The study followed six people who were attempting to discontinue the use of antipsychotics. Two of them succeeded in altogether discontinuing the medication, while two others experienced a worsening of their psychotic symptoms during the process. One person was able to lower their dosage significantly, and the last person is still in the process of tapering off the medication. The study, led by Sofie Norlin Mølgaard of Copenhagen University Hospital, presented these 6 cases to highlight the diverse experiences of individuals attempting to taper off and discontinue antipsychotic medication.

The authors write:

“Some patients with schizophrenia might be overmedicated, leading to unwanted side effects and the wish to reduce their medication. The patients in our study illustrate how guided tapering of antipsychotic medication done jointly with the patient can lead to improved emotional awareness and the development of effective symptom management strategies. This may, in turn, lead to a greater sense of empowerment and identity and give life more meaning, supporting the experience of personal recovery.”

This study, published in BMC Psychiatry, examines the techniques used by the clinic to assist patients during tapering. The patients’ journeys are unique, and the research showcases their individual paths. Although not all patients are entirely successful in discontinuing their medication, the process itself helps to significantly improve their sense of independence and overall recovery.

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The present research aimed to present the diversity of service user experience of careful and closely monitored tapering of antipsychotics. To achieve this goal, the researchers present 6 case studies from a Denmark clinic specializing in guided tapering of antipsychotics.

To be seen at the clinic, service users must be between 18 and 64 years old and have a schizophrenia diagnosis, according to the International Classification of Mental and Behavioral Disorders—10th edition. Additionally, service users must agree to take their prescribed antipsychotics and adhere strictly to the clinic’s tapering schedule. Service users must also be available to speak weekly by telephone and attend monthly appointments.

Exclusion criteria include psychiatric hospitalization in the past six months, substance abuse that could limit the service user’s ability to attend appointments and a high risk of suicide or violence. Service users may also be excluded from clinic services if a psychiatrist concludes tapering may be dangerous.

Each clinic service user is evaluated monthly using the Positive and Negative Syndrome Scale (PANSS), an assessment tool that measures the severity of schizophrenic symptoms. The dose of antipsychotics is reduced by 10% each month. After half the initial dose is reached, tapering slows to a 5% reduction each month. In consultation with clinic staff, the service user decides when to stop tapering. The clinic continues service user observation for six months after the service user chooses to stop tapering or reaches discontinuation.

Service user A had been prescribed the long-acting injectable (LAI) form of aripiprazole for several years. When he came to the clinic, he was prescribed 400 mg/month and had an initial PANSS score of 70. After 12 months of careful tapering, he was able to discontinue his antipsychotic use altogether. At the end of the clinic’s 6-month observational period after discontinuation, service user A had a PANSS score of 38. After 12 months of no antipsychotic use, service user A has not reported any psychotic symptoms.

Service user B had been taking antipsychotics for more than ten years. When he first came to the clinic, service user B was taking 300 mg/month of LAI aripiprazole. His initial PANSS score was 66. After ten months of careful tapering, service user B took his last 80 mg of LAI aripiprazole, and his PANSS score had reduced to 52. After 14 months of antipsychotic discontinuation, service user B has not reported any psychotic symptoms.

Service user C had been taking antipsychotics for several years. When she came to the clinic, she had been taking 20mg/day of aripiprazole for the past year and had an initial PANSS score of 40. After six months, she had tapered her dose down to 5 mg/day and decided to stop the tapering there. Four years after tapering service, user C still hears a supportive voice in her head, but this does not cause any uneasiness or suffering, and she does not experience any other psychotic symptoms.

Service user C reported that tapering her dose made her more emotionally available, and she felt “in charge of her own life.”

Service user D was taking 10 mg/day of aripiprazole and had an initial PANSS score of 34 when he first came to the clinic. After receiving clinic services, service user D revealed that he had not been taking his medication regularly. He was then switched to 200 mg/month of LAI aripiprazole. After four months, his dose was tapered to 120 mg/month. Service user D then began experiencing increased psychotic symptoms, including auditory and visual hallucinations, and his PANSS score increased to 40. He also had to take sick leave from his job. The clinic then adjusted his dose to 300 mg/month. After two months, his PANSS score had dropped to 31, and he was able to return to work. Although he was not able to discontinue his antipsychotic use, service user D reports: “I think the time in the clinic has been good. I’m sad that I couldn’t do without medication, but now I know medication is important for me.”

Service user E was taking 200 mg of LAI aripiprazole every 5th week and had an initial PANSS score of 59 when she came to the clinic. Her aripiprazole dose was changed to 160 mg/month by clinic staff. After two months of tapering service, user E’s PANSS score increased to 62. She reported feelings of being watched and was scared of others. Two weeks later, service user E experienced an increase in psychotic symptoms, including intrusive thoughts, derealisation, and persecutory delusions. Her PANSS score increased to 67, and clinic staff boosted her antipsychotic dose to 300 mg/month with an additional 5 mg/day. Service user E was subsequently hospitalized for 11 days as a result of her psychotic symptoms. She stabilized two months later, and her PANSS score improved to 48.

Service user F had been treated with multiple antipsychotics as well as electroconvulsive therapy for his persistent and treatment-resistant delusions of clairvoyance and telepathy. When service user F came to the clinic, he was taking 175 mg/day of clozapine and 250 mg/day of amisulpride. He had an initial PANSS score of 85. After 16 months, service user F has reduced his clozapine use to 12.5 mg/ day. He has not experienced any increase in psychotic symptoms and has the same level of function as when he first came to the clinic. Service user F is still in the process of tapering and plans to discontinue clozapine use over the next four months.

The authors contend that while tapering antipsychotics may involve some risks:

“Determining whether the current antipsychotic dose is still needed can only be ascertained by reducing the dose, and, as most side effects are dose-dependent, treatment with the lowest effective dose is of crucial importance.”

The authors report that while not all service users are successful in their attempts to taper and/or discontinue antipsychotic use, their attempts at discontinuation and the support of clinic staff give service users a sense of autonomy and empowerment. Four of the six service users included in the current work reported increased emotional awareness, leading to better stress management strategies and increased feelings of recovery.

The authors acknowledge one major limitation of the current research. The 6 cases presented in the current work were chosen to demonstrate the diversity of tapering experiences and are not qualitatively representative of the service user experience of tapering antipsychotics. This means the results are not generalizable to any population.

Discontinuation of antipsychotics is difficult due to the withdrawal symptoms that often accompany the process, especially if careful tapering is not observed. Previous research has found that success in discontinuing antipsychotics is reliant on multiple factors such as internal resources, systematic factors, and access to supportive figures such as medical professionals and friends/family. Numerous studies have found that slow tapering is the best strategy to mitigate the adverse effects of withdrawal, such as psychotic symptoms. These psychotic withdrawal symptoms are often mistaken for a return of the initial psychosis, although this is less likely when slow and careful tapering is observed.

****

Mølgaard, S. N. et. al. (2024). Clinical experiences of guided tapering of antipsychotics for patients with schizophrenia– a case series. BMC Psychiatry 240. (Link)

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The post Case Studies Reveal Patient Empowerment Through Tapering Antipsychotics appeared first on Mad In America.

Additionally, one study examined in the current research, headed by Evagelia Andrianopoulou of the National and Kapodistrian University of Athens, found that children exposed to atypical antipsychotics during the third trimester of pregnancy were much more likely to be diagnosed with autism.

The authors note that in many cases, the developmental delays linked to in-utero antipsychotic exposure were short-lived and disappeared after the exposed child was 6-12 months old. The authors write:

“Our meta-analysis showed a significant association between prenatal exposure to antipsychotics and an increased risk of adverse outcomes in the child related to attention deficit hyperactivity disorder, social-emotional-mental development, and motor delay. Although we believe that the current data are insufficient to conclude that antipsychotics in the perinatal period cause increased morbidity, these results highlight that women receiving antipsychotic drugs in the perinatal period represent a population at higher risk for adverse outcomes for their children.”

The post Study Links Prenatal Antipsychotic Exposure to Developmental Delays and ADHD appeared first on Mad In America.

The authors note they were unable to investigate withdrawal psychosis, withdrawal dyskinesia, rebound psychosis, or supersensitivity psychosis due to a lack of World Health Organization codes (WHO). The authors write:

“Our results suggest that there might be a risk difference for WDS between antipsychotics. Tiotixene, pimozide, and quetiapine were associated with a higher risk of reporting a WDS, whereas this risk was lower with chlorpromazine, clozapine, and fluphenazine. We could not address the issue of withdrawal psychosis, withdrawal dyskinesia, rebound psychosis, or supersensitivity psychosis due to the lack of specific WHO medDRA coded terms to identify potential cases.”

The post Study Highlights Difficulty of Antipsychotic Withdrawal appeared first on Mad In America.

The current research, headed by Luis M. Garcia-Marin of the QIMR Berghofer Medical Research Institute, additionally finds that service users with ADHD and PTSD diagnoses were more likely to discontinue antidepressants while those with higher educational attainment were less likely to do so. The authors write:

“The two most common side effects, reduced sexual function and weight gain, were not associated with increased odds of treatment discontinuation. Anxiety, agitation, suicidal thoughts, vomiting, and rashes were associated with higher odds for treatment discontinuation, as were lifetime diagnoses of PTSD, ADHD, and a higher neuroticism score. Educational attainment showed a negative (protective) association with discontinuation across medications.”

The post Common Side Effects Leading to Antidepressant Discontinuation appeared first on Mad In America.

One of the key findings of the study was the prevalence of TESD among respondents, with approximately 19% reporting sexual dysfunction associated with at least one antidepressant. What’s concerning is that despite the significant impact of sexual dysfunction on patients’ quality of life, many did not discuss these issues with their healthcare providers. This lack of communication underscores the need for improved patient-physician dialogue in the management of depression and antidepressant therapy.

“The impact of TESD was based on respondents’ experiences with current ADs and use of ADs in the prior 12 months rather than identified from retrospective claims data, in which TESD is highly underreported,” the authors write. 

“Labeling for SSRIs, SNRIs, and some serotonin modulators now requires inclusion of information about sexual side effects in the warnings and precautions and patient counseling sections in package inserts of serotonin reuptake inhibitors, as well as in patient medication guides.”

The study also sheds light on the factors influencing patients’ decisions to continue, switch, or discontinue antidepressant treatment. Provider recommendations, treatment efficacy, and medication side effects were identified as major determinants in these decisions, highlighting the importance of personalized care approaches in managing MDD.

The post Antidepressant Use Linked to Sexual Dysfunction, Why Aren’t Prescribers Discussing It? appeared first on Mad In America.

The authors write:

The post SSRI Withdrawal has Social, Cognitive, and Emotional Consequences appeared first on Mad In America.

The goal of the current research was to examine associations between antidepressant use during pregnancy and child development at 2 years old while controlling for maternal depressive and anxiety symptoms. In other words, the authors wanted to ensure the associations they were seeing were related to antidepressant exposure rather than maternal depressive/anxiety symptoms.

To achieve this goal, the authors used data from the 3D Cohort Study of pregnant women in Quebec, Canada. Women were recruited for this research during the first trimester of pregnancy. In order to be included in the 3D cohort Study, women had to be between 18 and 47 years old and speak either French or English. Women were excluded due to current intravenous drug use, severe or life threatening illness, and multiple gestation pregnancies.

Additional inclusion criteria for the current research included the children being tested between 18 and 30 months for language development in either French, English, or Spanish. Children were excluded from the current research if they were diagnosed with a condition known to interfere with child development. In total, the current study included 1,489 mother-child pairs.

The authors used a maternal medication log to assess antidepressant use during each trimester as well as a questionnaire to collect data on antidepressant use in the three months prior to pregnancy. Demographic information was obtained through a prenatal questionnaire during the first trimester. Maternal depression/anxiety was measured using 2 self report surveys, the Center for Epidemiologic Studies – Depression Scale during the first trimester, and the Perceived Stress Scale during the second trimester. Cognitive and motor skills were measured in the children at 2 years of age using the Bayley Scales of Infant and Toddler Development — Third Edition (BSID-III). Language skills were evaluated using a short form of the MacArthur Communicative Development Inventories (MCDI) in which the parents reported which words their children could say from a list of 100 words.

4.1% of mothers reported antidepressant use during pregnancy. Of the participants using antidepressants, 96.2% reported daily use. The data showed a mild association between in utero antidepressant exposure and lower BSID-III scores at 2 years of age. Both fine and gross motor skills were effected. There was no association between in utero antidepressant exposure and cognitive skills as measured by the BSID-III or language skills as measured by the MCDI. Additionally, there was a marginal association between in utero antidepressant exposure and reduced cognitive ability, but this association was not present after multiple linear regression analysis.

The strongest associations found in the current research were for gestation duration and birthweight (longer gestation meant higher birthweight), and depressive symptoms and perceived stress (more perceived stress meant more depressive symptoms).

There was a mild association between maternal depressive symptoms and antidepressant use with a stronger (but still mild) association between antidepressant exposure and perceived stress. Maternal perceived stress was also weakly associated with lower scores for children in measurements of cognitive, fine motor, and language skills. Higher gestational age was marginally related to higher scores in measures of cognitive, language, and fine motor skills. Higher birthweight was marginally related to higher scores when measuring cognitive, fine motor, and gross motor skills.

The authors acknowledge several limitations to the current study. Antidepressant use was low in their participants. This means the researchers were not able to consider the dose, duration, type, or timing of antidepressant exposure in the current study. Medication logs were self reported by participants. This could lead to under-reporting due to misunderstanding or stigma around antidepressant use. The language assessment used only considered vocabulary. Additionally, the language assessment was based on reports by the parents rather than an objective measure of vocabulary. This research was conducted on women from Quebec, Canada with relatively high incomes and levels of education, significantly limiting generalizability to other populations. The authors conclude:

Previous research has linked in utero exposure to antidepressants to an increased risk for speech disorders, neonatal withdrawal syndrome, and poor neonatal outcomes. SSRI exposure in particular has been linked to reduced brain volume and delayed neonatal adaptation. The risks associated with antidepressant use during pregnancy are likely downplayed by many professionals. In an interview with Mad in America, Dr. Adam Urato emphasizes the importance of counseling around the use of psychopharmaceuticals during pregnancy due to the risks associated with these drugs.

****

Tanguay N, Abdelouahab N, Simard M-N, Séguin JR, Marc I, Herba CM, MacLeod AAN, Courtemanche Y, Fraser WD and Muckle G (2023), Antidepressants use during pregnancy and child psychomotor, cognitive and language development at 2 years of age—Results from the 3D Cohort Study. Front. Pharmacol. 14:1252251. doi: 10.3389/fphar.2023.1252251 [full text]

The post Antidepressant Exposure In Utero May Negatively Impact Motor Skills in 2-Year-Old Children appeared first on Mad In America.

According to the current research, led by Le Zhang of the Karolinska Institutet in Sweden, service users are at a 4% greater risk of cardiovascular disease (CVD) for each year of ADHD drug use. The largest increase in risk for cardiovascular disease occurs in the first three years of ADHD drug use. Children and adults see a similar pattern of risk when these drugs are used long-term. The authors write:

The goal of the current research was to examine the link between the use of drugs meant to treat ADHD and the risk of developing CVD. To achieve this goal, the authors used several databases that track diagnoses, prescriptions, and demographics of people residing in Sweden. They used the National Inpatient Register for data on diagnoses, the Swedish Prescribed Drug Register for data on prescriptions, the Longitudinal Integrated Database for Health Insurance and Labour Market studies for socioeconomic data, and the Swedish Cause of Death Register for data on participant deaths.

The authors examined data from everyone living in Sweden aged 6-64 who received an ADHD diagnosis or drugs to treat ADHD between January 1, 2007, and December 31, 2020. Data on 278,027 service users were explored for inclusion in the study.

19,192 service users were excluded due to having a CVD diagnosis before using ADHD drugs, being prescribed ADHD drugs to treat something other than ADHD,  and emigrating or dying before the start of the research. Of the 258,835 service users who met the inclusion criteria, 10,842 received a CVD diagnosis after using drugs meant to treat ADHD. After excluding those with short follow-up periods (3 months or less) and those without a matched control case, the authors had 10,388 service users with a cardiovascular disease diagnosis paired with 51,672 control cases (with no CVD when the research began).

In the overall sample used in the current research, ADHD drug use for 1 to 2 years is associated with a 4% – 9% increased risk of CVD. 2 – 3 years of drug use is associated with a 10% – 15% increased risk of CVD. 3 – 5 years of drug use is associated with 23% – 27% increased risk of CVD. More than five years of drug use is associated with a 20% – 23% increased risk of CVD.

For people between the ages of 6 and 24, ADHD drug use for 1 – 2 years is associated with a 5% – 8% increased risk of CVD. 2 – 3 years of drug use is associated with an 18% – 21% increased risk of CVD. 3 – 5 years of drug use is associated with 22% – 25% increased risk of CVD. More than five years of drug use is associated with a 30% – 35% increased risk of CVD.

For people between the ages of 25 – 64, ADHD drug use for 1 – 2 years is associated with a 5% – 10% increased risk of CVD. 2 – 3 years of drug use is associated with a 6% – 12% increased risk of CVD. 3 – 5 years of drug use is associated with 23% – 29% increased risk of CVD. More than five years of drug use is associated with a 16% – 19% increased risk of CVD.

The authors note that the increased risk of CVD when taking ADHD drugs was mainly present for two conditions: hypertension and arterial disease. The use of ADHD drugs for 3 – 5 years was linked to a 72% increased risk of developing hypertension and a 65% increased risk of developing arterial disease. At five years of ADHD drug use, service users are at 80% increased risk for developing hypertension and 49% increased risk of developing arterial disease. The present research found no increased risk for the use of ADHD drugs in developing arrhythmias, heart failure, ischemic heart disease, thromboembolic disease, or cerebrovascular disease.

The authors acknowledge several limitations to the current study. They used recorded diagnoses of CVD for their analyses, which could have missed some service users with CVD that had not yet been diagnosed. This means the association between ADHD drug use and CVD may be stronger than the present research indicates.

The authors used data on prescriptions of ADHD medication, but there is no guarantee that service users took their medication as prescribed. Due to confounding variables and the observational nature of the study, this research cannot speak to causality, meaning the researchers simply observed a link between ADHD drug use and CVD. They cannot say if the ADHD drugs actually caused CVD. The present research also excluded service users with pre-existing CVD. The data was collected exclusively in Sweden, so generalizability to other populations is limited. The authors conclude:

Previous research has found that long-term use of ADHD drugs is linked to growth suppression. The addictive nature of these drugs also means service users can experience withdrawal symptoms when attempting to discontinue their use. ADHD drug use has also been linked to hallucinations. Adults receiving treatment for ADHD report a low quality of life, and experts have said that in most cases, the risks associated with ADHD drugs outweigh the benefits.

****

Zhang, L. et al. (2023). Attention-Deficit/Hyperactivity Disorder Medications and Long-Term Risk of Cardiovascular Diseases. JAMA Psychiatry. doi.org/10.1001/jamapsychiatry.2023.4294. (Link)

The post ADHD Drugs Linked to Cardiovascular Disease appeared first on Mad In America.

A new research article authored by Kickan Roed, Niels Buus, Julie Midtgaard, and colleagues, published in Qualitative Health Research, finds that there is reluctance among mental health staff to allow service users to make decisions regarding their own treatment. The findings were concerning: despite the increasing debate surrounding the balance between benefits and treatment-related side effects of long-term antipsychotic maintenance, many healthcare professionals remain hesitant to support tapering efforts.

This often leaves the difficult task of tapering medications to the service user alone. The authors write:

The aim of this study was to investigate the perspectives of mental health professionals on reducing the use of antipsychotic medications. The researchers also aimed to determine how mental health staff perceive their rights and responsibilities, as well as the rights and responsibilities of service users.

To achieve this goal, 39 mental health workers from two regions in Denmark were recruited for the study, and six focus groups were conducted between May and June of 2022. Participants included various mental health staff positions, with registered nurses (13) and nurse assistants (15) being the majority. Sixteen participants worked in community services, 13 in inpatient services, and 10 in outpatient services, with an average of 13 years of experience in the mental health field. During the focus group sessions, participants were presented with claims related to the use of antipsychotic drugs in individuals diagnosed with psychotic disorders, to create tension and stimulate discussion.

Three researchers carefully examined the transcripts and audio recordings of each focus group. They observed that mental health staff tended to hold one of three positions about service users tapering antipsychotic drugs and recorded the data around these three positions.

The authors identified the following three positions around the question of tapering antipsychotic drugs:

• “No, patients will eventually realize that they need the medication.”
• “Yes, but tapering means running a big risk of relapse in symptoms.”
• “Yes, we need to welcome risks to support personal recovery.”

During the focus groups, some participants expressed more than one position, but staff members aligned mainly with one position. It is important to note that these positions were not tied to specific settings, professional experience, age, or gender.

Those participants who believed that patients would eventually realize their need for medication saw antipsychotic drugs as effective in reducing symptoms of psychosis. They compared these drugs to other drugs used to treat physical illnesses, such as insulin. They viewed schizophrenia as a chronic illness and believed that symptom remission indicated that antipsychotic drugs were working and should be continued. These participants tended to avoid discussing the adverse effects caused by antipsychotic drugs.

These participants relied heavily on the concepts of “compliance” and “illness insight,” in which not taking antipsychotic drugs when prescribed was seen as non-compliance and evidence that the service user lacked insight into their condition. Tapering was viewed mainly as a negotiation tactic in which staff could eventually persuade the service user to take the full dose.

These participants often questioned the authenticity of service user preferences by, for example, dismissing requests for tapering as service users falling for a trend or acting on impulse. Mental health staff endorsing this position saw themselves as having the right to authorize patient wishes and the responsibility to protect society from psychotic service users. They viewed service users as ideally passively receiving the treatment offered.

Participants endorsing the position “Yes, but tapering means running a big risk of relapse in symptoms” regarded antipsychotic drugs as helpful in controlling symptoms and allowing for recovery from psychotic disorders. While this group viewed antipsychotics as an integral part of treatment, they also acknowledged that drugs were often overused as the cheaper treatment option and likely relied on so heavily as a way to discharge service users quickly.

These participants endorsed tapering as a good clinical practice to be instituted when service users were stable. While tapering was viewed positively in preventing overmedication and adverse drug effects, this group did not view service user preference as primarily important in this process.

This group expressed several concerns about tapering antipsychotic medications. These participants endorsed both the risk of relapse and the risk of drug abuse as reasons not to taper antipsychotic drugs. They believed tapering should only be attempted with service users who had not had multiple psychotic episodes and only during prolonged stable phases.

These mental health workers position themselves as well-informed professionals with the right to protect service users. This means service users are viewed as vulnerable people with the right to be protected from harm.

Participants endorsing the position “Yes, we need to welcome risks to support personal recovery” viewed schizophrenia spectrum disorders as transient with symptoms that come and go. This group was in favor of tapering at the service user’s request as a way of upholding service user rights and honoring their preferences.

They also preferred to reevaluate service user’s prescriptions frequently as service users developed and learned coping strategies, to find the lowest amount of medication that could be used to manage symptoms.

This group typically reported discussing tapering with service users as part of a constant conversation about how prescribed drugs worked for them. They emphasized monitoring service user triggers, stressors, and other warning signs that may signify relapse throughout the tapering process. They also emphasized identifying effective coping strategies to help combat relapse.

Tapering was also viewed as beneficial to recovery, as service users were better able to connect and participate in recovery-oriented activities once they were no longer on high-dose antipsychotic medications.

These mental health workers positioned themselves as having limited knowledge, so they sought the experiential knowledge of the service users they worked with. They also viewed themselves, as a result of constant dialogue with service users, as sometimes knowing the service users better than the service users knew themselves. In their eyes, this gave them the right to speak for service users in decisions around medication and tapering.

There are several limitations to the current research. Participants were recruited exclusively from two Danish regions, severely limiting generalizability to other populations. The sample size is also small, limiting generalizability even within the two Danish regions where the research was conducted. The authors conclude:

Research has shown that antipsychotic drugs have many adverse long-term effects. Antipsychotic use is associated with early death, dementia, sexual dysfunction, and brain damage. It is also common to prescribe these drugs without informed consent.

Some studies suggest that tapering antipsychotic drugs can reduce the risk of psychotic symptoms. However, tapering is best done very slowly to avoid withdrawal symptoms and relapse.

****

Roed, K., Buus, N., Nielsen, J., Christensen, P., & Midtgaard, J. (2023). Mental health Staff’s Perspectives on tapering of Antipsychotic Medication: a focus group study. Qualitative Health Research. https://doi.org/10.1177/10497323231195821  (Link)

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The researchers also found that certain factors made it more likely for an older adult to be prescribed multiple medications, such as being older, unmarried, living in a rural area, having a non-western background, or having physical illnesses. However, having a history of using antidepressants or having a psychiatric diagnosis did not necessarily make it more likely for someone to be prescribed multiple medications.

This study highlights the importance of being aware of the potential risks of polypharmacy, especially in older adults, and the need for healthcare providers to consider the medications they prescribe to their patients carefully. The authors explain:

According to the authors, nearly 1 in 10 older adults deals with depressive symptoms. Antidepressants are commonly the first line of treatment for such patients. Additionally, many of these older adults also have other physical and mental health issues for which drugs are often prescribed. As a result, many older adults take multiple medications at once, which increases the likelihood of PIMs. The current work aimed to examine polypharmacy and PIM in adults aged 65 and older.

The authors examined Denmark’s Civil Registration System data to accomplish this goal. This system collects demographic and healthcare information on everyone born, alive, or residing in the country. For the current study, the authors looked at adults aged 65 and over that redeemed a prescription for antidepressants at a Danish community pharmacy between January 1st, 2015, and December 31st, 2019 (n = 261,479).

The authors used this data to determine when older adults were given multiple prescriptions in addition to antidepressants and to determine when individuals may have been given drugs with dangerous interactions. The authors also looked at demographic information such as sex, age group, education, marital status, ethnicity, place of residence, etc., to determine if any of this information was predictive of polypharmacy and PIMs.

Overall, 73% of the individuals examined were prescribed multiple medications (using at least five concurrent drugs) and antidepressants. However, some subgroups were more at risk for polypharmacy than others, including older adults (83% in those over 86 years old), people with somatic and psychiatric diagnoses (93% in those with a high comorbidity score), and people with higher numbers of hospital visits (87% in those with three or more somatic hospital contacts within the past year).

Overall, 56% of the individuals examined were prescribed PIMs while taking antidepressants. 33% were prescribed at least one drug that could have dangerous interactions with their antidepressants, and 23% were prescribed more than 1. PIMs were most associated with those of older age (81-85 years old), short or medium educational attainment, widowed/separated/single marital status, rural residence, non-western ethnicity, and somatic hospital visits and diagnoses. The authors note that the prescription of PIMs decreased during the period they examined (2015-2019).

The authors acknowledge several limitations to the current work. First, they defined concurrent medication use as medications with at least a 1-day overlap, which could lead to overestimation. Second, the data they used only indicated that people had filled various prescriptions, not that they had taken the prescribed drugs. Third, the authors had no data on medications administered in hospitals or sold over the counter at pharmacies and so could have missed some instances of polypharmacy and PIMs. Fourth, it was not possible to determine the severity of symptoms in the population examined. There may be significant differences in polypharmacy and PIM based on severity that the current work could not address.

Lastly, 25% of the population examined in the current study used antidepressants for the first time. First-time users may have significant differences in terms of concurrent medication use, depression treatment, and comorbidities. The present study’s population was overwhelming Danish and white, drastically limiting generalizability to other people.

The authors conclude:

Other researchers have written about the increase in older adults being prescribed multiple medications simultaneously. This trend is concerning because pharmacies likely miss half of these dangerous drug combinations.

Researchers have commented on the dangers of polypharmacy and inappropriate medication at length, including that older adults on multiple medications, are more likely to go to the hospital for adverse drug reactions. In addition, research has linked polypharmacy to cognitive decline (especially in elderly patients), neuroleptic malignant syndrome, and premature death.

****

Ishtiak-Ahmed, O. Köhler-Forsberg, E.L. Mortensen, et al., Concurrent use of polypharmacy and potentially inappropriate medications with antidepressants in older adults: A nationwide descriptive study in Denmark during 2015–2019, General Hospital Psychiatry (2023).

The post Alarming Overprescription Patterns for Older Adults on Antidepressants appeared first on Mad In America.

The authors state that although “antidepressant discontinuation syndrome” (ADS) (also, and perhaps more accurately, known as antidepressant withdrawal) has been linked to suicidal ideation, no suicide attempt had been reported in the academic literature until the publication of the present work. While the suicide attempt examined here likely had several intertwined causes, the authors argue that antidepressant withdrawal contributed and may have played a central role. They write:

As the chemical imbalance theory of depression has been debunked, the use of antidepressants to correct that fabled imbalance has come under increased scrutiny. Research has shown that antidepressants show no clinically significant difference from placebo in treating depression. The clinically insignificant treatment effect of antidepressants likely only applies to 15% of the population, meaning 85% of people prescribed antidepressants are exposed to the risks with no hope of benefit.

One study found that antidepressants do not improve the quality of life in users. Another piece of research found that antidepressants worsened long-term outcomes for sufferers of depression. Antidepressants pose health risks to babies when exposed during pregnancy, may blunt our ability to feel empathy, and can lead to sexual dysfunction.

Multiple studies have linked antidepressants to increased suicide risk, with one reporting that using antidepressant drugs more than doubles the risk of suicide. These drugs have also been linked to increased instances of violence. Overall, suicide rates did not decrease with the advent of antidepressants. However, suicide rates have risen as the use of antidepressant drugs has become more common.

Likely, antidepressants do not prevent suicide. Moreover, due to the lack of evidence of efficacy in treating depression, and the numerous ill effects linked to antidepressant use, some researchers have even declared that antidepressants should not be used to treat depressive disorders in adults.

A meta-analysis found that antidepressants are ineffective for children and adolescents. In addition, these drugs are linked to increased suicide risk and more attempts at self-harm in children. However, that did not stop psy-professionals from increasing antidepressant prescriptions for children by 41% between 2015 and 2022.

Past research has likely misclassified symptoms of antidepressant withdrawal as a relapse of the initial depression. Another study indicated that antidepressant withdrawal is frequently mislabeled as medically unexplained symptoms, functional neurological disorder, and bodily distress syndrome.

Research has shown that stopping antidepressants can have dangerous long-term effects, with the safest method being very slow tapering of these medications.

The current work presents a case study of a 22-year female previously diagnosed with major depressive disorder, generalized anxiety disorder, alcohol use disorder, and anorexia nervosa. Seven days after stopping her antidepressant, which she had used for two years, she was admitted to an emergency room after taking half a bottle of acetaminophen with alcohol in a suicide attempt.

She reported no suicidal ideation before withdrawing from antidepressants. 4 days after her withdrawal, she began to experience intermittent dizziness, muscle aches and pains, and the sensation of electric shocks. She also reported fatigue, anhedonia, loss of appetite, and suicidal ideation during her stay in the emergency room.

She was admitted to a voluntary inpatient treatment facility where antidepressants were given. After four days, her depressive and ADS symptoms had subsided, and she was discharged from the inpatient facility with a new prescription for antidepressants.

The authors note that ADS is typically linked with antidepressants with a short half-life. However,  in the current case study, ADS was observed in a patient taking an antidepressant with a longer half-life. The authors conclude that the risk of ADS is not binary, with some antidepressants posing a risk while others are safe. Instead, the danger of ADS lies on a spectrum. Given individual differences in metabolizing antidepressants, the authors report that all antidepressant medications could cause ADS.

The authors then point to this case study as exemplifying the difficulty in pinpointing the causes of suicidality. While diagnostic criteria may be helpful to some extent, there are no diagnoses for ADS or suicide. So diagnoses are greatly limited in their ability to predict and trace the causes of suicidal behavior.

In the current case, substance-induced depressive disorder was considered as a possible cause of the suicide attempt. However, the patient reported that her alcohol use was unchanged. It is also possible that chronic alcohol use, as well as ADS, contributed to her suicide attempt. As these threads are impossible to tease apart, the authors state that they cannot rule out multiple causes for her suicide attempt.

They conclude that suicide is difficult to predict and causes are mysterious, so anyone considering withdrawal from antidepressants should do so while under close monitoring.

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Waldvogel, N., & Akira, A. (2022). Antidepressant discontinuation syndrome resulting in a suicide attempt. The Journal of Clinical Psychiatry, 83(6). https://doi.org/10.4088/jcp.22cr14562 (Link)

The post Antidepressant Withdrawal Linked to Suicide Attempt in Case Study appeared first on Mad In America.

The initial review, authored by Taishiro Kishimoto and colleagues, stated that LAI antipsychotics were more effective than oral antipsychotics in reducing hospitalization and relapse. However, on closer scrutiny, Cosgrove and colleagues found that the evidence was of low quality, riddled with bias, and vulnerable to industry corruption. They then provide recommendations on how to reduce bias and improve the quality of evidence when systematic reviews are conducted by authors who have industry ties.

They write:

There has been an ongoing debate about whether LAIs are more effective than oral antipsychotics. MIA previously covered this debate between Cosgrove and Kishimoto and their colleagues, where some of these issues were raised and addressed.

There are serious concerns about patient rights and safety with LAIs, so investigations that find that LAIs are no more effective than oral antipsychotics are especially pertinent to gauge harm and adverse effects. In addition, antipsychotic drug studies tend to have significant reporting bias, with many obscuring adverse outcomes.

Psychiatry has been long plagued by influence from the pharmaceutical industry. More recently, similar criticisms have been levied against other medical sciences. There are obvious financial conflicts of interest that can undermine the integrity of research and more subtle implicit biases that might lead researchers to spin their abstracts or misinterpret data. In addition, researchers have noted deceitful practices common in clinical trials that can manipulate outcomes.

The World Health Organization’s Mental Health Gap Programme conducted the systematic review under investigation. This program has not escaped critique by researchers who question its claims of universality about mental illnesses and the technology it uses to diagnose and intervene.

Cosgrove and colleagues note that this review has significant clinical consequences for patient care and rights and has already received attention as both clinicians and researchers tend to trust systematic reviews. It is thus essential that the evidence these reviews are built on is of superior quality.

Systematic reviews are supposed to comprehensively and robustly comb through relevant studies. However, if the studies under examination are biased or of poor quality, the review can reflect similar bias, and its conclusions can be equally flawed.

The authors recommend that it is crucial that low-quality RCTs (Randomized Controlled Trials) and studies that are at risk of bias (RoB) should undergo sensitivity analyses, especially since it has been repeatedly found that industry-sponsored studies tend to favor industry treatment. A recent Cochrane review directly implicated systematic reviews, finding that reviews authored by those with financial conflicts of interest tend to be of lower quality and favor the industry.

Cosgrove and colleagues critique numerous decisions made by the authors of the systematic review that led to favorable conclusions about LAIs.

First, the studies of the most dubious quality, the pre-post studies, produced the most favorable results for LAIs. The more rigorous Randomized Controlled Trials produced the least favorable results. The review researchers should have explicitly highlighted this for clinicians to exercise informed decisions.

More importantly, patients need accurate and relevant information to make informed decisions about their treatment. This includes knowing about its possible adverse effects. Kishimoto and colleagues did not focus enough on the harm that LAIs can produce or the fact that the number needed to treat in order for one patient to show benefit is 539. Cosgrove and colleagues write:

Kishimoto and colleagues failed to consider the extent to which many studies were not properly randomized, their allocation concealed, and their outcomes blinded. Only 19% of the RCTs included were properly randomized. A sensitivity analysis that excludes investigations with a high risk of bias would have been helpful but was not performed. As MIA had previously reported:

Lastly, the review measured disease-centric outcomes (decreased hospitalization or relapse) and not patient-centric, thus ignoring patient choice, desires, or needs. Disease-centric outcomes are known to be more industry-friendly. As the importance of shared decision-making with clients has become apparent, this decision to ignore what patients value is egregious.

Cosgrove and colleagues also point to the significant extent to which the authors of this review are tied to the pharmaceutical industry. They write:

While these ties do not automatically mean that researchers intentionally manipulated their data, such relationships can create implicit bias and influence how the data is interpreted, what might be highlighted (weak low, quality pre-post studies), and what is left out (harm profiles and patient-centered outcomes).

Since the FDA or the European Medicines Agencies do not regulate systematic reviews, the lack of transparency is deeply concerning, as Kishimoto and colleagues have stated that they will not make their data available for sharing.

The authors lay out several recommendations if unbiased systematic reviews have to be conducted by people with ties to the industry.

First, reviewers must be more transparent and open about their uncertainty and highlight weak evidence since these results have direct consequences for clinical guidelines and thus patient care.

Second, systematic reviews need to enhance their independence from industry conflict. For example, Cochrane requires at least two-thirds of the review team to have no conflicts of interest, but PRISMA guidelines, followed by Kishimoto, do not have this requirement.

Third, reviewers need to be more discerning about the studies they allow into their review. In this case, the low-quality pre-post studies favored LAIs and underestimated the risks involved.

Lastly, it is essential to focus on patient-centric outcomes; studies that focus on the lived experience of patients have highlighted some of the adverse effects of antipsychotics that are overlooked in traditional study designs.

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Cosgrove L, Mintzes B, Bursztajn HJ, D’Ambrozio, G, Shaughnessy AF (2022). Industry effects on evidence: A case of long-acting injectable antipsychotics Accountability in Research. DOI: 10.1080/08989621.2022.2082289 (Link)

The post Industry Corruption in Systematic Review for Injectable Antipsychotics appeared first on Mad In America.

As the evidence against the serotonin theory of depression grows each day, many psychiatrists have claimed that the field never truly embraced this damaging and incorrect theory. To test whether psychiatry championed the serotonin theory of depression, the current work examines highly cited reviews of the causes of depression, highly cited papers that discussed depression and serotonin, and several textbooks published between 1990 and 2012. Despite contemporary psychiatrists’ claims to the contrary, all of the textbooks examined and nearly all academic papers supported this theory despite the lack of evidence.

Despite the psy-disciplines knowing that the serotonin theory was incorrect as far back as 1970, modern psychiatrists are still pushing this debunked theory, even as others claim the psy-disciplines never truly embraced it. The serotonin theory led to the common misunderstanding that depression was caused by a “chemical imbalance” in the brain, which led to an explosion in the sale of antidepressants to treat this supposed chemical imbalance. This series of events, paired with the lack of evidence for the serotonin theory, has caused some researchers to wonder if the serotonin theory was, in truth, a marketing scheme carried out by the pharmaceutical industry.

Although antidepressants are still commonly prescribed to treat depression, their efficacy is questioned. The little evidence that does exist is at high risk for bias. There is no evidence that antidepressants treat a “chemical imbalance” in the brain. The lack of evidence for antidepressant efficacy, paired with the mounting evidence of their detrimental effects, has caused some researchers to declare, “It’s time to stop recommending antidepressants for depression.”

The theory that chemical imbalance in the brain causes depression began in the 1960s. Researchers initially focused on noradrenaline rather than serotonin as the problematic neurotransmitter. However, serotonin replaced noradrenaline as the key neurotransmitter in the chemical imbalance theory in the late 1980s, just as pharmaceutical companies rolled out selective serotonin reuptake inhibitors.

In the 1990s, the pharmaceutical industry began aggressively branding depression as an imbalance of serotonin in the brain and SSRIs as a “magic bullet” that could correct this problem. The American Psychiatric Association parroted this pharmaceutical industry misinformation in a 2005 patient leaflet declaring, “antidepressants may be prescribed to correct imbalances in the levels of chemicals in the brain.”

The branding of depression as a chemical imbalance and SSRIs as the remedy has paralleled a massive increase in antidepressant prescriptions. According to the authors, belief in the debunked chemical imbalance theory is common among people using antidepressants. This belief also encourages people to request antidepressants and discourages them from trying to stop taking these drugs.

In 2005, Jeffrey Lacasse and Jonathan Leo published a paper detailing the disconnect between pharmaceutical industry advertising and what the evidence actually said about chemical imbalance theory. This paper inspired prominent psychiatrists to defend the debunked theory by explaining that a “chemical imbalance” was a metaphor rather than a literal description of reality. As the evidence against chemical imbalance theory mounted, many within the psy-disciplines began claiming that psychiatry had never truly embraced “chemical imbalance theory” but that it was instead pushed by the pharmaceutical industry directly to the public with little involvement from the psy-disciplines.

The authors investigate the claim that the psychiatric profession did not promote serotonin theory by analyzing influential research articles and textbooks published between 1990 and 2012. The current research examines 30 reviews of the causes of depression, 30 highly cited papers that explored the connection between serotonin and depression, and a sample of influential textbooks.

23 of the 30 reviews discussed the chemical imbalance theory of depression. And 2 of the seven that did not discuss chemical imbalances were explicitly dedicated to environmental factors of depression. Eleven reviews thoroughly and unequivocally supported the serotonin theory. Additionally, nine reviews proposed that while serotonin was not the primary or only cause of depression, it was involved in depression in a similar manner described by pharmaceutical industry misinformation. Only one paper came out unequivocally against the chemical imbalance theory.

Most of the papers the current research examined explicitly support the hypothesis that serotonin is involved in depression. Four papers admitted that the connection between serotonin and depression was inconclusive but suggested that serotonin was likely involved in depression.

While all the textbooks acknowledged that the causal relationship between serotonin and depression was an unproven hypothesis, they all provided some support for that unproven hypothesis. In addition, the textbooks all dedicated a disproportionate amount of space to describing serotonin systems and how they may affect depression. The authors conclude:

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Ang B., Horowitz M. & Moncrieff J., Is the chemical imbalance an ‘urban legend’? An exploration of the status of the serotonin theory of depression in the academic literature, SSM – Mental Health (2022), DOI: https://doi.org/10.1016/j.ssmmh.2022.100098.(Link)

The post Did Psychiatry Ever Endorse the Chemical Imbalance Theory of Depression? appeared first on Mad In America.

The authors examined 450 posts from the website www.askapatient.com, 50 posts each relating to the nine most used ADs: sertraline, citalopram, paroxetine, escitalopram, fluoxetine, venlafaxine, duloxetine, mirtazapine, and bupropion. Overall, satisfaction with antidepressant medication was inversely correlated with adverse side effects. Bupropion, citalopram, and venlafaxine showed the highest satisfaction ratings, with sertraline, paroxetine, and fluoxetine showing the most complaints of “emotional blunting.”

The authors write:

Although ADs are commonly prescribed to treat depression, many researchers have criticized their use based on their numerous side effects and dubious efficacy. In addition, the usefulness of ADs is likely overestimated in the academic literature due to corrupt publication practices. The minimal benefits paired with the risks of using these drugs have led some researchers to call for an end to professionals recommending ADs to treat depression.

ADs are commonly prescribed for diagnoses other than depression as well. Although the evidence of usefulness is scant, more than a quarter of Americans with chronic low back pain are prescribed an AD. Although there is little evidence for its efficacy, ADs are also prescribed for many other chronic pain diagnoses such as arthritis, migraines, and fibromyalgia.

ADs have been linked to increased suicide risk and increased instances of violence. One study found that ADs worsen long-term outcomes overall, with people that received no treatment faring better than those that received AD medication.

With prominent psychiatrists declaring that ADs are likely over-prescribed and the numerous negative side effects service users experience from these drugs, many AD users are seeking strategies for discontinuing AD use. Even when advised by medical professionals to discontinue AD use, many service users are afraid to quit the drugs due to biomedical understandings of their condition and the lingering side effects of withdrawing from ADs. Research has found that many popular websites incorrectly promote this biomedical view while systematically overestimating the benefits and underestimating the risks of ADs.

The present study explains that although several different ADs with unique treatment mechanisms exist, there are no biomarkers to indicate which AD may be most beneficial for each service user. In the absence of biological data to predict which drug best treats depression, the authors argue that a suitable alternative method would be to use service user opinion and experience data to decide which drug to prescribe.

The authors used www.askapatient.com, a website dedicated to cataloging service user experiences of different medications, to collect data on opinions around different ADs. The authors randomly selected 1000 posts that reported on one of nine commonly used ADs: sertraline, citalopram, paroxetine, escitalopram, fluoxetine, venlafaxine, duloxetine, mirtazapine, and bupropion. They further pruned these 1000 posts using the following inclusion criteria: the AD was used in an appropriate dosage range, the AD was used for at least four weeks, the indication for the AD had to be reported, and fewer than 50 posts about that AD had already been extracted. The final data set consisted of 450 posts, 50 for each of the nine most used ADs.

Sexual disturbances were most frequently reported with SSRI and SNRI drugs (sertraline, citalopram, paroxetine, escitalopram, fluoxetine, venlafaxine, and duloxetine). Few users of the dopaminergic drugs (mirtazapine and bupropion) experienced sexual disturbances as a side effect of AD use. Sedation was most reported by participants using mirtazapine and fluoxetine. Insomnia was most reported by participants using bupropion.

42% (189 participants) reported adverse emotional effects from AD use. Emotional blunting was reported by 18% of participants, emotional hyperactivity by 14.7%, and withdrawal by 14.7%. Emotional blunting was most common in participants using SSRIs (paroxetine, sertraline, and fluoxetine) and least common in those using bupropion and mirtazapine.

Bupropion had the highest satisfaction rating, with citalopram and venlafaxine a close second. Participants with anxiety disorders and more prolonged treatment durations generally reported more satisfaction with their ADs. The adverse effect most associated with low satisfaction ratings were suicidality, irritability, emotional blunting, cognitive disturbances, and withdrawal symptoms.

The authors acknowledge several limitations to the current research. The data came from a website on which people spontaneously post about their experiences. This means the participants are self-selected and may not represent a proper random sample. The data is self-reported, meaning the participants could be lying or exaggerating. There is also no way to know if the adverse effects reported came from the ADs or other confounding factors present in the participant’s experience. Lastly, the emotional blunting reported by many participants could also be a symptom of the underlying depression rather than an effect of the ADs. The authors conclude:

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Camino S, Strejilevich SA, Godoy A, Smith J, Szmulewicz A (2022). Are all antidepressants the same? The consumer has a point. Psychological Medicine 1–8. https:// doi.org/10.1017/S0033291722000678 (Link)

The post Patient Reports Reveal SSRI Antidepressants Often Lead to Emotional Blunting appeared first on Mad In America.

The researchers also found that 31% of participants would like to stop antipsychotic medication with professional help, and 45% wanted to reduce their dose of antipsychotics. The authors write:

Long-term antipsychotic use has come under scrutiny by voices from within and beyond the psy-disciplines. Antipsychotic use causes several undesirable side effects with dubious evidence for their benefits. For example, research has linked antipsychotic use with increased risk of dementia, brain atrophy in children, worsening cognitive functioning, and breast cancer. Research has also linked antipsychotic use with damage to several parts of the brain.

The largest survey conducted to investigate service user experience of antipsychotics saw more than half of the participants report only negative effects of antipsychotic use. Research has found that greater exposure to antipsychotics is associated with worse long-term outcomes, while discontinuing antipsychotics improves cognitive functioning. The recovery rate in service users who stop using antipsychotics within two years is six times higher than those who use them for longer. Research has also found that these drugs are commonly prescribed without informed consent, with many people never being told about the likely negative effects of their use.

Recently, professional psy organizations have begun to recognize the need to discontinue long-term antipsychotic use, with more than one author publishing guidelines on how to taper antipsychotics to avoid withdrawal symptoms safely. Research has shown tapering to be the most effective method to discontinue antipsychotic use. With many psychiatrists unwilling to help their patients come off these medications, service users have found support for discontinuing their use in internet forums.

The current research investigated service user attitudes towards antipsychotic medication. The authors relied on face-to-face interviews in which they asked structured and open-ended questions about their antipsychotic use. The authors recruited participants from community mental health services and primary care practices throughout London between April 2016 and August 2017.

To be included in the present research, participants had to have a schizophrenia spectrum disorder diagnosis (schizophrenia, schizoaffective disorder, delusional disorder, or other psychotic disorder), at least two previous psychotic episodes, or 1 episode that lasted more than a year, be currently prescribed antipsychotic medication and be stable for the past three months (not requiring acute or inpatient care). In addition, people that were legally compelled to take antipsychotics were excluded from this research.

The majority of participants were diagnosed with schizophrenia (70%), with an additional 18% having a diagnosis of schizoaffective disorder. 36% of participants had been in contact with mental health services for more than 20 years. The mean length of antipsychotic use was 16.5 years.

One-third of the participants were happy with their medications and had no plans or desire to discontinue their use. 19% of participants accepted that they would remain on these drugs long term but did so reluctantly. 18% said they were not content with taking antipsychotics long-term. 24% accepted present antipsychotic use but did not see themselves taking these drugs indefinitely.

When asked about the possibility of discontinuing antipsychotic use with professional help, one-third of the participants said they would definitely like to try. An additional 21% expressed interest but reported serious concerns about the consequences. Another 21% wanted to discontinue use at some time in the future, but not presently. 25% of participants reported they did not want to stop using antipsychotics.

When asked about the possibility of reducing antipsychotic medication with professional help, 45% of participants said they would definitely like to decrease their use, with 13% saying they would be willing to try. 14% of participants were open to reducing their medication in the future but not presently. 21% reported that they did not want to reduce their use of antipsychotic drugs.

Of the participants that did not want to discontinue their antipsychotic use, 70% gave the reason of fear of relapse. Other common reasons given for continuing to use these drugs included: maintaining stability, producing general improvement, reduction in positive symptoms like hallucinations, the calming effect they produce, and reduction of agitation and suicidal thoughts. 24% report they take antipsychotic drugs primarily because a doctor told them to.

Of the participants that wanted to discontinue or reduce their antipsychotic use, 74% gave the reason that they were concerned about the adverse effects and the actual/potential impact on their physical health. The most common adverse effects the participants wanted to avoid were: sedative effects, weight gain, shaking/twitching/stiffness, cognitive/emotional capacity, and sexual functioning.

The authors acknowledge several limitations to the current study. First, responses are likely not generalizable to the greater population. Second, people who agree to participate in research are likely more adherent and accept treatment than others. Third, the sample consisted of people with long histories of mental health service use which likely biases them towards more acceptance of medication use.

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Crellin, N. E., Priebe, S., Morant, N., Lewis, G., Freemantle, N., Johnson, S., Horne, R., Pinfold, V., Kent, L., Smith, R., Darton, K., Cooper, R. E., Long, M., Thompson, J., Gruenwald, L., Freudenthal, R., Stansfeld, J. L., & Moncrieff, J. (2022). An analysis of views about supported reduction or discontinuation of antipsychotic treatment among people with schizophrenia and other psychotic disorders. BMC Psychiatry, 22(1). https://doi.org/10.1186/s12888-022-03822-5 (Link)

The post Many Service Users Interested in Decreasing Antipsychotic Use with Professional Help appeared first on Mad In America.

This view of depression is becoming increasingly mainstream within the psy-disciplines and is currently endorsed by the United Nations, the World Health Organization, and various service user movements. The authors write:

While still very common, the use of antidepressants to treat depression has come under increasing criticism from voices within the psy-disciplines. Prominent voices from within the field argue, for instance, that antidepressants are likely overprescribed.

Recent research has found antidepressant use largely ineffective in treating depression while likely worsening long-term outcomes. Antidepressant use has also been linked to several mild and severe side effects, including emotional numbness, feeling foggy/detached, sexual dysfunction, drowsiness, and an inability to feel empathy. In addition to these common reactions to antidepressants, research has also linked antidepressant use to increased risk of death, increased suicide risk, and an increased risk of violence.

Research has found ECT to be ineffective compared to a placebo for treating depression and preventing suicide while putting service users at increased risk of brain dysfunction and mortality. Audits of ECT use have revealed problems with administration and monitoring of the procedure, making it impossible to guarantee the safety of service users receiving ECT. In addition, ECT can result in permanent memory loss and has caused cognitive impairments in some service users severe enough to prevent them from returning to work.

The current work appears in Psychological Medicine, a leading international journal within the psy-disciplines. This article was commissioned by the journal’s editor, prominent psychiatrist Sir Robin Murray. The inclusion of this piece in a mainstream journal at the request of a well-known psychiatrist may suggest that a paradigm shift is occurring within the psy-disciplines away from the biomedical understanding of depression as a brain disease towards a socially informed model that understands depression mostly as a reaction to difficult life circumstances.

Read, and Moncrieff begin with a critique of the biomedical model of mental health. Antidepressants and ECT are both an attempt to correct an underlying biological issue that supposedly causes depression. However, proponents of these treatments have been unable to pinpoint any biomarkers or show any significant evidence that some biological dysfunction actually causes depression. They write:

Though many within the psy-disciplines subscribe to a biopsychosocial model of mental illness, the psychological and social layers are commonly understood as secondary to the supposed primary underlying biological dysfunction. A dysfunction that, if it does actually exist, we are at present unable to treat.

According to the authors, this results from the dominance of the biomedical model of mental illness. While many within the field pay lip service to the psychological and social causes of depression, the biomedical model forces them to prioritize biological causes and, therefore, biological solutions such as antidepressants and ECT, despite their ineffectiveness and possible negative effects.

According to the authors, antidepressants are likely no better than placebos at easing depression. When research compares antidepressants to placebo in terms of the commonly used Hamilton Depression rating scale, the antidepressants result in a difference of 2 points. Research has shown that a difference of 3 points or less indicates no change, with an 8 point change indicating mild clinical improvement.

The authors note that antidepressant efficacy within these data sets is artificially inflated due to publication bias, meaning the actual advantage over placebo is likely even less than indicated by the 2 point Hamilton Depression rating scale change.

Placebo trials are commonly conducted by pharmaceutical companies with a financial interest in out-performing placebos. Still, these drugs rarely produce better outcomes than a placebo and often fare even worse in clinical practice where they are used to treat a supposed chemical imbalance. The authors write:

Rather than viewing antidepressants as correcting a likely mythical chemical imbalance, the current work envisions antidepressants as a psychoactive drug that alters normal mental activity. Some of these changes may be desirable in people experiencing depression (such as a blunting of emotions). However, many of these drugs effects, such as sexual dysfunction and withdrawal from discontinuation, range from irritating to agonizing for users.

The authors suggest that psy-professionals and service users need to realistically evaluate these drugs’ negative and positive effects rather than asserting their correction of an as of yet undiscovered chemical imbalance.

Similar to antidepressants, ECT is supposed to correct some underlying, as of yet unseen, biological dysfunction to treat depression. This treatment works by damaging the brain, sometimes resulting in a temporary lifting of depressive symptoms. Walter Freeman, an ECT proponent, wrote in 1941:

Again, similar to antidepressants, ECT has shown little advantage over placebo treatments known as sham ECT. The authors write:

In addition to the short-lived, no better than placebo treatment of depressive symptoms, ECT is also associated with memory loss and cognitive impairments.

The authors assert that antidepressants and ECT, rather than treating an underlying illness, alter normal brain activity and occasionally obscure depressive symptoms. While these interventions may seem helpful to alleviate acute depression in the short term, their long-term effects are not well understood and have been detrimental to many people.

The authors point towards a paradigm shift away from the biomedical model of mental illness within the psy-disciplines as necessary to address the true underlying causes of depression: difficult life circumstances. They write:

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Read J, Moncrieff J (2021). Depression: why drugs and electricity are not the answer. Psychological Medicine 1–10. https://doi.org/10.1017/S0033291721005031

The post Shifting Away from ECT and Antidepressants for Depression appeared first on Mad In America.

He points out that these drugs alter our neurobiology, causing sometimes permanent and irreversible changes. He argues that these changes can turn what may have been transient symptoms into chronic, and in some cases, lifelong, mental illness. By using psychotropics to treat symptoms and alleviate acute short-term suffering, practitioners may be paradoxically increasing the duration of suffering.

New research has questioned the efficacy of antidepressants and investigated the potential harms of long-term use. Researchers have noted that in a nine-year follow-up comparing depression patients that took antidepressants versus those that did not, antidepressants appeared to worsen long-term outcomes. This was true even when researchers controlled for depression severity. In addition to the lack of efficacy and potential for harm, antidepressants are likely overprescribed.

Recently, more attention is being paid to the difficulties of withdrawing from antidepressant medications after long-term use. In some cases, recovery from these medications can span decades, with withdrawal symptoms commonly misdiagnosed as a return of the initial mental illness. Even when these drugs work as intended, the adverse effects can be severe.

Similarly, antipsychotics have a wide range of well-documented negative long-term effects. Recent research has shown that antipsychotic use damages several areas of the brain, increases the risk of dementia, and is associated with early death. Researchers have also found that when people diagnosed with schizophrenia discontinue antipsychotic use, their cognitive functioning improves.

Turabian begins by problematizing the overmedicalization of distress by doctors. Both overdiagnosis and misdiagnosis are increasing, and so is the usage of psychotropic drugs, leading to polypharmacy — doing more harm than good. Most importantly, there is a severe shortage of research on the long-term effects of psychopharmaceuticals.

The author has conducted a review and reflected on personal experience to write about the consequences of liberally using psychopharmaceuticals in the long run, especially for issues of anxiety and depression. He specifies that the article should be considered his personal view on the issue.

The author writes that psychiatry mistakenly follows the logic behind antibiotics in calling its treatments antidepressants and antipsychotics. These names are metaphors that assume that psychiatric issues are threats that come from outside and harm the host and thus need to be removed. This metaphor has allowed the discipline to look past the numerous adverse effects of their treatments. The dangerous assumption that keeps harming patients is that what makes them feel better is also what keeps them well.

Turabian lists several reasons we should be wary of antidepressants – the effect sizes of their efficacy in clinical trials are small, long-term effects are unexamined, psychotherapies and psychosocial treatments often show similar or better outcomes without adverse effects of the drugs, and “only one in nine patients benefit from antidepressants.”

Mood disorders are often transient states caused by distressing life circumstances and would have been resolved with “watchful waiting” instead of a premature antidepressant prescription. Many of these drugs produce lasting changes in the bodies of patients. For example, benzodiazepines can lead to neurocognitive changes, and in zebrafish, early exposure to antidepressants can be seen in three generations of offspring. The author emphasizes that one of the main effects of psychotropics is suppression:

Often, in the case of antidepressants, the long-term effects are the opposite of the initial ones, leading to iatrogenic comorbidity. In other words, antidepressants can lead to chronic depression and increase susceptibility to depressive episodes. Similar findings have been reported for psychosis where dopamine supersensitivity can be caused by long-term use of antipsychotics, in turn leading to more florid psychosis.

Biomedical understandings of anxiety and depression can also harm patients by blocking recovery. Instead of seeing oneself as changing and responsive to the environment, these neurochemical understandings force people to see (and experience) their distress as internal and permanent. It leads them to ignore the social conditions that might be causing it. The disease model focuses on symptom removal (as is true for most medicine), and thus the patient’s internal state is often considered insignificant. The experience of anxiety or depression becomes meaningless, and they are only seen as states to be eradicated.

On the other hand, non-biological models often consider symptoms and distress to be meaningful, context-sensitive, and even useful as they can make a person re-evaluate their self, relationships, and world. This points to an essential difference in the way these two models see causality:

Thus, in focusing on symptoms removal and not meaning, drugs often render the patient passive – numbing feelings, thwarting problem-solving, hindering memory processes and concentration, and creating dependence. Consequently, they hinder the processes of psychotherapy that could have helped the patient.

Turabian concludes by noting that these drugs have numerous effects at multiple levels beyond just neurotransmitter communication. The impact on people, such as changes in thoughts, moods, feelings, behavior, etc., are often a cause of side effects such as loss of cortical gray matter. He concludes:

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Turabian, J (2021). Psychotropic Drugs Originate Permanent Biological Changes that go Against Resolution of Mental Health Problems. A View from the General Medicine. Journal of Addictive Disorders and Mental Health. (Link)

The post Overuse of Psychiatric Drugs is Worsening Public Mental Health, Doctor Argues appeared first on Mad In America.

Growing up in 1970’s Oakland and Berkeley, California, Hansen witnessed the consequences of deinstitutionalization and mass incarceration policies firsthand. Losing family members to both the prison and mental health systems gave her a personal understanding of the social and structural failures she interrogates in her work today. She also draws on the principles she learned as a participant in AIDS-related activism to mobilize community organizations and champion mutual aid groups in combatting our current mental health crises.

In this interview, Hansen discusses how race and class affect psychiatric diagnoses and subsequent treatment, the moral implications of psychiatric diagnosis, structural competency, and more.

The transcript below has been edited for length and clarity. Listen to the audio of the interview here.

Richard Sears: First, will you tell us a bit about what brought you to your work? How did you end up interested in psychiatry and anthropology? More specifically, how did you end up looking at these questions about intersectionality and psychiatric diagnosis?

Helena Hansen: Since I’m speaking to a contributor to Mad in America, let’s start by saying that it’s probably because I was “mad,” as in angry.

My childhood was profoundly shaped by the mental health system in California. I grew up in the seventies in Oakland and Berkeley, California, at the height of deinstitutionalization. The mental hospitals were being closed with a verbalized motive of getting people out into the community and not confined in mental hospitals, but there was nothing on the other end, no community services, no supports. I remember on my way to school and back, there were a lot of people sleeping on the streets, and I had to find my way through a maze of people who clearly had just been totally abandoned.

The other part of that story is that mass incarceration was starting, and many people who otherwise might have been in the mental health care system were instead in the carceral system. It got personal in that three of my uncles were caught up in it. I grew up largely in the home of my grandparents. My mother was a single mother raising me in Oakland, and my grandparents had a cycle of my uncles in and out as they lost their own independent housing and had to move home. They struggled with drugs and what we might have called a psychiatric crisis. They were often brought home by the police, and they went in and out of jail.

One of them ended up dying in a mental hospital. He got one of the few remaining beds in California but probably was medicated with antipsychotics that ended up stopping his heart. Two of my uncles were arrested on drug charges. They were probably using drugs because of the mental distress that they were going through. It was a really hard time to be a black man in Oakland and Berkeley.

They were both involved in the civil rights movement and had experienced a lot of repression and oppression. So likely, as a result, they had issues that we could label with psychiatric diagnoses, basically distress. I think drug use was a way of coping for them. But, unfortunately, they ended up in the prison system with those struggles.

With the war on drugs came a lot of police surveillance and arrests. This is what I grew up with. I grew up in a home where my grandparents, my mother, and I were always in fear that we’d come home to a police car. There was a lot of anxiety, a lot of emotional distress.

When I got into medical school, it was on the heels of my own participation in AIDS activism. I graduated college in the early nineties, just as AIDS activism was really peaking. The thing that inspired me about AIDS activism was the grassroots nature of it. In a very creative way, the people directly affected by HIV were on the frontlines. They had a lot of success, making changes in public policy and medical practice and shifting what research and clinical care got funded.

That really inspired me. I think it was because I had seen the other end. I’d seen how horrible it can be to have no voice in the mental healthcare system, no voice in drug policy. So, inspired by AIDS activism, I decided to try to make the change from within medicine. I majored in biology, and it seemed like a natural step to get into medicine.

I wanted to study medicine with another kind of political consciousness that was deliberate from the beginning. That’s why I combined it with anthropology. I found that anthropology was a counter-cultural way of looking at questions of medical practice and the assumptions that psychiatrists and others brought to their work.

Sears: Can you talk a bit about how race, class, gender, etc., can affect psychiatric diagnosis?

Hansen: I’ll try to answer it from two different angles.

The first is a bit more intuitive. I was a psychiatry resident at NYU in 2005 and trained in Bellevue hospital, which was New York City’s largest public hospital. It takes people from all over the city and has historically been known for its psychiatric care. Many of the patients were on Medicaid or uninsured. We would get people from the homeless shelters. We would get people from low-income areas in the South Bronx, Harlem. We got new immigrants looking for mental health care. We got people from all over.

The very high-end New York University (NYU) Langone Hospital was just three blocks up the street. It accepts private insurance on the psychiatric unit. A lot of the patients we saw there were sons and daughters of psychiatrists, doctors, lawyers, celebrities, etc.

What really struck many of my classmates in our psychiatry training and me was the contrast between how we saw people treated at the exclusive NYU hospital and how we saw people treated at Bellevue. We saw people who would come in with very similar symptoms but get radically different diagnoses.

The reason for that radical difference was really the life circumstance and the goals of “care.” For example, somebody comes into Bellevue with mood symptoms, with hallucinations. Let’s say they’re coming from the homeless shelter or they’re unemployed or uninsured. We would really steer them towards a schizophrenia diagnosis.

At Bellevue, because it was so understaffed, a lot of times, what was used to treat schizophrenia would be highly sedating antipsychotics like Zyprexa. The purpose was to keep people quiet because we’re dealing with an overcrowded and understaffed ward. These medications come with some serious side effects (including weight gain, diabetes, and heart disease). Still, we used the diagnosis because it was easier for people to get Social Security if they had a schizophrenia diagnosis. It was well-intentioned.

Classism also likely played a role here because so many of us were worried for our safety. My classmates grew up in neighborhoods where they did not encounter black men as friends or as colleagues. And they saw them on TV as very violent individuals. This was, of course, part of the logic. We want to keep these large black men quiet. But some of it was well-intentioned to grant access to Social Security benefits. Otherwise, they don’t have anything to survive on once we discharge them. With the schizophrenia diagnosis, maybe they can qualify for what tiny amount of supportive housing there might be out there in New York.

Contrast that with Langone Hospital, where we’re confronted with the daughter of a fellow psychiatrist who might’ve been in graduate school, and we’re trying to get them back on track to have a professional career. You don’t want to give somebody like that a schizophrenia diagnosis. That’s not going to help them finish grad school or get a job so that a bipolar disorder diagnosis might be more appropriate. That’s thought of as somehow less severe, less threatening to a professional career. The medications we used were designed to keep them alert and enable them to finish their studies or succeed as professionals.

It was race and class reasoning; it’s not just out of the blue. It’s not like randomly doctors think, “oh, I hate black people.” It’s a part of an entire system in this country of race and class hierarchy. Medical care is just one little piece of that. Medical care is designed to keep people where they are in the hierarchy. That’s one version of the story.

There is a second way to look at this problem. Over the past decade, I’ve been studying the pharma industries and what I’ve come to call racial capitalism. Through interviews with people in different parts of the pharmaceutical industry—people who are doing the drug development, people who are visiting doctors and basically advertising their products through promotional dinners and gifts and things like that, people who are prescribing and people who are consuming—I’ve discovered that there’s a whole race and class logic to how the pharmaceutical industry is set up. For example, it’s entrenched in psychotropic medications like antipsychotics and antidepressants because these are considered “lifestyle drugs.”

There’s no explicit biomarker. You can’t do a blood test to decide if someone should get an antidepressant or an antipsychotic. It’s an expandable category, and you can designate who the people that should get these medications are, which means that it has been a gold mine for pharmaceutical industries.

Since the era of Prozac, pharma industries have really focused a lot on psychotropic drugs as a category because they’ve been extremely lucrative. The more they’ve been able to define emotional distress as a biologically treatable brain disorder, the more money they’ve made. Race and class logics are integral to that.

We have a system in our country of race and class apartheid regarding who has access to what kinds of medical care. We have a public and uninsured track, and then we have a privately insured track. So the pharma industries have been extremely deliberate about which drugs they are developing and marketing for which market. It’s very clear that at least two and probably more markets divide along these lines. Psychotropic drugs are right in the center of that.

I already mentioned the highly sedating antipsychotics that were used at Bellevue Hospital when I was training. The pharma industry is very savvy about this stuff, and they do it in ways implicit and secretive as well as explicit. They market drugs according to race and class strata, so you’re going to see a lot more of those heavily sedating antipsychotics in hospitals like Bellevue. You’re going to see drugs like Abilify, which don’t have all those side effects, being marketed to a white clientele in private hospitals.

I’ll give you another example. ADHD is a diagnosis that has been controversial because it’s a category that’s radically expanded over the past few decades, a lot of it thanks to pharmaceutical industry marketing in the United States. We prescribe 10 times as much medication for ADHD than many European countries that outlaw the kind of marketing and promotions that we have here. Stimulants have been shown to improve academic performance in children, whether or not they meet the criteria for ADHD diagnosis. So, what you see is a market segment for ADHD medication, stimulants in particular, among more affluent, largely white children.

On the other hand, children who meet the criteria for ADHD who are poor and largely black and brown overwhelmingly get prescribed off-label antipsychotics because they come to medical attention through teachers who feel that they need to be behaviorally controlled in the classroom. So there’s been a very deliberate marketing strategy underlying that as well. Teachers and parents in public schools are subject to a certain kind of marketing around medications. Then more affluent parents are subject to another kind of marketing around stimulants that improve educational outcomes.

I’ve discovered that race and class are absolutely baked into our pharmaceutical industries and mental health system. I do think the fact that “mental illness” is so politically marginalized makes it even easier for pharmaceutical industries to take advantage of healthcare systems and to be negligent about the implications of this stuff.

Sears: Are certain groups more at risk of misdiagnosis and mistreatment in psychiatry than others?

Hansen: I think the “mental health care system”—and I put that in quotes because it’s not a system to promote mental health—reflects the political disempowerment or impairment of the groups involved.

What my uncles experienced is just a reflection of where they stood in the political-economic hierarchy of society. I think that mental health care is like an index of where people are in the power hierarchy. I’m not going to say that wealthy people in this country necessarily have good mental health care. I think we’re in a system that is crazy-making for everyone.

An interesting study came out almost a decade ago by social epidemiologists Richard Wilkinson and Kate Pickett. They compare industrialized nations by health outcomes against measures of social inequality. What they find is that the more socially unequal the country, the worse the health outcomes.

For example, in the US, we have the worst distribution of income. We also always come out the worst in measures of mental and physical health. I want to emphasize that the severe inequalities we have in this country give us all bad physical and mental health outcomes. The same study found that the wealthiest people in industrialized nations in the most unequal countries (like the US) have worse life expectancies and worse mental health outcomes than the wealthiest people in more equal countries. The soundbite from the study was that inequalities are bad, even for the rich.

It’s well documented that poor, black, and brown people don’t get a treatment that follows professional society guidelines. They get a lot more in the way of dangerous over-sedating drugs and multiple drugs that interact, which reflects that the doctor hasn’t taken any time to think through the regimen or the side effects. They get restrained a lot more often.

I was describing the wards at Bellevue that were totally overcrowded and understaffed. You had frightened nurses and frightened floor attendants that were very quick to put people in four-point restraints or put them in a seclusion room. In contrast, in a better-funded ward, like up the street at the NYU hospital, you had staff trying to talk people down if they were having an emotional outburst. They had soothing music and calming rituals instead of four-point restraints.

These days what you’re seeing is both too much “care,” in the way of over-medicating people and over restraining people, as well as abandonment. Insurance companies will only pay for a few days of hospitalization. So what you get is people coming in serious crises, getting a bunch of strong antipsychotics to sedate them, getting into restraints, and then being released a few days later with no plans for housing support, no plans for social support, and no plans for continuity of care.

I don’t think the answer is more medications and more restraints. I think the answer is we must look at what kinds of community supports we have. We need a more equal distribution of resources and the things that would develop our communities economically. I’m not advocating for more restraints or more polypharmacy; I’m saying that we have really used “mental illness” as a way of abandoning a large swath of people who are largely poor. Remember, wealthy people don’t get the best mental health treatment in unequal countries either. I think the answer is that we need a better society.

There are ways forward, but one of the biggest challenges is the unraveling of the social fabric of our communities. Our communities have a lot of disorganization, and people are becoming socially isolated. Sociologists have documented that many signs of distress, including drug overdose, are directly linked to feelings of isolation and the disintegration of community organizations and sources of social support.

Instead of debating how we can get more medications to people, we need to debate how we can foster community, economic, and social development. How can we support social connections and supportive communities?

Sears: What can we do to start rebuilding our communities?

Hansen: Over the past decade, my colleagues and I have been building a movement that we call structural competency.

I think many of us have been exposed to the idea of cultural competency. The idea is that if we’re going to try to address differences in health outcomes and healthcare by race, class, etc., we need to pay attention to culture. That sounds good, but in practice, what it’s meant in medicine and psychiatry has been that we kind of blame the victim. We act as though the reason why the outcomes are so bad for poor people, for black and brown people, is their beliefs and behaviors. We really need to look at the economic decline and the accompanying social isolation and disintegration of community organizations and support.

We need to be looking not at the level of an individual patient’s beliefs and behaviors, but we need to look at what’s available in the community. Who can we partner with in these communities in community organizations, mutual aid organizations, etc.? Who can we partner with to support our patients? I’m using the language of patients because I work in a psychiatry department, but I realize that there’s a movement not to refer to people as patients. What can we do to help people in their communities? What about institutions that are relevant to people’s health outcomes, but aren’t really part of the healthcare system, like housing agencies, criminal legal systems, schools, and parks? How can we collaborate with them for health-promoting initiatives and public policies?

There are lots of things that psychiatrists and other clinical practitioners can do to promote health in these areas. It does involve a lot of collaboration because we don’t necessarily learn how to do community organizing in medical school and clinical training. Still, there’s a lot we can do if we partner with community organizers.

I’m inspired by the new generation of mental health practitioners because I see residents and interns, and trainees do things very differently. I’ll give you an example. A group of residents in New Haven at Yale that I’ve been working with have been partnering with urban farms. They’ve been partnering with organizations that assist undocumented migrants. They’ve been partnering with mutual aid organizations, including theater and arts organizations that have in them people with lived experience of serious mental health distress. They’re also working with policymakers. They hosted a series of conferences called Rebellious Psychiatry. They invited policymakers and started to think about how mental health practitioners can partner with people with lived experience to get better public policies in place. As a result, they managed to get some laws regarding affordable housing and supportive housing in Connecticut passed. I look to things like that as inspiration for how we can do our business differently.

We need to address the root of the problem. The root of the problem is not the beliefs and behaviors of individual patients. It is rather this pathogenic society with seriously oppressive public policies. The issues with affordable housing and bad economic policies have left people with insecure employment and no benefits. These people are stranded and hurting. One thing that we have that’s great in this country is a history of community and grassroots organizing and mutual aid. And again, I take my inspiration from the AIDS epidemic. AIDS activism achieved a whole lot.

Sears: A lot of moving parts there, but there are definitely things we can do, I think.

Hansen: Mad in America is no small part of it.

Sears: I agree. Can you talk to us about what patients or service users can do to protect themselves in these healthcare systems?

Hansen: I mentioned mutual aid, and some of these organizations are national in scope. Some are founded and run by people with lived experience.

One such organization is the Icarus Project. They have, for example, a guide to tapering off medications, which is something that psychiatrists are not trained to do. I’ve seen people from the Icarus Project bring this guide into their psychiatrists and teach their psychiatrists how to taper them off of certain medications that are problematic for them.

There’s a lot that mutual aid organizations can do to help people understand the problems they’re having with the mental health system differently and understand their rights and how to push back.

One of the huge problems with giving somebody a psychiatric diagnosis is that it automatically associates them with all of the stereotypes and all the baggage of images of people with psychiatric diagnoses over the past century. It really weighs people down. Not only does it objectively make it harder for them to get jobs and housing etc., but I think it also makes it harder for people to feel good about themselves, to have faith in themselves and their own internal compass.

One thing that’s great about mutual aid organizations is that when you’re with other people who’ve been through that, you begin to understand yourself not as a flawed individual but rather as somebody who’s felt the impact of an oppressive system. That makes all the difference in the world because it puts you in the position to fight back, to fight for your place at the table. That’s why I think mutual aid is so critical in all of this.

I have colleagues that are threatened by that. I know psychiatrists who will say, “Mutual aid organizations are antipsychiatry, they’re out to get me, and they’re run by people who are deluded, people who think they don’t have a problem and they don’t realize they need help.” I think that kind of defensiveness is a sign of the insecurity that we have in our field. I think it’s an unfortunate cop-out because we know that psychiatry as a field is not having the positive impact that it should.

We know there’s something wrong with the way we practice. If we could just be curious and if we could just learn from people with lived experience, we’d see that mutual aid is one of the most powerful things that people can seek out for themselves.

We’ve been encouraging people to seek out mutual aid organizations. We have encouraged them to question their diagnoses and really think carefully about what kinds of treatments seem to benefit them or not. I hope more of my colleagues do not react like they’re threatened and are much more curious and supportive.

Sears: How do issues of morality end up influencing psychiatric diagnosis?

Hansen: Psychiatric diagnoses can be weaponized against people and can take away their legitimacy as moral actors. So I think one of our most important jobs, if we’re going to advocate for a better approach to mental distress, is to provide the conditions for people to get their moral agency back. That’s really what I was talking about regarding trusting one’s own compass.

One of the first things a mainstream psychiatrist (the kind who might get defensive about mutual aid) might do is question the judgment of the person who is coming in distress. We use the term “insight.” If somebody is hospitalized, day by day, we must document in the patient chart how much insight they have about their mental illness. When somebody accepts our terms of their mental illness, then they have insight. That’s what we reward, and that’s when we can discharge them. I think it reflects the power inequalities involved and how we’ve misused psychiatric care to enforce power hierarchies. Therapeutically, it’s exactly the wrong approach.

What we want to do is help people to trust themselves because that’s part of the crisis that they may be having. Often, they’re trying to express a critical truth. I think the stereotype that the media and the public have is that if somebody is psychotic, it means they just have wildly crazy and unpredictable associations in their head that aren’t at all rooted in reality. I think that’s totally wrong.

If you spend enough time with people who have a psychotic episode, you realize that there is a coherence to the story they’re telling; there’s some truth there. If you spend enough time with them and if they spend enough time with themselves, they can get to that. It often has to do with trauma. It often has to do with a really horrifying experience they’ve had that they couldn’t resolve in another way—other than going to the kind of symbolic realm of psychosis—but there’s a truth there. I think the first thing to do is to acknowledge that truth.

Sears: You’ve written about “context-free neuroscience” in psychiatry. What do you mean by this?

Hansen: Psychiatrists would really love to see mental health treatment become applied neuroscience. They just want to boil everything down to the brain because that would give the field of psychiatry a lot more prestige. It would give it a veneer of scientific control. A lot of my colleagues think it would get rid of the stigma of psychiatric diagnosis. Now that is a delusion.

When my sociology colleagues actually research this, they find that people who believe in the brain disease model actually stigmatize people with psychiatric diagnoses more because they think, “Oh, it’s biological, It’s something that is hereditary that can’t be changed. I wouldn’t want my son or daughter marrying anybody with that diagnosis. I don’t want to move in next to them.”

It’s a fallacy, but many of my colleagues think if we could just boil it down to the brain, it’ll de-stigmatize mental illness because it’ll hold people blameless. It doesn’t necessarily hold them blameless, but it does take away their moral agency. It consigns people to a category where you just can’t expect them to participate in their own decision-making and so forth.

These days, we in psychiatry are beholden to this idea that neuroscience will produce magic bullet solutions on the molecular level and that we can identify everything in the brain. This ideology ends up reinforcing the same class and race hierarchies that we were discussing. It presents itself as neutral because you’re talking about a brain. It doesn’t matter where somebody lives. It doesn’t matter the color of their skin, what their job is. It’s just the brain. It shouldn’t matter where they live, what they do, who they are.

This kind of molecular universalism is expressed in the kinds of images put in psychiatric journals these days. You’ll see an image of a brain scan. That is the image of contemporary psychiatric research; it’s just the brain. It doesn’t matter who this person is.

What that ends up doing is completely distracting us as psychiatrists, policymakers, and consumers from all of the social determinants of health. We end up not asking questions like, why is it that certain groups suffer so much more than others? Why are certain groups so much more likely to get certain diagnoses? Why are they so much more likely to die prematurely with this diagnosis? It erases neighborhood conditions. It erases public policies. It erases race and class. It prevents asking about housing policy and how it relates to elevated mortality among people who have psychiatric diagnoses. What about drug war policies?

That’s what I mean by context-free neuroscience. I think that ideology, that kind of worship of the brain and molecular solutions, has worsened many of our mental health problems because it’s detracted from any kind of attention or investment in the social determinants.

Sears: Can you recall any significant pushback or criticism you’ve experienced due to your critical view of psychiatry? Is it ever tough to be a psychiatrist with a critical perspective?

Hansen: Thank you for that question. I feel very lucky. I think being an anthropologist has insulated me on the one hand. On the other hand, I don’t have the National Institute of Mental Health running after me trying to give me grants. I’ve gotten a little bit of money from the National Institute on Drug Abuse when I managed to disguise myself as somebody who could produce data supporting the benefits of buprenorphine and medication for opioid dependence. But I haven’t had a lot of NIH funding, and I certainly don’t get asked to serve as a division chief or chair or anything.

But there are these rare pockets where everybody’s running to me for help in addressing a crisis. I’ll give you an example. I (and colleagues like me) are typically pretty marginalized within psychiatry. Over the past year, we have seen huge inequalities in COVID deaths by race, and huge upticks in overdose deaths, particularly among black and brown people, but also many poor white people. There’s all this emphasis right now on racism, inequalities, and health. So, psychiatry departments and the American Psychiatric Association are scrambling to show that they’re attending to these issues. All of a sudden, I’m being invited to serve in many positions I wasn’t before.

This year has been an interesting experiment, and I think groups like Black Lives Matter had a lot to do with that. When you ratchet things up to a certain level of attention, then you can get an institutional response. I think that my fear is that this is just for show and that it’s temporary. Maybe as soon as the cameras are gone, we’re going to go back to ignoring social determinants.

That’s what my colleagues and I are trying to figure out: How can we keep the pressure on around social determinants of mental health and structural racism in mental health? How can we make sure that this continues and that it builds? I don’t have the answer to that, but I think it has something to do with organizing efforts like Mad in America to push back against the status quo.

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MIA Reports are supported, in part, by a grant from the Open Society Foundations

The post Combatting Structural Racism and Classism in Psychiatry: An Interview with Helena Hansen appeared first on Mad In America.

The authors also explain that while these medications can be useful and minimally harmful for short-term treatment, the risk of adverse effects from long-term use makes discontinuation an attractive option for many. They write:

The use of antipsychotic medications has come under increasing scrutiny as their adverse long-term effects have begun to surface in academic literature. Some authors have pointed to the poor long-term outcomes for people experiencing first-episode psychosis with greater exposure to antipsychotics. There is also research suggesting the experience of people using antipsychotics is mostly negative and that as few as 1 in 5 people may experience any benefits beyond placebo.

As the current research suggests, service user choice and shared decision making (as opposed to decisions made by authorities on the part of the service user) have become increasingly important in healthcare. While psychiatry has had some unique issues with service user agency and shared decision making, the current authors are not the first to suggest that antipsychotic use should ultimately be a choice.

Evidence has existed since at least the 1970s that drug-induced dopamine supersensitivity can cause psychosis. In line with the current research, Horowitz has found in past research that sudden discontinuation of antipsychotics could cause a relapse of psychosis not seen in low-dose patients using antipsychotics.

There is also evidence that “treatment-resistant” schizophrenia is strongly linked to dopamine hypersensitivity, and that same supersensitivity can even cause once useful drugs to lose their efficacy over time.

While the current research acknowledges the usefulness of antipsychotics in short-term treatment, the authors are warier of the long-term adverse effects outweighing the benefits. They also point to patient preference as playing an important role in the treatment and note that when psychiatrists ignore patient preference for discontinuation of antipsychotic medications, this may cause an abrupt and dangerous cessation resulting in withdrawal symptoms rather than a steady, expert-assisted tapering.

According to the authors, antipsychotics work by acting as an antagonist for many of our receptors (blocks them from being activated), perhaps dopamine most importantly. If we are exposed to dopamine antagonists over a long enough period of time, our brains react by creating more dopamine receptor sites. This state of heightened dopamine receptors is what they call dopamine hypersensitivity.

When an antipsychotic is abruptly discontinued, the heightened dopamine receptors (that had been blocked by the drug) are flooded with dopamine. A similar process happens with many neurotransmitters and their receptor sites under the influence of antipsychotics. This is correlated with many adverse withdrawal effects.

The authors divide these withdrawal symptoms into three groups: somatic symptoms, motor symptoms, and psychological symptoms. Somatic withdrawal symptoms, such as nausea, sweating, and diarrhea, usually start within a few days and last a few weeks. These symptoms are likely a result of acetylcholine antagonism and the subsequent flood during antipsychotic discontinuation. Motor withdrawal symptoms can include dyskinesia, parkinsonism, and neuroleptic malignant syndrome.

These adverse effects can last for months or years. Psychological withdrawal symptoms include psychosis, persecutory delusions, and other psychotic symptoms (often misunderstood as a return of the initial psychosis rather than a withdrawal symptom).

The authors argue that often the appearance of psychosis after discontinuing antipsychotics is a withdrawal symptom rather than a return of the initial psychosis. They present two pieces of evidence to support this argument.

First are the instances of people that have never experienced psychosis having psychotic symptoms after abrupt withdrawal from dopamine antagonists. In some cases, these symptoms persisted until the dopamine antagonists were readministered. For example, in one case where a dopamine antagonist was not reintroduced, the psychotic symptoms persisted for 10 months.

The authors also point to the timing of relapse psychosis in people diagnosed with schizophrenia. Research has found that 48% of psychotic relapse occurs within 12 months of discontinuing antipsychotics, with 40% of those occurring in the first 6 months. After the initial 12 month period, psychosis relapse was observed at only 2% per year. Additionally, evidence suggests that the longer a patient uses antipsychotics, the greater their risk of psychosis during withdrawal.

Although the current standard guidelines ignore tapering, the current research suggests that the worst of these withdrawal symptoms can be avoided by slowly discontinuing these medications rather than stopping them abruptly. This is because when a person gradually tapers down the dose of antipsychotics, the number of dopamine receptors does not change radically, and we do not experience the dopamine hypersensitivity that likely leads to psychotic withdrawal symptoms.

The authors recommend spending months or more likely years coming off of these drugs. Then, to safely discontinue their use, a person would need to reduce the dose by one quarter to one half and maintain that new dose for 3-6 months. They would then repeat the process until they take about 1/40 of the initial dose before complete discontinuation.

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Horowitz, M. A., Jauhar, S., Natesan, S., Murray, R. M., & Taylor, D. (2021). A method for tapering antipsychotic treatment that may minimize the risk of relapse. Schizophrenia Bulletin, 47(4), 1116–1129. (Link)

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