship between brain structure and substance use,” Miller said in a press release. “The hope is that these types of studies, in conjunction with other data on environmental exposures and genetic risk, could help change how we think about the development of substance use disorders and inform more accurate models of addiction moving forward,” Miller said. Reevaluating Causal Assumptions In an accompanying editorial, Felix Pichardo, MA, and Sylia Wilson, PhD, from the Institute of Child Development, University of Minnesota Twin Cities, Minneapolis, suggested that it may be time to “reevaluate the causal assumptions that underlie brain disease models of addiction” and the mechanisms by which it develops, persists, and becomes harmful. Neurotoxic effects of substances are central to current brain disease models of addiction, wrote Pichardo and Wilson. “Substance exposure is thought to affect cortical and subcortical regions that support interrelated systems, resulting in desensitization of reward-related processing, increased stress that prompts cravings, negative emotions when cravings are unsated, and weakening of cognitive control abilities that leads to repeated returns to use.” The editorial writers praised the ABCD Study for its large sample size for providing a level of precision, statistical accuracy, and ability to identify both larger and smaller effects, which are critical for addiction research. Unlike most addiction research that relies on cross-sectional designs, the current study used longitudinal assessments, which is another of its strengths, they noted. “Longitudinal study designs like in the ABCD Study are fundamental for establishing temporal ordering across constructs, which is important because establishing temporal precedence is a key step in determining causal links and underlying mechanisms.” The inclusion of several genetically informative components, such as the family study design, nested twin subsamples, and DNA collection, “allows researchers to extend beyond temporal precedence toward increased causal inference and identification of mechanisms,” they added. Note: This article originally appeared on Medscape .

TOPLINE: About one third of US adults aged 50-80 years report feeling lonely and socially isolated, a new study of data from 2018-2024 shows. While the levels have returned to the pre-pandemic range, investigators say the findings suggest clinicians should screen for loneliness and isolation. METHODOLOGY: Researchers conducted a nationally representative survey of US adults aged 50-80 years through the University of Michigan National Poll on Healthy Aging at six timepoints between 2018 and 2024. Data collection involved online surveys conducted using the Ipsos KnowledgePanel from 2018 to 2021, transitioning to online and phone surveys conducted using the National Opinion Research Center AmeriSpeak panel from 2022 to 2024. Sample sizes ranged between 2051 and 2576 respondents, with completion rates ranging from 61% to 78% across the survey periods. TAKEAWAY: Loneliness rates among adults aged 50-80 years showed notable fluctuation, starting at 34% (95% CI, 31.7%-36.2%) in 2018, rising to 41% (95% CI, 39.1%-43.7%) in 2020, and returning to 33% (95% CI, 31.7%-35.1%) by 2024. Social isolation showed a similar pattern in the study group, starting at 27% (95% CI, 24.5%-28.8%) in 2018, peaking at 56% (95% CI, 53.4%-58.1%) in 2020, and declining to 29% (95% CI, 27.5%-30.9%) by 2024. Higher loneliness and social isolation rates were frequently reported among individuals who did not work, lived alone, had lower household incomes, and had self-reported fair and poor physical and mental health than those who reported excellent, very good, or good health. IN PRACTICE: The findings suggest that “much like routinely asking about diet and exercise, clinicians should consider screening older adults for loneliness and social isolation and connect them with appropriate resources,” the investigators wrote. SOURCE: The study was led by Preeti N. Malani, MD, MSJ, University of Michigan Medical School, Ann Arbor, Michigan. It was published online on December 9 in JAMA. LIMITATIONS: The study was limited by possible recall bias, reliance on self-reported data, lack of longitudinal results, and differences in survey timing, panels, and question framing across years. The findings may not have been applicable to excluded groups such as nursing home residents or individuals aged > 80 years, which limited their generalizability. DISCLOSURES: The study was supported by AARP and Michigan Medicine and the Department of Veterans Affairs, Veterans Health Administration, and Health Systems Research. One author reported receiving consulting fees and honoraria from various organizations. Details are provided in the original article. Note: This article originally appeared on Medscape .

Key Takeaways Neuroplasticity is central to psychiatry, with brain health factors like nutrition and exercise being crucial for its optimization. BDNF is a key intermediary in neuroplasticity, with decreased levels associated with psychiatric disorders. Treatments like psychotherapy, ECT, and certain medications enhance BDNF, promoting neuroplasticity. Medication-assisted psychotherapies using psychoplastogens show promise but face regulatory challenges. A new treatment paradigm is needed in psychiatry to support enduring neuroplastic changes for optimal patient outcomes. As Psychiatric Times celebrates its 40th year, psychiatry’s tapestry is just beginning. The threads that currently exist seem to be weaving into a magnificent fabric that we have named neuroplasticity. Our challenge and opportunity is to optimize all of the threads we currently understand and remain open to the many additional threads that are currently unknown or just beginning to appear. Some of the most important threads that facilitate brain health, which provides a necessary foundation for neuroplasticity to occur, get lost in the Western medical model treatment process, where time is limited and interventions commonly focus on medications and procedures. We know now that the same factors that maximize cardiac health also maximize brain health: healthy blood pressure/cholesterol levels/blood glucose/body mass index, minimal substance use, quality sleep, good nutrition, physical activity, ability to manage stress, and supportive relationships. In addition to these, the brain thrives when it is learning new information, encountering novel experiences, and solving problems. Although certainly not a panacea, neuroplasticity provides hope that we have an inborn ally during our journey toward healing and maximum functioning. The Birth of Neuroplasticity In the 1970s, experimental research that involved severing the afferent neuron of a monkey’s limb just before where it enters the spinal cord to ascend to the brain led to the revolutionary field of neuroplasticity. This research extended into the early 1990s when it demonstrated that the monkey’s brain undergoes cortical remapping and connects to any adjacent active neurons when it ceases receiving input from the deafferented limb. Thus, the neuroplasticity property of the human brain was born. Learning Music as a Model During that early excitement, researchers looked for potential models that could quantify brain changes over time in an activity that required rigorous ongoing training. Researchers hypothesized that musicians provided an ideal model to study brain plasticity by using neuroimaging to monitor brain structure and function before and after a period of intensive training. Another research team reported on structural brain changes in early childhood following 15 months of musical training. Structural changes correlated with improvements in relevant motor and auditory musical skills.3 Similarly, a review of studies looking at changes in brain structure and function in musicians after their musical practice, magnetic resonance imaging demonstrated structural plasticity while neurophysiological activation patterns demonstrated functional plasticity. The authors concluded “experience can shape brain anatomy and brain physiology. BDNF: A Proxy for Neuroplasticity An established intermediary in the process of neuroplasticity is brain-derived neurotrophic factor (BDNF), which is present throughout the peripheral and central nervous systems, especially in the hippocampus and prefrontal cortex. BDNF has been shown to facilitate the maturation, differentiation, and longevity of neurons. One well-established pathway involves a presynaptic glutamate surge. Postsynaptically, this agonizes AMPA-glutamate receptors, which induces production of BDNF. BDNF agonizes tropomyosin-related kinase B receptors, which promote a cascade of molecular events, culminating in increased activity of the mammalian target of rapamycin (mTOR). mTOR serves as the orchestrator of the synthesis of scaffolding proteins and dendritic growth/synaptogenesis. Many psychiatric disorders are associated with decreased levels of BDNF compared with those found in healthy individuals. A growing literature has looked at serum and/or plasma BDNF levels as a proxy for neuroplasticity in patients pre- and post treatment. The strongest data supporting BDNF as a proxy for neuroplasticity comes from research in psychopharmacology, with a growing body of evidence supporting BDNF’s role in psychotherapy. Psychotherapy and Other Treatments Jeffrey Schwartz, MD, a pioneer in demonstrating the ability of cognitive behavior therapy to change brain chemistry without medications in patients with obsessive-compulsive disorder,6 demonstrated a significant bilateral decrease in caudate nucleus metabolic rates of glucose through positron emission tomography after 10 weeks of intensive exposure-response prevention and cognitive behavior therapy treatment, resulting in symptomatic improvement. Subsequent research has supported the hypothesis that psychotherapy can facilitate a rewiring of the brain through the production of increased BDNF. Other investigators have even hypothesized that good quality psychotherapy may facilitate interbrain plasticity between the therapist and patient during their sessions as a result of recurrent exposure to high interbrain synchrony that can lead to enduring neuroplastic changes in the patient that are then activated in relationships outside of therapy. Beyond psychotherapy, there are other treatments that impact neuroplasticity. Electroconvulsive therapy (ECT), one of psychiatry’s oldest treatments, has demonstrated increased BDNF levels in individuals with medication-resistant depression. For most patients, the significant increase in BDNF appeared 1 month after the completion of the ECT. Psychopharmacology One intriguing property of certain psychiatric medications is their effect of increasing BDNF, sometimes as soon as several hours after administration. We are early in understanding the effect on BDNF by specific antidepressants and antipsychotics, although it is well-documented that BDNF plays an important role in depression, bipolar disorder, and psychosis, especially in the hippocampus and the prefrontal cortex. Lithium is an example of such an agent. It has been shown to upregulate BDNF, and chronic treatment with lithium has demonstrated an associated increase in BDNF when administered in therapeutic as well as low doses in both the hippocampal and cortical regions of the brain. Neuroimaging studies have demonstrated an association between long-term lithium treatment and increased gray matter volume in the ventral prefrontal cortex and other brain regions related to cognition and emotional processing. It has also been proposed that chronic lithium treatment in patients with bipolar disorder may delay or decrease the risk of the onset of dementia. Medication-Assisted Psychotherapy Psychoplastogens are a molecularly diverse class of medications that initiate rapid neuronal plasticity via the rapid production of BDNF.16,17 These medications include 3,4-methylenedioxymethamphetamine (MDMA), ketamine, esketamine, psilocybin, and lysergic acid diethylamide (LSD). The downstream effect is increased activity of mTOR. With medication-assisted psychotherapies (MAPs), the psychoplastogens are administered to patients early in treatment and commonly in a small number of doses—usually between 1 and 3—in the presence of the psychotherapist(s) with whom they will work intensively (for up to as many as 15 sessions). Hypothetically, the psychoplastogen (eg, MDMA) increases patients’ access to difficult psychological material, it facilitates a meaningful experience with a strong emotional response (as with psilocybin/LSD), and/or it creates a window of neuroplasticity that can enhance improved functioning of a dysregulated circuit (as with ketamine/esketamine). With all 3 agents, an extended period of neuroplasticity may allow for significant and enduring changes in neuronal connectivity through the intensive psychotherapeutic process that is an integral part of the treatment. (Disappointingly, MAP received a setback in August 2024 when the FDA decided against approving MDMA-assisted psychotherapy and requested an additional phase 3 study.) Conclusion Thirty years ago, the medical profession and neuroscientists believed that the human brain was fully wired at birth. In retrospect this was naive, as we have the ability to learn new information, languages, musical instruments, and technical skills, and adapt to significant changes throughout our lives. Where but in the brain would the capacity for all of this learning, adaptation, and mastery occur? The catch is that it takes time, motivation, practice, and intention for us to orchestrate this neuroplasticity. In my opinion, the current structure of clinical psychiatric practice lacks these qualities, with a focus on the 15-minute medication check as the common standard time spent with a patient. If our treatment goal is to facilitate enduring neuroplastic changes in our patients’ brains, we must create a new treatment paradigm that supports that process. Then we can truly continue to weave our tapestry. Note: This article originally appeared on Psychiatric Times .

Key Takeaways Cannabis-induced psychosis complicates criminal responsibility, with settled insanity as a potential defense if symptoms persist beyond intoxication. Legal standards for insanity and diminished capacity vary by jurisdiction, affecting the applicability of voluntary intoxication as a defense. Understanding the relationship between substance use and mental health is crucial for forensic evaluations, especially with increasing cannabis prevalence. Case Study “John,” a 25-year-old man with no prior criminal history, was arrested after breaking into a convenience store in the middle of the night and assaulting the clerk with a knife. Witnesses reported erratic and violent behavior, including shouting about being chased by invisible enemies. Upon arrest, John was incoherent, disoriented, responding to internal stimuli, and exhibiting signs of paranoia. He was charged with assault with a deadly weapon. While incarcerated for several months, John continued to exhibit signs of psychosis and was found incompetent to stand trial. His family revealed that John had heavily used high-potency cannabis for several years and had experienced increasing paranoia and auditory hallucinations over the past year. After more than 6 months of involuntary treatment with antipsychotic medication, John was ultimately deemed competent to stand trial. At trial, John’s defense team contended that he was not guilty by reason of insanity, asserting that his prolonged cannabis use had led to a state of settled insanity, which he was experiencing at the time of the crime. However, the prosecution countered by pointing to the fact that John’s psychosis resulted from voluntary intoxication, a condition often excluded from insanity defenses. Criminal Responsibility Findings from studies have shown an increased use of cannabis in the US resulting from its legalization for recreational purposes. However, findings from studies on the effects of recreational cannabis legalization on mental health issues have shown mixed results. Recent cases have highlighted the relationship between cannabis and criminal responsibility, particularly with regard to intoxication and its impact on a defendant’s mental state. Criminal responsibility refers to the extent to which a person can be held legally accountable for committing a crime. In such cases, defendants may raise various mental defenses to argue that their mental state at the time of the offense diminishes or negates their responsibility for the act. The insanity defense is one of the most well-known mental defenses. The exact standard for determining legal insanity has differed across time and jurisdictions, but it typically means that due to a mental illness or defect, an individual cannot recognize an act is wrong, fails to understand the nature or quality of the act, or is unable to control their behavior. Typically, a substance-induced disorder resulting from the voluntary consumption of an intoxicating substance, such as cannabis, does not constitute a mental disease or defect for the purposes of the insanity defense. However, in certain jurisdictions, the defense of settled insanity may offer an alternative route for defendants whose cannabis use leads to prolonged psychotic symptoms. If it can be shown that substance use triggered or worsened psychotic symptoms that continued beyond the acute effects of intoxication, the defendant may be eligible to use the defense of settled insanity. Settled Insanity The standard for settled insanity varies by jurisdiction and is not always clearly defined. Although the specific criteria may differ across regions, the challenge of separating the effects of mental illness from substance use remains consistent. Establishing a clear timeline for the onset of substance use and symptoms of mental illness can be difficult and at times even impossible. Evidence indicating that the defendant showed signs of mental illness close to the time of the offense but prior to substance use or that the symptoms present during the offense persisted beyond the effects of intoxication may support the determination of settled insanity. For instance, the persistence of psychotic symptoms far beyond what would be expected from cannabis intoxication alone, requiring significant clinical intervention, could support an opinion of symptoms that are more settled and not merely a result of acute intoxication. Once it is established that a lasting impairment may be at play, the forensic evaluator must assess whether the symptoms meet the statutory criteria for the insanity defense. Experts assessing defendants for a potential insanity defense in cases involving substance use may consider examining the factors outlined in the Table. Diminished Capacity All crimes, except strict liability offenses (where the prosecution is not required to prove that the defendant had intent or knowledge of committing the crime), require both an action (actus reus) and criminal intent (mens rea). If mens rea is absent, an individual cannot be found guilty of a crime that necessitates intent. Courts distinguish between general intent and specific intent crimes, with voluntary intoxication being relevant to the latter. Specific intent crimes require not only the intent to perform the criminal act but also the intention to achieve a specific result. If cannabis intoxication impaired the defendant’s ability to form this specific intent, it could serve as a partial defense. For example, a defendant charged with a specific intent crime, such as first-degree murder, may argue that due to cannabis-induced psychosis, they were unable to premeditate or intentionally carry out the killing. This in turn could result in a reduction of charges. A general intent crime requires that the defendant intended to commit the criminal act but not necessarily to achieve a particular result. For these crimes, it is enough that the individual acted with a wrongful purpose, even if they did not intend to cause a specific outcome. Voluntary intoxication is never accepted as a defense, not even a partial one, for general intent crimes. Mitigation Voluntary intoxication may be considered during the sentencing phase of a criminal proceeding. Some jurisdictions allow judges to consider the defendant’s intoxicated state when determining the severity of the sentence. In Texas, for example, voluntary intoxication may be cited as a mitigating factor in sentencing. A mitigating factor is a circumstance or piece of evidence that can reduce the severity of a defendant’s sentence or level of criminal responsibility, even if they are found guilty of a crime. Mitigating factors do not excuse the crime but help explain why it may have occurred, suggesting that a lesser punishment is more appropriate. Concluding Thoughts The laws regarding voluntary intoxication and mental health defenses differ significantly among jurisdictions, making it important for forensic psychiatrists to be well-versed in the legal standards of the area where a case is being tried. Whether or not voluntary intoxication can be used to argue diminished capacity or as a mitigating factor at sentencing varies widely. The recognition of settled insanity where long-term substance use results in lasting mental impairment even after intoxication has ended adds another layer of complexity. Understanding the complex relationship between substance use and mental health is critical to providing thorough and well-informed evaluations. Staying up to date on both the evolving science of substance-induced psychiatric conditions and jurisdiction-specific legal standards ensures that forensic assessments remain aligned with contemporary practices and legal standards. As cannabis and other substances become more prevalent in legal contexts, expertise in this area will only grow in importance. Note: This article originally appeared on Psychiatric Times .

The number of US adults who will develop dementia each year is projected to increase from approximately 514,000 in 2020 to about 1 million in 2060, new research shows. In addition, the lifetime risk of developing dementia after age 55 is estimated at 42%. The research showed that the relative growth in dementia cases is particularly pronounced for Black adults. These new findings researchers say, “highlight the urgent need for policies that enhance healthy aging, with a focus on health equity.” “The aging of the population means that the increased burden of cognitive decline and dementia, particularly among the oldest age group, is going to be significant, and we need to be prepared for it,” study investigator Josef Coresh, MD, PhD, director of the Optimal Aging Institute at NYU Grossman School of Medicine, New York City, told Medscape Medical News. He added that dementia may be preventable through such strategies as controlling vascular risk factors, treating sleep disorders, detecting and correcting hearing loss, managing mood disorders, and improving access to social support. The findings were published online on January 13 in Nature Medicine . Diverse Cohort, More Rigorous Methodology Over the past century, the US population has aged substantially, resulting in a rise in late-life diseases. Once an uncommon condition, dementia now affects more than 6 million Americans. The lifetime risk for dementia is a critical public health measure that can be used to raise awareness, enhance patient engagement in prevention, and inform policymaking, the investigators noted. The often-cited Framingham Heart Study estimates that 11%-14% of men and 19%-23% of women will develop dementia during their lifetime. But, as Coresh noted, these estimates were based on a predominantly White, relatively affluent, and well educated cohort, as well as limited means of determining dementia cases. In contrast, this new study is based on a more diverse cohort and used more rigorous methodology, Coresh said. “It’s capturing the latest decade of risk, from age 85 to 95 years,” which is important because people are living longer, he added. The report analyzed data collected from 1987 to 2020 from 15,043 participants in the Atherosclerosis Risk in Communities (ARIC) study. Drawn from four US communities, these individuals were all dementia-free of dementia at age 55. One of the study sites was Jackson, Mississippi, where Black individuals comprise 82% of the population. Black individuals accounted for 26.9% of the total study population, 55.1% of participants were women, and 30.8% carried at least one copy of the apolipoprotein E (APOE) epsilon 4 allele (28.1% with one copy and 2.7% with two copies). Over the past three decades, study participants underwent clinical examinations, including cognitive testing, laboratory testing, and both in-person and telephone interviews. In addition to interviews, the ARIC study uses review of hospital records and death certificates to determine dementia, with cases adjudicated by a committee assisted by a computer algorithm. Over a median follow-up of 23 years, 3252 new cases of dementia were identified. At age 55, researchers estimated the lifetime risk for dementia (up to age 95) to be 42% (95% CI, 41-43). The cumulative incidence of dementia remained relatively low between 55 and 75 years of age (3.9%) but rose significantly beyond that. Over a median follow-up of 23 years, there were 3252 incident cases of dementia. The lifetime risk for dementia was higher in women (48%; 95% CI, 46-50) vs men (35%; 95% CI, 33-36) and in Black individuals (44%; 95% CI, 41-46) vs White individuals (41%; 95% CI, 40-43). Additionally, Black individuals experienced an earlier median age of dementia onset (79 years) compared with White individuals (82 years). “By age 75, the risk is 3% in our White participants and 7% in our Black participants, so the racial difference is expressed early, and it stays to age 85 and then sort of closes and becomes smaller by age 95,” said Coresh. Structural Racism The racial disparity in dementia risk may reflect the impact of structural racism and socioeconomic inequality, including limited access to quality education and nutrition, said Coresh. Additionally, it could be influenced by poorer access to healthcare and a higher prevalence of vascular risk factors, such as hypertension and diabetes, he added. “People who were born in the South a long time ago may not have had the same opportunities as people in other areas and of other races and ethnicities.” The substantially higher risk among women is thought to reflect women’s longer life expectancy. Adults with two copies of the APOE epsilon 4 allele had a higher lifetime risk for dementia (59%; 95% CI, 53-65) compared with those with one copy (48%; 95% CI, 45-50) and those with no copies (39%; 95% CI, 37-40). Dementia also occurred earlier in APOE epsilon 4 carriers (median age, 79 years in those with two copies, 81 years in those with one copy, and 82 years in those with no copies). Applying the lifetime risk estimates to US Census population projections, the researchers predict the annual number of incident dementia cases will increase from about 514,000 in 2020 to 1 million in 2060. The number of individuals who will develop dementia each year is expected to nearly double among White individuals and triple among their Black counterparts. These findings highlight the importance of addressing the growing number of Baby Boomers transitioning into the oldest age group, Coresh noted. As more individuals live into their 80s and beyond, the medical community must focus on managing early symptoms and implementing effective prevention strategies, he added. Such strategies should include managing risk factors, such as social isolation, disordered sleep, mood issues, poor cardiovascular health, and uncorrected hearing loss, he said. As it stands, research suggests only about 20% of US adults meet recommended lifestyle and cardiovascular health targets, and only 30% of older adults with hearing loss are using a hearing aid. Dementia before age 75 may be underestimated in the study because up until this age, dementia was ascertained retrospectively with phone interviews and review of hospital and death records. Other limitations of the study include the lack of external validation of the results, limited generalizability of the projections to the entire US population, and exclusion of racial groups other than White and Black from the analysis. A Crisis in the Making Commenting for Medscape Medical News, Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, said the new findings reinforce what the Alzheimer’s Association has long emphasized: that the risk and prevalence of Alzheimer’s disease and other dementias are expected to rise significantly in the coming years. “There’s an urgent need to address the crisis of Alzheimer’s disease and dementia in this country and globally,” she said. These new data confirm the high risk for dementia among minority groups as well as women who have often been underrepresented in research, said Carrillo. The good news, though, is that this is “an exciting and hopeful time” in the field, with Alzheimer’s treatments being approved that slow the progression of early disease and with more treatments in the pipeline. “There are also better ways available now to detect and diagnose Alzheimer’s, and we’re learning more every day about risk reduction for Alzheimer’s and all other dementias,” Carrillo said. Carrillo added the Alzheimer’s Association is leading the U.S. POINTER Study, a 2-year clinical trial evaluating whether lifestyle interventions targeting risk factors can protect cognitive function in older adults at increased risk for cognitive decline. Results of that study will be reported later this year at the Alzheimer’s Association International Conference. She also pointed to last summer’s Lancet Commission Report showing that 40% of global dementia is potentially avoidable with behavioral and lifestyle changes. “The main message is that there’s hope that we can, in fact, change the trajectory,” that by making such changes, “we won’t hit the numbers that this new paper talks about until 2060.” However, she noted there’s still more work to be done. For example, she said, there’s an urgent need for more research into how to detect dementia as early as possible. Carillo emphasized the importance of checking patients’ blood pressure and cholesterol, and conducting other tests to determine risk and discuss lifestyle changes that could result in dementia risk reduction. Note: This article originally appeared on Medscape .

Older adults with major depressive disorder (MDD) exhibit riskier driving behaviors than their nondepressed peers, including hard braking, cornering, and unpredictable driving patterns, new research showed. Data for the study came from commercial vehicle data trackers installed in participants’ vehicles. After about a year of follow-up, investigators found that MDD was associated with an increase in the amount and severity of risking driving, even after controlling for antidepressant use. Late-life depression often goes undiagnosed, and the new findings highlight the importance of routine depression screening and targeted interventions to ensure driving safety among older adults, the study team said. “By using longitudinal, real-world driving data rather than controlled settings or self-reports, the study provides robust evidence of how MDD influences driving behaviors in day-to-day contexts,” first author Ganesh M. Babulal, PhD, OTD, with the Department of Neurology, Washington University School of Medicine in St Louis, told Medscape Medical News. “By analyzing the influence of antidepressant use and overall medication load, the study disentangles the effects of MDD from those of driver-impairing medications, further clarifying the unique contributions of depression to driving behaviors,” Babulal noted. The study was published online on December 30 in JAMA Network Open . Road Risks As the number of older adults grows, safe driving practices in this age group become increasingly crucial. By 2050, one quarter of drivers in the United States will be older than 65 years. MDD affects about 8% of US adults and is linked to cognitive impairments that may compromise driving safety. Prior studies revealed a link between depression and increased car crash risk, regardless of age. And earlier research by Babulal and colleagues showed that older adults with depression were three times more likely to receive a marginal or failing score on a standardized road test. To further study the issue, Babulal and colleagues examined the impact of MDD on naturalistic driving behaviors among older adults using longitudinal data. Participants were recruited from the Driving Real-World In-Vehicle Evaluation System Project, where their daily driving behaviors were recorded using commercial vehicle data loggers installed in their personal vehicles. The cohort included 85 adults with MDD (mean age, 69 years; 71% women) and 310 adults without MDD (mean age, 70 years; 49% women). The majority of participants in both groups were non-Hispanic White individuals. Based on intercepts, adults with MDD had a propensity toward riskier driving habits with a higher frequency of speeding events and spending more time on the road than those without MDD, they found. Additionally, during a mean of 1.1 years of follow-up, compared with older adults without MDD, those with MDD exhibited significantly more hard braking (P < .001) and hard cornering events per trip (P = .04) over time. They also traveled farther from home and visited more unique destinations (P < .001 for both). Over time, older adults also displayed increased entropy in driving patterns (P < .001), indicated less predictable driving routes. “Driving unpredictability, as evidenced by increased random entropy, highlights the unique challenges posed by MDD in maintaining safe driving practices,” the researchers wrote. Adjusting for antidepressant use, which could impair driving, or total medication burden did not change the findings, suggesting MDD independently affects driving. “Most importantly, our findings demonstrate that MDD — a common and treatable illness in older adults — was associated with an increase in both the amount and magnitude of risky driving behaviors over time,” the researchers wrote. The researchers noted that the study did not account for changes in depression severity over time and other psychiatric conditions co-occurring with MDD were not adjusted for. Also, situational factors like weather or traffic conditions were not assessed. Clear Clinical Implications There is a “pressing need” for targeted interventions to manage and mitigate the driving risks associated with late-life depression, the researchers wrote. “The study emphasizes the need for interventions tailored to the mental health and driving behaviors of older adults. These could include cognitive retraining, driver rehabilitation programs, and routine depression screening to enhance road safety and preserve independence,” Babulal told Medscape Medical News. “Encouraging older adults with MDD to self-regulate their driving habits (e.g., avoiding night driving or high-traffic situations) and educating them about potential driving challenges related to their condition can enhance safety,” he added. Commenting on this study for Medscape Medical News , Ipsit Vahia, MD, McLean Hospital, Belmont, Massachusetts, and Harvard Medical School, Boston, said it “adds nuance to our understanding of how depression can impact driving among older adults.” “While the connection between depression and a higher incident of crashes is known, this study demonstrates an association with riskier driving behaviors such as speeding,” Vahia said. “It highlights the importance of clinicians proactively initiating discussion of driving and safety when working with older adults with depressive symptoms.” Note: This article originally appeared on Medscape .