Are there potential problems in the latest study on antipsychotic medication reduction and discontinuation? Psychiatry A study on antipsychotic medication reduction and discontinuation came out yesterday with fanfare. The fanfare was basically because the principal investigator is a self-proclaimed critical psychiatrist with many criticisms of psychiatric medication and the results of her trial contradicted the primary hypothesis of the study and that was: “Our hypothesis was that antipsychotic reduction would improve social functioning with only a small increase in relapse rate.” Relapse rate in this case was defined as rehospitalization and the authors subsequently state that they thought a 10% rate of relapse would be “acceptable.” The irony of this situation (ideology versus real world treatment) was not lost on anyone. Several people seemed to congratulate the authors on publishing results inconsistent with their ideology although the study was so embedded in the UK research infrastructure – I doubt that not publishing it would have been an option. As a clinical trialist myself – the research seems to present several problems and creates several questions that could suggest that it was designed to optimize the likelihood that antipsychotic medication could be reduced and possibly discontinued. Before I get into those scenarios let me briefly summarize the results. The paper is open access and can be downloaded as well as another paper that describes the research protocol. In the study there were two arms an antipsychotic maintenance arm (N=127) and a reduction arm (N= 126). Diagnoses were taken from clinical information and the clinical staff had treatment responsibility for the patients. In those patients who were randomized to dose reduction, a tapering protocol was suggested to the clinical staff and if it went well at some point the option for a more rapid taper or discontinuation was offered. The research staff monitored the protocol. Baseline and outcome measure included a number of checklists to assess side effects, sexual side effects, positive and negative symptoms, quality of life, and social outcomes at the reassessment points. Raters were blinded but the measures are essentially self report. The ultimate result was that the risk of adverse outcomes was worse in the reduction arm with no associated improvement in social functioning. He are some potential issues that I noticed based on my experience in clinical trial design and on research review boards. 1. Recruitment – described in the following: “Participants were recruited from 19 National Health Service Trust mental health organisations across England. Potential participants were identified initially by clinical staff or recruited through advertisements placed in clinical settings and social media; those patients who expressed an interest in participating were sent further information”. Not enough information. What did the advertisements say? Were subjects aware of who was running this trial and what the goal of the research was? Were the patients asked why they were interested in participating in this trial? Were they asked what they think about taking a medication? Did the subjects have any exposure to the considerable press that the critical psychiatry group and the principal investigator generate? Descriptions in the lay press have been demonstrated to have significant effects on perceived side effects – even to the point of creating a nocebo effect (6) – is there any reason to think that a group emphasizing side effects and minimizing any therapeutic effects might have a similar impact? If that is the case – how would it affect this trial? 2. Inclusion/Exclusion criteria – “Exclusion criteria included being considered by a clinician to pose a serious risk of harm to self or others were the individual to reduce their antipsychotic medication, being mandated to take antipsychotic medication under a section of the Mental Health Act, having been admitted to hospital or treated by a crisis service for a mental disorder within the last month, lacking capacity to consent, having insufficient spoken English, pregnancy, breastfeeding, and being involved in another trial of an investigational medical product; eligibility was assessed by researchers and confirmed by the Principal Investigator for the site.” Practically all the exclusion criteria result in a population that may be more likely to discontinue antipsychotic medications with less difficulty. Consistent with this is the antipsychotic doses of both the reduction and maintenance arm of 300 mg chlorpromazine equivalents (on average). According to the Maudsley Prescribing Guidelines (4) 300 mg chlorpromazine is considered the minimally effective dose of medication for relapsing schizophrenia. Whether this was a representative sample of the 4109 patients put forward for research by clinicians a comparison of the demographics and medication doses would have been of interest. Selection bias may also be evident in the Consort diagram (page 4). After subjects consented to be contacted by the research team (N= 958) – a total of 562 declined participation. Was that because they did not want to take the chance of randomization to a medication reduction? 3. Diagnoses – the diagnosis required was schizophrenia or non-affective psychoses with recurrent episodes. The diagnoses were taken from clinical records. Considerable heterogeneity is introduced with the non-specific category of psychoses with an unpredictable course for which the concept of maintenance medication was not intended. 4. The Dose Reduction - The description of the dose reductions in the paper is confusing. It starts out describing individualized reductions every 2 months based on starting doses but at some point states the patient is allowed to discontinue the medication if the dose reduction has been going well or reduce at a rate of the equivalent of 2 mg haloperidol/day. 2 mg/day of haloperidol is not a slow reduction and it is a departure from reduction every 2 months. Some of the authors here have written about antipsychotic withdrawal reactions – how is the more rapid dose reduction or optional abrupt discontinuation justified? 4. Safety Monitoring/Informed Consent: The more clinical trials I read (and I have read thousands) – the more I want to see the consent form that each patient signs. Some of the authors here continuously talk about medication side effects. In fact – the principle investigator (PI) has stated that in her opinion that modern psychiatric medications work in a "drug centered" rather than a disease centered model by producing side effects like sedation, cognitive impairment, dysphoria, and loss of libido (5). In that model, symptoms of mental illness are muted by side effects rather than effectively treated. The model essentially denies the possibility of effective treatment without medication side effects. Of course, there are medication side effects but consent forms also must contain a discussion of the risks of the intervention. How are they listed when the investigators do not believe they can be directly addressed? Were the subjects told about the risk from medication discontinuation of recurrent psychosis, suicidal thinking, and death? That seems especially relevant in a study where the intervention arm had twice as many deaths as the maintenance arm . Along those same lines – the protocol paper for the study (2) states that a Data Safety and Monitoring Board (DSMB) assessed the ongoing safety of the protocol and made recommendation to a Programme Steering Committee providing independent oversight – even to the point of stopping the protocol if there was a substantial increase in adverse events related to the intervention. Was there a threshold? In this case why was that threshold not met? In the trials I have been involved with the PI and the physician responsible for monitoring safety (typically me) had to clearly delineate a safety plan if any of the research subjects developed medical or psychiatric complications from the intervention. In this case that responsibility seems to have been delegated to the clinicians originally treating the patient. In the reported causes of death of the trial participants – how is the death of a research subject in the reduction arm attributed to antipsychotic medication when they have been on a low dose, were being followed clinically in an outpatient clinic, and their dose was presumably being reduced? One patient in each arm died of an “accidental overdose”. What medication was implicated in the accidental overdoses? This protocol is also a case of shifting risk for the research to the clinicians. Here the research staff designs an intervention that likely will lead to worsening clinic status and the subjects are followed in a treatment as usual manner. Were any additional safeguards in place for that eventuality? For example – were the subjects informed that they could contact the principal investigator or research coordinator if things were not going well? These all seem like significant safety questions to me. 5. Social Functioning Scale (SFS) to measure the primary outcome - The measured results with this scale are in the top line of Table 2 at 6, 12, and 24 months. The scale has 79 items that are assigned to assess social functioning. Is there a problem with taking a cross sectional sample of people stabilized on medications and hypothesizing they will function better being tapered off antipsychotic medication? There is an obvious problem and that is there is no accounting for the improvement in social functioning due to the medication in the first place. In other words - what would the subjects have scored leading up to and during the episode of acute or recurrent psychosis - the reason they are taking the medication in the first place. What would the trajectory of these scores be over time? Stabilization of psychosis involves a lot more than treating hallucinations, delusions, and thought disorder symptoms. With stabilization there is an improvement in social behavior. The design of the trial suggests that the problem began with medications rather than a significant psychiatric disorder. There is a concept in clinical psychiatry and that is trying to get the patient as close as possible to their baseline level of functioning. That requires a knowledge of what they were like before the onset of illness and restoring as much functional and social capacity as possible. That also typically means minimal to no medication side effects if possible. 6. What is supported reduction of antipsychotic medication? Is there a protocol that I missed? I could not find what this means anywhere in either the protocol or final paper or in the supplementaries. If I was tapering an antipsychotic medication I would meet more frequently with the patient, inform them of what we need to watch for, have additional caregiver and family involvement, and encourage them to call me at specific signs of early problems due to the dosage reduction. In a research protocol, research staff would call and check on how the subject was doing. I would call all of that treatment as usual (TAU) when it comes to antipsychotic medication reduction. Is supported reduction more than that? Even TAU has been implicated as a potential placebo enhancing effect. Did it have that effect on the intervention in this case? 7. The overstated conclusion: “Our findings provide information for people with schizophrenia and related conditions about the probable medium-term impact of reducing the dose of their antipsychotic medication, and they highlight the need for collaborative decision-making based on the sharing and careful consideration of all the evidence.” Actually, it doesn’t. This is what clinical psychiatrists do and more specifically it is what I did for 35 years of practice. I can still recall community psychiatry seminars with Len Stein, talking about dosage reductions of antipsychotic medications and the implication of a WHO international study looking at that problem in schizophrenia. That seminar was in 1986. Collaborative decision making seems to be the latest term for informed consent and therapeutic alliance. Informed consent means that the patient is given enough information and discussion so that they can make a decision about the direction of their care including any medications, tests, or other interventions used. The therapeutic alliance is the affiliative relationship between the patient and physician aligned to address the patient's problems and diagnoses. It is by longstanding definition a collaboration. What the authors did encounter but did not discuss was the tendency of people on antipsychotics to just discontinue them (several in the maintenance group did this), how much withdrawal was encountered, and why there were no group categorical differences in side effects with the taper. According to the Glasgow Antipsychotic Side-effect Scale (GASS) guidelines all subjects remained in the moderate side effect range. And if medications work through side effects as the critical psychiatrists say why did the subjects in the dose reduction group worsen? Those are a few of the problems that jumped out at me as I read this paper and the associated backgrounder. As can be seen from the above discussion many of these design factors potentially optimize the intervention group in the direction of proving the authors’ hypothesis. It also limits generalizability to other clinical settings. That makes the result of the trial even more significant. It also raises some issues that seem more prominent in recent years as pharmaceutical conflict of interest seems to ring hollow. Is there an ideological conflict of interest and how is it determined? How does it affect research design, results, and the discussion of research findings? The Recent Takedowns of Adult ADHD Psychiatry seems doomed to argue endlessly about whether certain conditions exist or not and whether they can be characterized by written criteria. The latter condition is the most easily dismissed since clinical training is necessary to recognize conditions. You cannot just sit in an office, read the DSM and call yourself a psychiatrist. Whether conditions exist or not is more debatable but often slides into rhetoric that suggests inadequate training, ignorance, and/or significant conflict of influence or undue influence by the pharmaceutical industry. Consideration of the undue influence can easily be applied at the global level since Pharma has massive marketing efforts, direct to consumer advertising in the US, and at least one major political party pulling for them. That brings me to the recent commentaries about adult ADHD (1, 2). The first reference (1) doubts that adult ADHD exists for the most part and sees the diagnosis primarily as the result of a marketing scheme by Eli Lilly for atomoxetine and ignoring affective temperaments and other states that may affect attention. Atomoxetine was invented as a norepinephrine reuptake inhibiting antidepressant and like other members of this class of drugs – it did not work for depression. Since it is not technically a stimulant it was tested for ADHD and found to be effective. It is unique relative to other ADHD medications and not surprisingly it was heavily marketed while on patent. The patent expired on May 2017. The years on the market patent protected were 2002-2017. The first references to the diagnosis of adult ADHD were noted in the 1980s. Reference 2 suggests that the diagnosis of ADHD in children in the US is around 2-3% with adult numbers half that based on the work of one author. Contrasting numbers of a lifetime prevalence in adults as 8.1% and surveys estimating current prevalence at 4.4% are described as “absurdly high” but qualified on methodology (surveys vs interviews). Some authors have the opinion that books published about adult ADHD like Ratey and Hollowell's Driven to Distraction were a major source of public interest in the diagnosis and instrumental in getting it into the public vernacular. Before I get started – let me say that the only stake I have in this argument is making sure that the complexity of the situation is adequately described. Practically all the pro/con arguments in psychiatry are gross oversimplifications and based on what I know about the literature – I had no reason to expect that this was any different. I am already on record on this blog describing how to diagnose and treat ADHD and not fall into the common problems of misdiagnosis, prescribing to people with substance use problems, or prescribing to people who view these medications as performance enhancers. I have successfully treated adult ADHD with both on and off label medications and can attest to the fact that it is a valid and treatable diagnosis. Let me start out by looking at the prevalence estimates. These figures are very popular in the press to indict diagnosticians in the United States compared with some European countries and sell more papers. The problem with prevalence estimate is that the range can vary significantly due to methodological differences in the surveys. That question was looked at (3) and the title of that paper asked if ADHD was “an American condition”. The authors reviewed 22 studies based on DSM-III criteria and 19 studies based on DSM-IV criteria. Twenty prevalence estimates were done on the US and 30 were done in other countries. They demonstrated that the range of prevalence across all studies was approximately the same and that ADHD was not just an American condition. Since then numerous prevalence studies have been done in other countries – more recently using DSM-5 criteria showing similar ranges. On the issue of adult ADHD, a recent review looked at the issue adult ADHD and symptomatic adult ADHD prevalence by the 6 WHO regions (4). Their overall goal was to determine the worldwide prevalence of adult ADHD. They looked at the issue of persistent or childhood onset ADHD and symptomatic adult ADHD with no evidence of childhood onset and estimated the prevalence of those two groups separately. The pooled prevalence of persistent adult ADHD was 4.6% and for symptomatic ADHD it was 8.83%. These authors also looked at prevalence by a list of demographic factors, diagnostic criteria, addition to geographic areas as well as the decreasing prevalence by age groups. This study raises the issue of whether ADHD can be acquired rather than be a childhood onset illness. The reality is that there are many paths to acquired attentional deficit that have been treated over the course of my 35 years in the field. The best examples are neurodegenerative diseases, strokes, and brain injuries. Neuropsychiatrists have written about treating the associated cognitive, mood, and motivational deficits with stimulants. But a more relevant question is whether mechanisms exist that can result in people with none of these acquired brain injuries. The answer comes from modern genetics. Polygenic risk scores (of all diseases) suggest that there are high risk individuals who show no evidence of an illness as adults. These examples of incomplete penetrance are usually explained as environmental factors, additional genetic dynamics such as aging or protective factors. I see no reason why these factors could not occur in an ADHD genotype after childhood. The other significant genetic factor is spontaneous mutation or as a recent commentator put it: “You don’t die with the genome you were born with.” Psychiatry has focused on familial studies for the past 50 years, but it is likely that significant numbers of most conditions occur as the result of spontaneous mutations rather than strictly hereditary transmission. That is borne out in clinical practice every day. The authors (1) make the argument that ADHD is not a “scientifically valid” diagnosis. They explain “these symptoms have not been shown to be the result of a scientifically valid disease (adult ADHD) and better explained by more classic and scientifically validated psychiatric conditions, namely diseases or abnormalities of mood, anxiety, or mood temperament.” Mood temperament is a stretch. It is rarely commented on in adult psychiatry and then in extreme cases. It is not contained in the DSM. Part of the reason is selection bias. Psychiatrists are seeing people who have failed multiple other treatments and I have referred to this as being the treatment provider of last resort. Another factor is that ADHD is a quantitative rather than qualitative disorder – that is the cognitive symptoms are at the extreme end of normalcy and it is difficult to draw a line to demarcate illness from normal in many cases. A comparable example from medicine is hypertension. The cutoff for what is considered hypertension has varied significantly over the decades (9, 10) and even now considers antihypertensive side effects as a qualifier for treatment. That means that for any 2 people with the same marginally elevated blood pressure only one might get consistently treated. At one point hypertension was considered by some physicians to be a necessary compensatory mechanism that should not be treated (10). On the issue of quantitative aspects of psychiatric disorders in general – dimensional approaches are often suggested as a solution and the question is whether they work any better than the impairment criteria used in the DSM. That is especially true in a clinical setting where a patient is presenting with a clear problem that they are asking for help with On the issue of validity, studies have been done demonstrating reliability and validity (8) on both the DSM criteria as well as various rating scales for adult ADHD that are consistent with the diagnosis. There have also been detailed discussions of how to approach the problem clinically (11). Those discussions include how to differentiate mood disorders from ADHD and how to approach the functional impairment criteria in the clinical interview. That brings me to the issue of temperaments mentioned in reference 1. Temperaments have been researched in various contexts in psychiatry over the past decades. Most psychiatrists of my generation first heard about them on child psychiatry rotations and the work of Stella and Chess. In adults, temperaments are more descriptions of hyperthymia, cyclothymia, and dysthymia and are generally considered in the differential diagnosis of subclinical mood disorders. The best example is hyperthymia and it has been referred to both as a temperament and a personality. Hyperthymic people are generally high energy, require less sleep, and are social, talkative, and outgoing. They may be very productive and have increased libido relative to their peers. In clinical interviews they may say that their friends think they are “bipolar” and need to be treated. But careful interviewing demonstrates that they lack the symptom severity and degree of impairment necessary for a diagnosis of bipolar disorder. Ideally the initial interview results in that formulation and the psychiatrist can advise the person about why treatment is not necessary. Reference 12 looks at the issue of temperaments in a retrospective controlled study of patients being treated with stimulants who were referred to a mood disorders clinic. The authors acknowledge the selection bias in their study design. I can not think of a better design to pick up misdiagnosed patients than this one. To cite one example – of the 87 amphetamine treated referrals only 50% had a past diagnosis of ADHD. The authors acknowledge that there is no standard way to determine affective temperaments and decide to use the TEMPS-A with a cutoff of 75% of the items. If you are able to find a copy of the TEMPS-A (it is not easy) – you will find a list of 50 true-false questions like “I’m usually in an upbeat or cheery mood.” The questions are reminiscent of the Minnesota Multiphasic Personality Inventory (MMPI) except there are far fewer questions. The scoring guide suggests that the TEMPS-A can discriminate between hyperthymic, cyclothymic, dysthymic, and irritable temperaments. It is validated in the usual ways. The relevant question is whether any diagnosis made with this checklist would deter you from treating a comorbid condition - like Adult ADHD? It is one thing to survey a misdiagnosed group with the TEMPS-A and consider the clinical implications, but another to consider the presenting problem possible ADHD and whether it should be treated. The arguments in reference 2 about overdiagnosis, the existence of adult ADHD, and the idea that ADHD can occur in adults without a childhood diagnosis can be challenged with the facts and references provided here. The fact that we are in the midst of a multigenerational drug epidemic in an increasingly intoxicant permissive society does not mean that a diagnosis, treatment, or problem does not exist. It does mean that all psychiatrists from the moment they enter practice must exercise extreme caution when prescribing substances that reinforce their own use. The most likely cause of overdiagnosis is not because adult ADHD does not exist, not because of drug promotion (most are generic including the non-stimulant alternatives), or because MDs are careless. There are basically two reasons. First – the difficulty of diagnosing quantitative conditions. Second – sociocultural factors that exist in the US. Performance enhancement is built on the myth that you can tune your brain (or any organ) with supplements, nutrients, or medications to become a superior human being. The reality is you can alter your conscious state to believe that – but in the case of stimulants it is unlikely. The only real performance enhancement occurs because you can stay awake longer to read more and there is some evidence that your belief system is altered so that you believe you are smarter (14). These are just two of the reinforcing properties of stimulants that can lead to accelerated use and addiction. That is my brief summary of the complexity of this situation. For more on my approach to adult ADHD. Heart Rate Variability I have been following heart rate variability (HRV) on my watch and three different apps for the past several years. HRV is defined as the slight variations between R waves in the standard ECG recording. I have included an example below, illustrating the R-R’ intervals (or RRI) and how they might vary over time. Since HRV became widely available as a measurement off a watch that is commonly worn by millions of people, the research on this measurement and the variable studied has increased significantly. For my purposes – HRV is thought to be an indicator of heart health and conditioning and possibly a marker of overtraining – but advice about that varies significantly. Some studies have shown that decreased HRV is associated with an increased risk of arrhythmias. My recent cardiac ablation and cardioversion seemed to present an ideal situation for further study. Before getting into those details the physiology of HRV needs to be considered. The dominant heart rhythm of a normal heart is determined by the sinoatrial (SA) node. This node contains a population of spontaneously depolarizing cells that determine the rhythm and rate of the heartbeat. In addition to the neurophysiology of that cell population several additional factors affect both the rate and HRV. Primary among them is autonomic innervation from both the sympathetic and parasympathetic systems and their effect at the SA node. Parasympathetic fibers from the vagus nerve modulate slower firing through the neurotransmitter acetylcholine (ACh). Sympathetic fibers increase the rate of firing through the neurotransmitter norepinephrine (NE). NE has a longer half-life than ACh, but vagal tone is thought to be the most significant determinant of HRV. That is in line with several clinical observations including lower baseline heart rates in conditioned athletes and higher heart rates in people with less conditioning or in stressful situations. What happened to my heart rate and HRV during the recent cardiac ablation for atrial fibrillation and subsequent cardioversion? To answer that question, I had to figure out how to get the data off my Apple Watch 5.0. The only approach I could find was to downloaded all of the collected Health App data as a CSV file and then plot it in Excel. There are some online sites that you can download the data to and then use the remote software for plotting, but I preferred to retain control over the data. If you decide to do that and have several years of data like I did – it takes a long time. It took about 5 hours in my case to download about 1G of data to a zip file. From there it is easy to open that file with Excel or other software and do the plots. A useful addition to the Health App would be able to download specific time intervals. I have done 2 plots so far based on average daily HRV and hourly HRV as shown below. The plots are interesting because it clearly shows an effect from the ablation, a 96-hour period of atrial fibrillation and atrial flutter, and the cardioversion. At the minimum the baseline HRV drops to a different baseline after the ablation. That is followed by a significant spike with the recurrence of afib/flutter. And then there is a return to the lower baseline after the electrical cardioversion. I rarely had any significant episodes over the course of a year and whenever I went back and reviewed HRV it was not significantly changed. Since all those episodes were typically less than 2 or 3 hours it may not have been long enough to see an HRV effect. Conversely spikes of 50-100 msec in the HRV recording were common and not associated with arrhythmias. In the case of the post ablation period the sustained rates were associated with spikes, but since atrial flutter is regular, the associated R-R’ intervals probably showed a more characteristic HRV. I would expect to see an increase in vagal tone and therefore HRV just related to the sustained high rates over 4 days. If increased vagal tone correlates with increased HRV that does not seem to be the case in these graphs. The graphs also seem to indicate to me that there may be a structural element to HRV – either in the anatomical configuration of the conducting cells, their altered physiology, or a combination. The main implication for me at this point is to cautiously restart my conditioning efforts and see what impact that has on the HRV baseline. A second question is whether my HRV will approach the pre-ablation baseline. Electrocardiograms (ECG) may provide some clues in that direction. I have listed them below for references. Significant changes occurred in the immediate post ablation ECG and the post cardioversion ECG. An additional thought is whether non linear analysis of the RR intervals would yield more information and easily interpretable graphics. I have used some of these attractor plots in the past and also applied them to single electrode analyses of normal controls and patients with Alzheimer's disease. In terms of ECG analysis - see figure 5 in reference 2. In terms of theory - these attractor diagrams also imply changes in biological complexity at either the structural or functional level. George Dawson, MD, DFAPA ECG time course (1 -> 5 are in sequence): 1. Baseline - preop ECG 2. Post ablation ECG (following day): 3. Post ablation ECG - note anterior T wave changes thought to be consistent with procedure. 4. Precardioversion ECG showing atrial flutter at a high rate (day 5 of this arrhythmia; post op day 14). 5. Post cardioversion ECG showing NSR but flipped T waves in V1-V3. 6. ECG follow up 2 weeks after cardioversion showing T wave normalization in anterior leads. Heart Rate Variability Some recent recovery in HRV after a long period of low numbers in the 7-37 msec range following ablation and cardioversion.

Primum non nocere: above all, do no harm! KEY POINTS Autonomy, non-maleficence, beneficence, and justice are ethical principles that guide mental health care. Having an intentional process of ethical deliberation is essential. Clinicians need to act in the best interests of the people, families, and communities they serve. Ethical principles are especially pertinent to the conduct of professionals in psychology and psychiatry. The hard work comes when principles are in conflict, and clinicians must consider what values, biases, and obligations matter most. In the field of biomedical ethics, Tom Beauchamp and James Childress have had a seminal role in articulating fundamental ethical principles that guide professional conduct in a vast range of related specializations such as medicine, psychology, social work, and other health or social care services. Their book, Principles of Biomedical Ethics, has served as a practical guide for the development of many codes of ethics prepared by professional associations and regulatory bodies that oversee psychotherapy in various parts of the world. These four principles stand out: Autonomy: A person’s right to act as a free agent and the need to respect the rights of others to make free choices (respect for the client’s autonomy, dignity, and right to self-determination). Non-maleficence: “Above all, do no harm” (Latin: primum non nocere), i.e., not engaging in intentional physical or emotional harm or in actions with a high risk of harm. Beneficence: Engage in actions that benefit others and promote the welfare of the person who is suffering (including the prevention and the mitigation of harm). This means directing treatment in a way that promotes the best interests of the person you are working with; be careful not to project your perception of what is ‘best’ onto others. Justice: Treat people in similar circumstances similarly, and acknowledge when a person's circumstances differ and may require additional support. Justice means upholding the dignity and honoring the rights of all people. Practicing equity, inclusion, and attempting to address systematic inequalities are central components of justice. Ethical principles Other Ethical Principles to Consider: Trust: All relationships are built upon the foundation of trust. Being truthful, loyal, honest, and honouring one's commitments can create better outcomes for the individuals and communities we hope to support. Care: Always consider the unique interpersonal factors at play in a situation and act from a place of care, kindness, and responsibility—mental health providers should be attuned to others' needs. Transparency: sharing information and creating accessibility to knowledge in an honest, clear, and straightforward way at a level the person or family can understand is important. Societal interest: Upholding personal responsibility to always act in the best interests of society. This list of principles is not exhaustive, and many other ethical principles may be applicable to the context of different situations. However, the application of principles can sometimes come into conflict when making decisions, which is where the process of ethical deliberation truly begins. Ethical Deliberation If, after an evaluation of existing laws and guidelines, there is still no clear decision, further deliberation is required to explore values, personal biases, goals, and intentions to inform how we should make decisions. A deliberative ethical process requires us to understand the perspectives of the appropriate stakeholders and consider relevant values. Some values may feel right, but may not apply to the context of the situation. Once this information has been gathered, there are likely a couple of reasonable options on the table. To decide what option is the “best,” clinicians can deeply reflect on each available pathway forward. Practically, this may look like analyzing which action aligns best with the relevant values and principles previously identified. Some clinicians attempt to develop rational arguments for each ethical position in a given situation and attempt to choose the most logically defensible position. It is imperative for mental health care providers to also listen to their intuition and "gut feelings"—these will often elicit emotions that help us identify when an ethical conflict is being experienced. In learning to listen to your gut feelings or identifying an "ick factor," clinicians can create an intentional space to reflect on the context of the situation and unpack why such feelings are arising. This intuitive response can allow clinicians to practice critical reflectivity, identify how values may be at play or in conflict in client scenarios, and how different decisions within treatment may have risks or benefits that warrant substantial considerations. A suffering person’s well-being demands that mental health care providers act not on their own emotions, but rather deliberately focus on the best interests of the individuals, families, or communities they serve. This also means that professionals need to consider the interpersonal and cultural contexts in which people find themselves. After all, none of us exist in a social, cultural, or political vacuum. There are many processes of reflection and ethical frameworks that can help mental health professionals act with integrity, intentionality, and logic. Such reflection takes time and energy, but it is a choice clinicians get to make to ensure that our professions are held to the highest standard and that persons who are suffering receive the best care possible.

The prevalence of sexual dysfunction remains high in people with schizophrenia, but treating comorbid depression could be effective in improving sexual health. A systematic review and meta-analysis published in JAMA Psychiatry found that both men and women with schizophrenia often reported sexual dysfunction. While some dysfunction is explained by schizophrenia, lower rates of dysfunction were associated with antidepressant use, suggesting that comorbid depression may underlie some of the sexual health issues. Attention to sexual health in schizophrenia has increased in recent decades, yet, there is an overall paucity of published data on the subject. The aim of this review and meta-analysis was to determine the prevalence of and common types of sexual dysfunction in people with schizophrenia. As such, review authors searched publication databases through June 2022 for relevant observational studies. A total of 72 studies published between 1979 and 2021 were included in this analysis. The pooled study population was comprised of 21,076 individuals with schizophrenia or schizoaffective disorder from 33 countries. Most studies (81.9%) used a standard questionnaire to assess sexual dysfunction, and the most frequently used instrument was the Arizona Sexual Experience scale (n=19 studies). The pooled prevalence of sexual dysfunction was 56.4% (95% CI, 50.5%-62.2%). When stratified by type of dysfunction, the most common was loss of libido (40.6%; 95% CI, 30.7%-51.4%; I2, 96%), followed by orgasm dysfunction (28.0%; 95% CI, 18.4%-40.2%; I2, 97%) and genital pain (6.1%; 95% CI, 2.8%-12.7%). "[I]mproving the screening and treatment of depression may be an effective strategy to improve sexual health in patients with schizophrenia." Stratified by gender, sexual dysfunction was reported by 55.7% (95% CI, 48.1%-63.1%) of men, along with erectile dysfunction (44.0%; 95% CI, 33.5%-55.2%) and ejaculation disorder (38.6%; 95% CI, 26.8%-51.8%). Women also reported sexual dysfunction (60.0%; 95% CI, 48.0%-70.8%), as well as amenorrhea (25.1%; 95% CI, 17.3%-35.0%) and galactorrhea (7.7%; 95% CI, 3.7%-15.3%). Of note, there was a high amount of heterogeneity observed in the comparisons for men (I2, 98%; P <.001) and women (I2, 96%; P <.01). In addition, leave-one-out analyses found significant publication bias for global sexual dysfunction (t, 5.63; P <.001), orgasm dysfunction (t, -3.85; P <.001), ejaculation disorder (t, -2.33; P =.03), and sexual dysfunction among men (t, 4.58; P <.001) and women (t, 2.25; P =.03). In subgroup analyses, rates of erection disorders were lower among patients using antidepressants (b, -6.30; 95% CI, -10.82 to -1.78; P =.006) and mood stabilizers (b, -13.21; 95% CI, -17.59 to -8.83; P <.001). Similarly, antidepressants (b, -6.10; 95% CI, -10.68 to -1.53; P =.009) and mood stabilizers (b, -11.57; 95% CI, -16.34 to -6.80; P <.001) were associated with lower rates of ejaculation disorders. The review authors concluded, “[I]mproving the screening and treatment of depression may be an effective strategy to improve sexual health in patients with schizophrenia.” These meta-analysis findings may be limited, as common factors associated with sexual dysfunction in the general population were not adequately explored in the underlying studies. Related Article: What is Schizophrenia? Special Considerations in Treating Women With Schizophrenia

Intermittent Use of Benzodiazepines BARCELONA — Intermittent benzodiazepine use significantly reduces the risk for falls, fractures, and mortality in older adults compared with chronic use of these medications, results of a large-scale study show. Investigators matched more than 57,000 chronic-benzodiazepine users with nearly 114,000 intermittent users and found that at 1-year, chronic users had an 8% increased risk for emergency department (ED) visits and/or hospitalizations for falls. Chronic users also had a 25% increased risk for hip fracture, a 4% raised risk for ED visits and/or hospitalizations for any reason, and a 23% increased risk for death. Study investigator Simon J.C. Davies, MD, PhD, MSc, Centre for Addiction & Mental Health in Toronto, Canada, said that the research shows that where possible, patients older than 65 years with anxiety or insomnia who are taking benzodiazepines should not stay on these medications continuously. However, he acknowledged that, "in practical terms, there will be some who can't change or do not want to change" their treatment. Wide Range of Adverse Outcomes The authors note that benzodiazepines are used to treat anxiety and insomnia but are associated with a range of adverse outcomes, including falls, fractures, cognitive impairment, and mortality as well as tolerance and dose escalation. "These risks are especially relevant in older adults," they add, noting that some guidelines recommend avoiding the drugs in this population, whereas other suggest short-term benzodiazepine use for a maximum of 4 weeks. Despite this, "benzodiazepines are widely prescribed in older adults. One study showed that almost 15% of adults aged 65 years or older received at least one benzodiazepine prescription. Moreover, chronic use is more common in older vs younger patients. Benzodiazepine use among older adults "used to be higher," Davies told Medscape Medical News, at around 20%, but the "numbers have come down," partly due to the introduction of benzodiazepine-like sleep medications but also due to educational efforts. "There are certainly campaigns in Ontario to educate physicians," Davies said, "but I think more broadly people are aware of the activity of these drugs, and the tolerance and other issues." To compare the risk associated with chronic vs intermittent use of benzodiazepines in older adults, the team performed a population-based cohort study using linked healthcare databases in Ontario. They focused on adults aged 65 years or older with a first benzodiazepine prescription after at least 1 year without taking the drugs. Chronic benzodiazepine use was defined as 120 days of prescriptions over the first 180 days after the index prescription. Patients who met these criteria were matched with intermittent users in a 2:1 ratio by age and sex. Patients were then propensity matched using 24 variables including health system use in the year prior to the index prescription, clinical diagnoses, prior psychiatric health system use, falls, and income level. The team identified 57,072 chronic-benzodiazepine users and 312,468 intermittent users, of whom, 57,041 and 113,839, respectively, were propensity matched. As expected, chronic users were prescribed benzodiazepines for more days than were the intermittent users over both the 180-exposure period, at 141 days vs 33 days, and again during a further 180-day follow-up period, at 181 days vs 19 days. Over the follow-up period, the daily lorazepam dose-equivalents of chronic users four times that of intermittent users. Hospitalizations and/or ED visits for falls were higher among patients in the chronic-benzodiazepine group, at 4.6% vs 3.2% in those who took the drugs intermittently. After adjusting for benzodiazepine dose, the team found that chronic benzodiazepine use was associated with a significant increase in the risk for falls leading to hospital presentation over the 360-day study period compared with intermittent use. (hazard ratio [HR], 1.08; P = .0124). Sex Differences In addition, chronic use was linked to a significantly increased risk for hip fracture (HR, 1.25; P = .0095), and long-term care admission (HR, 1.32; P < .0001). There was also a significant increase in ED visits and/or hospitalizations for any reason with chronic benzodiazepine use vs intermittent use (HR, 1.04; P = .0007), and an increase in the risk for death (HR, 1.23; P < .0001). A nonsignificant increased risk for wrist fracture was also associated with chronic use of benzodiazepines (HR, 1.02; P = .8683). Further analysis revealed some sex differences. For instance, men had a marked increase in the risk for hip fracture with chronic use (HR, 1.50; P = .0154), whereas the risk was not significant in women (HR, 1.16; P = .1332). In addition, mortality risk associated with chronic use was higher in men than in women (HR, 1.39; P < .0001 vs HR, 1.10; P = .2245). The decision to discontinue chronic benzodiazepine use can be challenging, said Davies. "If you're advising people to stop, what happens to the treatment of their anxiety?" He said that there are many other treatment options for anxiety that don't come with tolerance or risk for addiction. "My position would be that intermittent use is perfectly acceptable while you bide your time to explore other treatments. They may be pharmacological; they may, of course, be lifestyle changes, psychotherapies, and so on," said Davies. If, however, patients feel that chronic benzodiazepine use is their only option, this research informs that decision by quantifying the risks. "We've always known that there was a problem, but there haven't been high-quality epidemiological studies like this that allowed us to say what the numbers are," said Davies. Confirmatory Research Commenting on the research for Medscape Medical News, Christoph U. Correll, MD, Professor of Psychiatry at the Zucker School of Medicine at Hofstra/Northwell, New York, NY, noted that the risk associated with benzodiazepine use, especially in older people, has been demonstrated repeatedly. "In that context, it is not surprising that less continuous exposure to an established risk factor attenuates the risk for these adverse outcomes," he said. Correll, who was not involved in the study pointed out there is nevertheless a "risk of residual confounding by indication." In other words, "people with intermittent benzodiazepine use may have less severe underlying illness and better healthy lifestyle behaviors than those requiring chronic benzodiazepine administration." Also commenting on the research, Christian Vinkers, MD, PhD, psychiatrist and professor of stress and resilience, Amsterdam University Medical Centre, Amsterdam, the Netherlands, said that it confirms "once again that long-term benzodiazepine use should not be encouraged." "The risk of falls, as well as cognitive side effects and impaired driving skills, with the risk of road accidents, make chronic overuse of benzodiazepines a public health issue. Of course, there is a small group of patients who should have access to long-term use, but it is reasonable to assume that this group is currently too large," he added.

Running Therapy Running therapy rivals antidepressant medication for the treatment of depression and anxiety, results of a new study show. However, running provides greater physical health benefits while adherence is greater with drug treatment. "Both interventions helped with the depression to around the same extent," study presenter Brenda W.J.H. Penninx, PhD, professor of psychiatric epidemiology at the VU University Medical Center in Amsterdam, the Netherlands, said in a release. However, medication "generally had worse impact on body weight, heart rate variability, and blood pressure, whereas running therapy led to improved effect on general fitness and heart rate," Penninx added. The findings were presented here at the 36th European College of Neuropsychopharmacology (ECNP) Congress, and recently published in the Journal of Affective Disorders. Research Gap Previous research suggests exercise interventions can have a therapeutic effect equivalent to antidepressants, but their impact on physical health has been "poorly examined in a psychiatric population, the investigators note. The authors note that depressive and anxiety disorders "cause immense suffering by compromising both mental and physical health," and the need for effective treatments is "pressing." Although antidepressant medication is considered a "standard first-line treatment" alongside psychotherapy, the drugs are "not effective for all and [are] often associated with side effects." The Mood Treatment with Antidepressant or Running (MOTAR) study was a partially randomized pragmatic trial in adults with depression and/or anxiety disorder, as determined using the DSM-IV algorithms with the Composite International Diagnostic Interview (CIDI). The 16-week intervention study included 141 patients with depression and/or anxiety. The mean age was 38.2 years and 58% were women. Participants were offered a choice of treatment: 16 weeks of treatment with the selective serotonin reuptake inhibitor (SSRI) escitalopram (Lexapro) or a 16-week group-based running therapy. Patients without a strong preference for treatment allocation were randomly assigned to either antidepressant medication or running therapy, while those unwilling to be randomized were allocated to their preferred intervention. A total of 22 patients were randomly assigned to receive antidepressant treatment and 13 to running therapy. A total of 36 participants chose antidepressant treatment, while 83 chose the running therapy. Running therapy involved 16 weeks of supervised 45-minute outdoor running sessions to a target of two to three sessions per week, in line with US Centers for Disease Control/American College of Sports Medicine recommendations. Physical Health Benefits Treatment adherence in the antidepressant group, defined as still using treatment at the post-treatment assessment, was 82.2% vs 52.1% among running therapy participants, where adherence was specified as completing more than 22 sessions. Remission was defined as no longer meeting the criteria of a current depressive or anxiety disorder via CIDI at week 16. On intention-to-treat analysis, this requirement was met by 44.8% of patients taking antidepressants and 43.3% of those in the running therapy group (P = .88). However, running therapy patients showed significant improvements in weight (P = .001), waist circumference (P = .011), systolic and diastolic blood pressure (P = .011 and P = .002, respectively), heart rate (P = .033), and heart rate variability (P = .006). The investigators note the more favorable physical health changes in the running therapy group were due to "larger improvements in the running therapy group but also due to larger deterioration in the antidepressant group."Antidepressants are generally safe and effective and work for most people, said Penninx. She also noted that untreated depression leads to worse outcomes, so "antidepressants are generally a good choice." Nevertheless, she said, "we need to extend our treatment arsenal as not all patients respond to antidepressants or are willing to take them." The study’s results, she added, suggest that "implementing exercise therapy is something we should take much more seriously, as it could be a good, and maybe even better, choice for some of our patients." Francesca Cirulli, PhD, senior researcher and group leader at the National Institute of Health, Rome, Italy, told Medscape Medical News the study is notable because it is one of the first to prospectively measure the effects of antidepressants and running on physical health. Cirulli suggested that running therapy could be tried ahead of treatment with antidepressants if patients prefer physical exercise and can adhere to it. However, she said, the findings also suggest that an increase in physical activity should accompany treatment with antidepressant medications. Overall, Cirulli said "the message should not be that everyone can be helped by running and antidepressants are bad," but rather "these are both helpful, but not excellent, interventions against depression." Important Limitations Commenting on the research Eduard Vieta, MD, PhD, chair of the Department of Psychiatry and Psychology at the University of Barcelona Hospital Clinic, Barcelona, Spain, noted the study has "very important limitations." Among the limitations: the inclusion of nonrandomized patients who received the treatment of their choice, causing obvious bias and the "lack of binding and power issues" over the number of patients enrolled. Vieta also told Medscape Medical News that the results "seem obvious, because it is known that exercise improves physical health." The trial therefore shows, "if you can find people who are able to do exercise while depressed and adhere to it, those would benefit from that practice," he noted. Also commenting on the research, Eric Ruhe, MD, PhD, Radboud University Medical Center, Nijmegen, the Netherlands, said the results are confirmatory and "again show physical health can influence mental health." However, Ruhe underlined, while it is "common practice" to allow patients to follow their treatment preference and is "understandable from a pragmatic point of view," the group comparison may be "biased" compared to a "truly randomized study." "For example, patients in the antidepressant group were more depressed, which might be associated with less chance of persisting engagement in the exercises," he said. "So, we have to be careful not to overinterpret the comparisons between groups, which the authors acknowledge properly." Turning to the difference in adherence between the two interventions, Ruhe said the results show adopting, and adhering to, a lifestyle habit is more difficult than taking a pill. "This is not exclusively found in psychiatry, indicating that we also have to focus on how to improve compliance to healthy behavior. This could have tremendous impact on healthcare more generally, but also on psychiatric diseases," Ruhe said. Source: MOTAR study was funded by a NWO-VICI grant. Funding for the inflammatory markers was provided by ZonMw: The Netherlands Organization for Health Research and Development.

A cancer diagnosis can bring feelings of confusion, anxiety, sadness, and helplessness. Many mesothelioma patients may feel overwhelmed as they search for stress reduction techniques while navigating their busy treatment schedule. There are many resources available for emotional support for cancer patients and their families, some of which are easy to practice at home. Mindfulness can help patients and their loved ones stay hopeful during a mesothelioma diagnosis. Mindfulness is awareness that arises when we purposely pay attention in the present moment without judgment. Mindfulness-based stress reduction (MBSR) programs can greatly impact cancer patients to manage their stress, pain, and illness. Cancer patients experience a variety of symptoms due to their condition and treatment side effects. MBSR has been proven to be effective in managing stress, anxiety, fatigue, headaches, and high blood pressure. Mesothelioma patients can expect to participate in interactive activities to engage and promote mindfulness meditation. Cancer patients will participate in support activities such as guided mindfulness practice, gentle stretching, yoga, and other activities to promote mindfulness to help them manage their illness. Classes will also provide patients with daily at-home activities to practice their mindfulness meditation skills in the comfort of their own home. Cancer patients and caregivers can both benefit from the techniques and practices of MBSR to reduce stress during their journey navigating a cancer diagnosis. Source: Kaitlyn Carlock- Advocacy Associate https://www.mesotheliomahope.com/

I remember what it was like to be a medical student at a well-known cancer hospital where patients were dying of cancer. In life's final stages, it was not uncommon for physicians to increase the dose of morphine; it alleviated pain, eased labored breathing, and yes, probably hastened the inevitable for patients who were in their final hours. In these scenarios, no one considered this euthanasia, and no one questioned whether it was the right thing to do. Fast-forward to 2023 when the act of a physician hastening a patient's death has become a controversial topic as criteria have expanded. Like all such topics in our polarized society, people aligned on sides, politics, and religion rush to the head of the room, legislation is proposed, and words take on new meanings. If you're in favor of legalization of clinician assistance in a patient's death, the term is medical assistance in dying (MAID). If you're opposed, the term is the more graphic physician-assisted suicide. The scenario is entirely different from what I saw in my medical school rotations decades ago. It's no longer an issue of easing the pain and discomfort of patients' final hours; the question now is whether, faced with a potentially terminal or progressively debilitating physical illness, a patient has the right to determine when, and how, their life will end, and the medical profession is given a role in this. In many places the bar has been further lowered to incorporate nonterminal conditions, and Belgium and the Netherlands now allow physician-facilitated suicide for psychiatric conditions, a practice that many find reprehensible. In these countries, patients may be provided with medications to ingest, but psychiatrists also administer lethal injections. While Belgium and the Netherlands were the first countries to legalize physician-facilitated death, it could be argued that Canada has embraced it with the most gusto; physician-assisted suicide has been legal there since 2016. Canada already has the largest number of physician-assisted deaths of any nation, with 10,064 in 2021 — an increase of 32% from 2020. The Canadian federal government is currently considering adding serious mental illness as an eligible category. If this law passes, the country will have the most liberal assisted-death policy in the world. The Canadian government planned to make serious mental illness an eligible category in March 2023, but in an eleventh-hour announcement, it deferred its decision until March 2024. In a press release, the government said that the 1-year extension would "provide additional time to prepare for the safe and consistent assessment and provision of MAID in all cases, including where the person's sole underlying medical condition is a mental illness. It will also allow time for the Government of Canada to fully consider the final report of the Special Joint Committee on MAID, tabled in Parliament on February 15, 2023." As a psychiatrist who treats patients with treatment-refractory conditions, I have watched people undergo trial after trial of medications while having psychotherapy, and sometimes transcranial magnetic stimulation or electroconvulsive therapy (ECT). The thing that is sustaining for patients is the hope that they will get better and go on to find meaning and purpose in life, even if it is not in the form they once envisioned. To offer the option of a death facilitated by the very person who is trying to get them better seems so counter to everything I have learned and contradicts our role as psychiatrists who work so hard to prevent suicide. Where is the line, one wonders, when the patient has not responded to two medications or 12? Must they have ECT before we consider helping them end their lives? Do we try for 6 months or 6 years? What about new research pointing to better medications or psychedelics that are not yet available? According to Canada's proposed legislation, the patient must be aware that treatment options exist, including facilitated suicide. Physician-assisted suicide for psychiatric conditions creates a conundrum for psychiatrists. As mental health professionals, we work to prevent suicide and view it as an act that is frequently fueled by depression. Those who are determined to die by their own hand often do. Depression distorts cognition and leads many patients to believe that they would be better off dead and that their loved ones would be better off without them. These cognitive distortions are part of their illness. So, how do we, as psychiatrists, move from a stance of preventing suicide — using measures such as involuntary treatment when necessary — to being the people who offer and facilitate death for our patients? I'll leave this for my Canadian colleagues to contemplate, as I live in a state where assisted suicide for any condition remains illegal. As Canada moves toward facilitating death for serious mental illness, we have to wonder whether racial or socioeconomic factors will play a role. Might those who are poor, who have less access to expensive treatment options and social support, be more likely to request facilitated death? And how do we determine whether patients with serious mental illness are competent to make such a decision or whether it is mental illness that is driving their perception of a future without hope? As psychiatrists, we often struggle to help our patients overcome the stigma associated with treatments for mental illness. Still, patients often refuse potentially helpful treatments because they worry about the consequences of getting care. These include career repercussions and the disapproval of others. When this legislation is finally passed, will our Canadian colleagues offer it as an option when their patient refuses lithium or antipsychotics, inpatient care or ECT?

Here is the basic principles behind Dr. Carl Jung's excerpt on how to own your yourself. Carl Jung (1875-1961) Carl Jung was an early 20th century psychotherapist and psychiatrist who created the field of analytical psychology. He is widely considered one of the most important figures in the history of psychology. Early Life Carl Gustav Jung was born in Switzerland in 1875 to Emilie Preiswerk and Paul Jung, a pastor. Because of his father’s faith, Jung developed a keen interest in religious history, but he settled on the study of medicine at the University of Basel. After he completed his medical degree, Jung joined the staff at Burghoelzli Clinic in Zurich, Switzerland as an intern to Eugen Bleuler, where he explored the unconscious mind and its related complexes. He also traveled to Paris to study under Pierre Janet in 1902. In 1905, Jung was appointed to the faculty at the University of Zurich where he worked until 1913. Jung married Emma Rauschenbach in 1903. The couple had five children and remained married until Emma's death in 1955, although Jung's extramarital affairs were extensive. Jung died in Switzerland in 1961. Professional Life Jung sent a copy of his book Studies in Word Association to Sigmund Freud in 1906, and Freud reciprocated by inviting Jung to visit Vienna. Their friendship lasted until 1913, at which time they parted ways due to a difference in academic opinion. Jung agreed with Freud’s theory of the unconscious, but Jung also believed in the existence of a deeper collective unconscious and representative archetypes. Freud openly criticized Jung's theories, and this fundamental difference caused their friendship and psychological views to diverge. Jung traveled throughout the world to teach and influence others with his psychoanalytical theories. He published many books relating to psychology, and others that seemed outside the realm science, including Flying Saucers: A Modern Myth of Things Seen in the Skies , which examined and dissected the psychological significance of UFO sightings. Jung’s work embodied his belief that each person has a life purpose that is based in a spiritual self. Through his eastern, western, and mythological studies, Jung developed a theory of transformation called individuation that he explored in Psychology and Alchemy , a book in which he detailed the relationship of alchemy in the psychoanalytical process. Source: GoodTherapy (2023)

In some cases, a recent stressors or sudden catastrophic event, failure or can leave people feeling desperate, unable to see a way out, and become a "tipping point" toward suicide. Suicide is one of the leading causes of death in the United States. It is the second leading cause of death for people aged 10 to 34. The highest rate of suicide occurs in persons 75 years of age or older. The impact of suicide in communities makes suicide a serious public health problem. In 2021 in the U.S., more than 47,000 people died by suicide and an there were an estimated 1.2 million suicide attempts according to the Centers for Disease Control and Prevention (CDC). This is one death by suicide every 11 minutes. (1, 2) Men were more than three times more likely than women to take their lives. Firearms are the most common method of suicide (used in about half of all suicides).Yet, suicide is preventable. Knowing the risk factors and recognizing the warning signs for suicide can help prevent suicide. Risk Factors, Warning Signs and Protective Factors Suicide is linked to mental disorders, particularly depression and alcohol use disorders, and the strongest risk factor for suicide is a previous suicide attempt. The Suicide Prevention Resource Center defines risk and protective factors and warning signs: Risk factors are characteristics that make it more likely that an individual will consider, attempt or die by suicide. Warning signs indicate an immediate risk of suicide. Protective factors are characteristics that make it less likely that individuals will consider, attempt or die by suicide. Suicide Prevention Risk Factors for Suicide Individual, relationship, community and societal factors can increase the risk of suicide such as: Previous suicide attempt(s). A history of suicide in the family. Substance use. Mood disorders (depression, bipolar disorder). Access to lethal means (for example, keeping firearms in the home or having access to unsecured prescription medications) Losses and other events (for example, the breakup of a relationship or a death, academic failures, legal difficulties, financial difficulties). History of trauma or abuse. Bullying. Chronic physical illness, including chronic pain. Exposure to the suicidal behavior of others. Social isolation. Historical trauma. Stigma associated with seeking help. In some cases, a recent stressor(s) or sudden catastrophic event, failure or can leave people feeling desperate, unable to see a way out, and become a "tipping point" toward suicide. A CDC report highlights the complexity of suicide.(3) While a mental health condition may be a contributing factor for many people, many factors contribute to suicide among people with and without known mental health conditions. A relationship problem was the top factor contributing to suicide, followed by crisis in the past or upcoming two weeks and problematic substance use. About half, 54 percent, of people who died by suicide did not have a known mental health condition, according to CDC.(4) However, many of them may have been dealing with mental health challenges that had not been diagnosed or known to those around them. Warning Signs of Suicide Often talking or writing about death, dying or suicide. Making comments about being hopeless, helpless or worthless. Expressions of having no reason for living; no sense of purpose in life; saying things like "It would be better if I wasn't here" or "I want out." Increased alcohol and/or drug use. Withdrawal from friends, family and community. Reckless behavior or more risky activities, seemingly without thinking. Dramatic mood changes. Talking about feeling trapped or being a burden to others. Protective Factors Contacts with providers (such as, follow-up phone call from health care professional). Effective mental health care; easy access to a variety of clinical interventions. Feelings of strong connections to individuals, family, community and social institutions. Strong sense of cultural identity. Problem-solving and conflict resolution skills. The CDC recommends a comprehensive public health approach to suicide prevention and it identifies several strategies that states and communities can undertake, including such measures as teaching coping and problem-solving skills to help people manage challenges, expanding options for temporary assistance for those in need and connecting people at-risk to effective and coordinated mental and physical health care. What You Can Do 988 Suicide Crisis and Lifeline has developed five steps to take to support a loved one that may be experiencing suicidal thoughts. Ask someone you are concerned about if they're thinking about suicide. Studies show that asking someone if they are having thoughts of suicide does not increase the likelihood of a completed suicide nor does it increase suicidal thoughts. Be there for them. This could be by phone or in person. Keep them safe. Reduce access to lethal means for those at risk. Help them connect with ongoing support. Follow up. Give them a call or visit. Send a text or an email to let them know that you are still present. Learn more and find resources at www.BeThe1To.com. Be the one to save a life. You can do something to prevent suicide. If you need help for yourself or someone else, contact the Suicide and Crisis Lifeline by calling or texting 988. You can also chat online at 988lifeline.org. Resources Crisis Resources - American Association of Suicidology Veteran's Administration Suicide Prevention Get Help - American Foundation for Suicide Prevention (AFSP) World Health Organization - Suicide Prevention Suicide Prevention Resource Center Suicide & Self Harm Injury Data, Centers for Disease Control and Prevention. We Can All Prevent Suicide : Lifeline (988lifeline.org) Take 5 to Save Lives References Centers for Disease Control and Prevention. 2022. Provisional Numbers and Rates of Suicide by Month and Demographic Characteristics: United States, 2021. Curtin, S.C., et al authors. Vital Statistics Rapid Release Report No. 24, September 2022. CDC. Facts about Suicide. https://www.cdc.gov/suicide/facts/index.html CDC. 2018. Fact Sheet: Suicide Rising Across the U.S. (.pdf) Centers for Disease Control and Prevention. Stone, et al. Vital Signs: Trends in State Suicide Rates – United States, 1999-2016 and Circumstances Contributing to Suicide – 27 States, 2015. Morbidity and Mortality Weekly Report. June 8, 2018. Vol.67, No.22.

Narcolepsy TOPLINE: Solriamfetol ― a medication approved for excessive daytime sleepiness caused by narcolepsy or obstructive sleep apnea ― significantly improved symptoms of attention-deficit/hyperactivity disorder (ADHD) and clinical impression of ADHD severity in a pilot study of adults with ADHD. METHODOLOGY: Solriamfetol is a dopamine and norepinephrine reuptake inhibitor that shares some of the properties of current ADHD medications. Researchers conducted a randomized, double-blind, placebo-controlled, dose-optimization trial of 75- or 150-mg solriamfetol in 60 adults with ADHD. For nearly all of the individuals who received solriamfetol, doses increased to 150 mg after the first week. The primary outcome was change in scores on the Adult ADHD Investigator Symptom Rating Scale (AISRS). Secondary outcomes included scores on the Clinical Global Impressions (CGI) scale and standard measures of executive function, behavior, and sleep. TAKEAWAY: By week 6, total AISRS score improved 25% for 52% of individuals to took solriamfetol, vs 17% of those who received placebo. Total AISRS score improved 50% by week 6 in 28% of those who took solriamfetol, vs 3.4% of those who received placebo. By week 6, CGI ratings of "much improved" or "very much improved" occurred in significantly more individuals who received solriamfetol than those who took placebo (45% vs 7%). Significantly more individuals who received solriamfetol than placebo self-reported improvements in executive function (69% vs 34%). Improvement in wakefulness was noted with solriamfetol, but that did not moderate the change in ADHD symptom burden. Solriamfetol was well tolerated, with no significant effect on sleep quality or blood pressure. Adverse effects that occurred at a higher rate in the treatment group than in the placebo group were typical for solriamfetol and sympathomimetic agents used for ADHD. IN PRACTICE: "Solriamfetol may be a safe and effective treatment for ADHD in adults. Larger studies replicating these findings could confirm the strong evidence of benefit and the tolerability of this agent as a treatment," lead author Craig B. H. Surman, MD, director of the Clinical and Research Program in Adult ADHD, Massachusetts General Hospital, said in a statement.

RESPECT YOURSELF - This Jordan Peterson Speech Is A Life Changing By: Dr. Jordan Peterson

How Many Hours a Day Do You Waste? Amazing video by Dr. Jordan Peterson about how productive we could be if we paid attention to the amount of time we waste each day. Productivity leads to longer longevity and satisfaction out of time... By Dr. Jordan Peterson Source: Dr. Jordan Peterson