Schizophrenia and bipolar disorder are serious mental illnesses that affect both males and females, but research in Acta Psychiatrica Scandinavica indicates that sex may influence the characteristics and course of these conditions.
The research included 1516 individuals from the multicentre PsyCourse Study: 543 with bipolar disorder, 517 with schizophrenia, and 456 healthy controls.
Several differences between groups and sexes were identified in age at diagnosis, age at treatment, illness duration, illicit drug use, and smoking. For example, females in the schizophrenia group were older than males at first outpatient treatment compared with females in the bipolar disorder group. Moreover, those who were older at first outpatient treatment presented a longer duration of illness. Regarding substance use, the highest rates were observed in males with schizophrenia. People with bipolar disorder showed better functioning and neurocognitive performance than those with schizophrenia. Among individuals with bipolar disorder, females reported better performance in verbal memory and psychomotor speed than males. Both females and males with serious mental illnesses showed higher rates of thyroid alterations than healthy controls.
“Our findings reveal a clear message: sex-sensitive treatment is essential for improving clinical outcomes, promoting healthy habits, and managing comorbidities,” said corresponding author Anabel Martinez-Arán, PhD, of the Hospital Clinic of Barcelona.
Every 34 seconds, someone in the United States dies from heart disease. As nearly half of the country suffers from some form of cardiovascular disease (CVD), another 1 in 4 adults experience a mental health disorder in their lifetime, signalling an inevitable overlap.
Now, a new report from Emory University shows that certain mental health conditions escalate the risk of developing heart disease by 50–100% – and adverse outcomes from existing heart conditions by 60–170%.
The report, published in The Lancet Regional Health-Europe, summarises cardiovascular health disparities among those diagnosed with depression, anxiety, schizophrenia, bipolar and post-traumatic stress disorders (PTSD). The article is part of a series aiming to raise awareness around disparities in CVD health in four populations: women, the elderly, racial minorities and those with mental health conditions.
Emory University professor Viola Vaccarino, MD, PhD, led this metareview linking mental health conditions to CVD, along with co-authors Amit Shah, MD, and Douglas Bremner, MD, also Emory professors.
The report associated the following conditions and their corresponding risks of developing CVD:
Major depression, 72%
PTSD, 57%
Bipolar disorder, 61%
Panic disorder, 50%
Phobic anxiety, 70%
Schizophrenia, nearly 100%
The research also shows that these conditions are associated with a poorer prognosis, greater risk for readmission and higher mortality from existing heart conditions. For example, major depression more than doubles the mortality rate in those with existing CVD.
Additionally, the report emphasises a bidirectional relationship. “More than 40 percent of those with cardiovascular disease also have a mental health condition,” adds Vaccarino.
The physiology of stress
According to the report, a well-documented relationship exists among depression, schizophrenia, PTSD, and abnormal stress responses in the autonomic nervous system (ANS) and hypothalamic-pituitary adrenal axis (HPA).
The former allows the brain to manage involuntary responses, such as functions of the liver, heart, sweat glands, and eye muscles. ANS also manages both acceleration and deceleration of these functions, regulating inflammatory responses. Since most major organs have ANS nerve endings, this system impacts most bodily functions.
The hypothalamic-pituitary adrenal axis (HPA) also influences immune response and metabolism, which can impact cardiovascular function.
According to the report, dysregulation of these systems creates “adverse downstream effects that can affect cardiovascular risk chronically, including increased inflammation, metabolic abnormalities, high blood pressure, enhanced systemic vascular resistance and autonomic inflexibility.” Inflammation has also been implicated in both the development of heart disease and mental health conditions.
Social determinants and quality of care
The role of social determinants of health in CVD disparities is critical. Those with mental health conditions may face disruptions and barriers in the continuum of care, such as affordability and accessibility. Compromised health literacy or communication can also impede access to health screenings and treatment.
Clinicians could also be challenged to care for patients with certain mental conditions, which can be compounded by stigma and existing models that fragment mental and physical health care. Stigmas are also present in the field of clinical research, where having a mental health condition is often an exclusionary criterion in randomised trials.
Moreover, according to the report, current prediction models don’t account for mental health disorders when forecasting the risk of developing heart disease.
Next steps toward a healthier future
To address the disparities of CVD among people with mental health disorders, the authors recommend an integrated approach with interdisciplinary care encompassing behavioural, mental and cardiovascular health.
“The tight connection between cardiovascular and psychological health warrants changes in the health care system that are more amenable to patients with comorbidities,” says Vaccarino. “A clinical team would be ideal for the care of these patients – a team of specialists, social workers, and nursing staff who work in collaboration to provide multidisciplinary care and resources.”
The report concludes that closing the health disparity gap upholds the rights of those living with a mental health condition to achieve the highest level of health and fully participate in society.
A new article published in the Canadian Medical Association Journal warns of the mental health dangers stemming from the increasing potency of cannabis. In Ontario, there has been a more than 14-fold increase in risk for visiting the emergency department for cannabis-related schizophrenic disorders. After a cannabis-induced psychotic episode, cessation of cannabis use is necessary to reduce the risk of relapse, and in severe cases, antipsychotics may be needed.
“Cannabis from the 2000s is not the same as in 2025,” said coauthor Dr Nicholas Fabiano, MD, resident and researcher with the Department of Psychiatry, University of Ottawa, Ottawa, Ontario. “THC content has increased by 5 times. This is likely a significant driver in the increasing link between cannabis use and schizophrenia.”
Cannabis potency is increasing — The concentration of tetrahydrocannabinol (THC) has increased fivefold in the last 20 years in Canada from about 4% to 20% in most legal dried cannabis.
High-potency and regular cannabis use is linked to increased risk of psychosis — The risk of psychosis is increased in people using high-potency THC (more than 10% THC), people using it frequently, and those who are younger and male. A history of mental disorders (depression, anxiety, etc) also appears to increase the risk.
Cannabis-induced psychosis and cannabis use disorder increase the risk of schizophrenia — A recent study of 9.8 million people in Ontario found a 14.3-fold higher risk of developing a schizophrenia-spectrum disorder in people visiting the emergency department for cannabis use and a 241.6-fold higher risk from visits for cannabis-induced psychosis.
Treatment requires stopping cannabis and taking medication — Continued use of cannabis after a first episode of cannabis-induced psychosis is linked to greater risk of returning symptoms. Antipsychotic medication can help people with severe and prolonged symptoms.
Behavioural options may help with cannabis cessation — Motivational interviewing or cognitive behavioural therapy by a physician or psychologist can help build skills to resist cravings and follow treatment recommendations.
Photoreceptor cells in the retina. Credit: Scientific Animations
Could the eyes, which are directly connected to the brain, hold clues to brain changes? An international team of researchers led by the University of Zurich and the University Hospital of Psychiatry Zurich has now tackled this very question. In their study, published in Nature Mental Health, the researchers examined whether changes in our nerve connections are linked to a genetic risk for schizophrenia, as impaired neural information processing is one of the main characteristics of the disorder.
Previous studies suggest that schizophrenia not only reduces volume of grey matter in the brains of those affected, but that it also leads to loss of retinal tissue. But whether these changes are the cause of schizophrenia or a consequence of the disorder has remained unanswered. Retinal health could also be affected by schizophrenia itself, for example, through antipsychotic medication, lifestyle factors or diabetes.
Extensive use of data from healthy individuals
“To investigate whether the risk of developing schizophrenia has an effect on the central nervous system, we examined tens of thousands of healthy individuals,” says Finn Rabe, first author of the study and postdoc at the University of Zurich. “We then calculated polygenic risk scores for each individual.”
The researchers were able to use extensive genetic and retinal data taken from the UK Biobank, a large biomedical database containing data from over half a million people. “You could say that the scale of the UK Biobank’s data has revolutionised biomedical research,” the researcher adds.
Thin retina, elevated risk
The study shows that higher genetic susceptibility to schizophrenia is indeed associated with thinner retinas. The effects are small, though, and can only be reliably demonstrated in large-scale studies. One of the study’s findings is that, unlike changes in the brain, changes in the retina are easy to detect using non-invasive and inexpensive retinal measurements. Thanks to optical coherence tomography, which can be described as a kind of ultrasound for the eye, retinal thickness can be measured in minutes.
This offers a promising outlook for prevention. “Our study shows the potential of using optical coherence tomography in clinical practice. But large-scale longitudinal studies are needed to examine how useful it will be for prevention,” says Finn Rabe.
Perspectives for new therapies
Another key finding of the study concerns genetic variants associated with inflammatory processes in the brain. These may also contribute to structural changes in the retina. The study thus offers further support for the inflammation hypothesis of schizophrenia, ie, the idea that inflammatory processes contribute to the development or progression of the disorder. “If this hypothesis is confirmed, inflammation could be interrupted by medication, potentially enabling us to improve treatment possibilities in the future,” says Rabe.
A new study, recently published in the journal Scientific Reports, has analysed and compared the fatty acids in the blood of individuals with schizophrenia, of those with cannabis use disorder and of those with both diagnoses, with the aim of shedding light on new biomarkers and improving the understanding of the biological relationship between the two disorders. The study also offers a powerful tool for identifying new biomarkers.
Cannabis is one of the most widely used substances in the world, with some 228 million users between the ages of 15 and 64. The risk of developing schizophrenia increases significantly with cannabis use, especially when it starts at a young age. What is more, it is estimated that approximately 10% of cannabis users will develop cannabis use disorder during their lifetime. Curiously, almost a third of individuals diagnosed with schizophrenia also meet the criteria for cannabis use disorder; and cannabis use disorder affects up to 42% of people with schizophrenia.
In this bid to shed light on the biological mechanisms that determine why some individuals develop schizophrenia while others only experience cannabis use disorder, despite similar levels of exposure to cannabis, the UPV/EHU’s Neuropsychopharmacology group has managed to detect “potential biomarkers in the blood that could help predict the risk some people have of developing a psychiatric disorder such as schizophrenia if they use cannabis”, explained Leyre Urigüen, coordinator of the study.
So, the research group compared the fatty acid content in the blood of samples taken from “a group of individuals with schizophrenia who did not use cannabis, a group who used cannabis and have developed a cannabis use disorder, a group with a dual pathology of schizophrenia with cannabis abuse, and a control group of individuals with neither a psychiatric disorder nor drug use”, explained Dr Urigüen. In the study they wanted to shed light on what happens “with people who use cannabis and develop schizophrenia; how do they differ from those who use cannabis and never develop a psychiatric disorder?” she added.
“We found considerable differences between these groups of individuals. By comparing the quantities of certain metabolites (fatty acids), we were able to perfectly differentiate between the three patient populations,” stressed the UPV/EHU researcher. “This indicates that there is an altered or different metabolism between these three groups.” In this study the Neuropsychopharmacology research group at the UPV/EHU detected “that some fatty acids differentiate between the cannabis-using group and the groups with schizophrenia and dual-diagnosis patients. These molecules could potentially be biomarkers”, said Urigüen.
Paving the way forward
The researcher is very hopeful about this finding: “I think it is important to be capable of finding blood biomarkers that can help predict the risk of developing a psychiatric disorder, such as schizophrenia due to cannabis use, and this study has proven to be the start of this way forward. Now this has to be disproved by studies with a larger cohort of people than the one we have analysed.”
In this respect, the researcher stressed that another of the strengths of the study is “the fine-tuning of plasma lipidomics in patients; in other words, the complete study of fatty acids (lipids). We are proposing a way of working that can be replicated by other groups, and that way, headway can be made in the specification of these metabolites”. This approach has been developed by the IBeA research group under the direction of the UPV/EHU professor Nestor Etxebarria. Both groups are working side by side on “various approaches to the study in which they are trying to find answers to these and many other questions”.
Auditory hallucinations are likely the result of abnormalities in two brain processes: a “broken” corollary discharge that fails to suppress self-generated sounds, and a “noisy” efference copy that makes the brain hear these sounds more intensely than it should. That is the conclusion of a new study published October 3rd in the open-access journal PLOS Biology by Xing Tian, of New York University Shanghai, China, and colleagues.
Patients with certain mental disorders, including schizophrenia, often hear voices in the absence of sound.
Patients may fail to distinguish between their own thoughts and external voices, resulting in a reduced ability to recognise thoughts as self-generated.
In the new study, researchers carried out electroencephalogram (EEG) experiments measuring the brain waves of twenty patients diagnosed with schizophrenia with auditory hallucinations and twenty patients diagnosed with schizophrenia who had never experienced such hallucinations.
In general, when people are preparing to speak, their brains send a signal known as “corollary discharge” that suppresses the sound of their own voice.
However, the new study showed that when patients with auditory hallucinations were preparing to speak a syllable, their brains not only failed to suppress these internal sounds, but had an enhanced “efference copy” response to internal sounds other than the planned syllable.
The authors conclude that impairments in these two processes likely contribute to auditory hallucinations and that targeting them in the future could lead to new treatments for such hallucinations.
The authors add, “People who suffer from auditory hallucinations can ‘hear’ sounds without external stimuli. A new study suggests that impaired functional connections between motor and auditory systems in the brain mediate the loss of ability to distinguish fancy from reality.”
New research led by King’s College London has found that thousands of DNA sequences originating from ancient viral infections are expressed in the brain, with some contributing to susceptibility for psychiatric disorders such as schizophrenia, bipolar disorder, and depression.
Around 8% of the human genome is made up of sequences called Human Endogenous Retroviruses (HERVs), which are products of ancient viral infections that occurred hundreds of thousands of years ago. Until recently, it was assumed that these ‘fossil viruses’ were simply junk DNA, with no important function in the body. However, due to advances in genomics research, scientists have now discovered where in our DNA these fossil viruses are located, enabling us to better understand when they are expressed and what functions they may have.
This new study, published in Nature Communications, builds upon these advances and is the first to show that a set of specific HERVs expressed in the human brain contribute to psychiatric disorder susceptibility, marking a step forward in understanding the complex genetic components that contribute to these conditions.
Dr Timothy Powell, co-senior author on the study and Senior Lecturer at the Institute of Psychiatry, Psychology & Neuroscience (IoPPN), King’s College London, said: “This study uses a novel and robust approach to assess how genetic susceptibility for psychiatric disorders imparts its effects on the expression of ancient viral sequences present in the modern human genome. Our results suggest that these viral sequences probably play a more important role in the human brain than originally thought, with specific HERV expression profiles being associated with an increased susceptibility for some psychiatric disorders.”
The study analysed data from large genetic studies involving tens of thousands of people, both with and without mental health conditions, as well as information from autopsy brain samples from 800 individuals, to explore how DNA variations linked to psychiatric disorders affect the expression of HERVs.
Although most genetic risk variants linked to psychiatric diagnoses impacted genes with well-known biological functions, the researchers found that some genetic risk variants preferentially affected the expression of HERVs. The researchers reported five robust HERV expression signatures associated with psychiatric disorders, including two HERVs that are associated with risk for schizophrenia, one associated with risk for both bipolar disorder and schizophrenia, and one associated with risk for depression.
Dr Rodrigo Duarte, first author and Research Fellow at the IoPPN, King’s College London, said: “We know that psychiatric disorders have a substantial genetic component, with many parts of the genome incrementally contributing to susceptibility. In our study, we were able to investigate parts of the genome corresponding to HERVs, which led to the identification of five sequences that are relevant to psychiatric disorders. Whilst it is not clear yet how these HERVs affect brain cells to confer this increase in risk, our findings suggest that their expression regulation is important for brain function.”
Dr Douglas Nixon, co-senior author on the study and and researcher at the Feinstein Institutes for Medical Research at Northwell Health, in the US, said: “Further research is needed to understand the exact function of most HERVs, including those identified in our study. We think that a better understanding of these ancient viruses, and the known genes implicated in psychiatric disorders, have the potential to revolutionise mental health research and lead to novel ways to treat or diagnose these conditions.”
Previous studies have questioned whether gut microbe imbalances and vitamin D deficiency may be linked to schizophrenia. New research published in Neuropsychopharmacology Reports now indicates that taking probiotics plus vitamin D supplements may improve cognitive function in individuals with the disease.
For the study, 70 adults with schizophrenia were randomised to take a placebo or probiotic supplements plus 400 IU vitamin D daily for 12 weeks. Severity of the disease and cognitive function were evaluated by tests called the Positive and Negative Syndrome Scale (PANSS) and the 30-point Montreal Cognitive Assessment (MoCA), respectively.
A total of 69 patients completed the study. The MoCA score increased by 1.96 units in the probiotic-containing supplement group compared with the placebo group. Also, the percentage of patients with MoCA scores of 26 or higher (indicating normal cognition) rose significantly in the intervention group. Between-group differences in PANSS scores were not significant.
“Probiotics may be a novel way to treat mental disorders by regulating gut microbiota,” said corresponding author Gita Sadighi, MD, of the University of Social Welfare and Rehabilitation Sciences, in Iran.
A global collaborative research group has identified brain energy metabolism dysfunction leading to altered pH and lactate levels as common hallmarks in numerous animal models of neuropsychiatric and neurodegenerative disorders. These include models of intellectual disability, autism spectrum disorders, schizophrenia, bipolar disorder, depressive disorders, and Alzheimer’s disease. The findings were published in eLife.
The research group, comprising 131 researchers from 105 laboratories across seven countries, sheds light on altered energy metabolism as a key factor in various neuropsychiatric and neurodegenerative disorders. While considered controversial, an elevated lactate level and the resulting decrease in pH is now also proposed as a potential primary component of these diseases. Unlike previous assumptions associating these changes with external factors like medicationa, the research group’s previous findings suggest that they may be intrinsic to the disorders. This conclusion was drawn from five animal models of schizophrenia/developmental disorders, bipolar disorder, and autism, which are exempt from such confounding factorsb. However, research on brain pH and lactate levels in animal models of other neuropsychiatric and neurological disorders has been limited. Until now, it was unclear whether such changes in the brain were a common phenomenon. Additionally, the relationship between alterations in brain pH and lactate levels and specific behavioural abnormalities had not been clearly established.
This study, encompassing 109 strains/conditions of mice, rats, and chicks, including animal models related to neuropsychiatric conditions, reveals that changes in brain pH and lactate levels are a common feature in a diverse range of animal models of conditions, including schizophrenia/developmental disorders, bipolar disorder, autism, as well as models of depression, epilepsy, and Alzheimer’s disease. This study’s significant insights include:
I. Common Phenomenon Across Disorders: About 30% of the 109 types of animal models exhibited significant changes in brain pH and lactate levels, emphasising the widespread occurrence of energy metabolism changes in the brain across various neuropsychiatric conditions.
II. Environmental Factors as a Cause: Models simulating depression through psychological stress, and those induced to develop diabetes or colitis, which have a high comorbidity risk for depression, showed decreased brain pH and increased lactate levels. Various acquired environmental factors could contribute to these changes.
III. Cognitive Impairment Link: A comprehensive analysis integrating behavioural test data revealed a predominant association between increased brain lactate levels and impaired working memory, illuminating an aspect of cognitive dysfunction.
IV. Confirmation in Independent Cohort: These associations, particularly between higher brain lactate levels and poor working memory performance, were validated in an independent cohort of animal models, reinforcing the initial findings.
V. Autism Spectrum Complexity: Variable responses were noted in autism models, with some showing increased pH and decreased lactate levels, suggesting subpopulations within the autism spectrum with diverse metabolic patterns.
“This is the first and largest systematic study evaluating brain pH and lactate levels across a range of animal models for neuropsychiatric and neurodegenerative disorders. Our findings may lay the groundwork for new approaches to develop the transdiagnostic characterisation of different disorders involving cognitive impairment,” states Dr Hideo Hagihara, the study’s lead author.
Professor Tsuyoshi Miyakawa, the corresponding author, explains, “This research could be a stepping stone towards identifying shared therapeutic targets in various neuropsychiatric disorders. Future studies will centre on uncovering treatment strategies that are effective across diverse animal models with brain pH changes. This could significantly contribute to developing tailored treatments for patient subgroups characterized by specific alterations in brain energy metabolism.”
The exact mechanism behind the reduction in pH and the increase in lactate levels remains elusive. But the authors suggest that, since lactate production increases in response to neural hyperactivity to meet the energy demand, this might be the underlying reason.
Photo by Inzmam Khan: https://www.pexels.com/photo/man-in-black-shirt-and-gray-denim-pants-sitting-on-gray-padded-bench-1134204/
Antipsychotic medications for serious mental illness like schizophrenia or bipolar disorder often causes metabolic side effects such as insulin resistance and obesity, leading some patients to discontinue the treatment.
Now, a pilot study led by Stanford Medicine researchers has found that a ketogenic diet not only restores metabolic health in these patients as they continue their medications, but it further improves their psychiatric conditions. The results, published in Psychiatry Research, suggest that a dietary intervention can be a powerful aid in treating mental illness.
“It’s very promising and very encouraging that you can take back control of your illness in some way, aside from the usual standard of care,” said Shebani Sethi, MD, associate professor of psychiatry and behavioral sciences and the first author of the new paper.
The senior author of the paper is Laura Saslow, PhD, associate professor of health behavior and biological sciences at the University of Michigan.
Making the connection
Sethi, who is board certified in obesity and psychiatry, remembers when she first noticed the connection. As a medical student working in an obesity clinic, she saw a patient with treatment-resistant schizophrenia whose auditory hallucinations quieted on a ketogenic diet.
That prompted her to dig into the medical literature. There were only a few, decades-old case reports on using the ketogenic diet to treat schizophrenia, but there was a long track record of success in using ketogenic diets to treat epileptic seizures.
“The ketogenic diet has been proven to be effective for treatment-resistant epileptic seizures by reducing the excitability of neurons in the brain,” Sethi said. “We thought it would be worth exploring this treatment in psychiatric conditions.”
A few years later, Sethi coined the term metabolic psychiatry, a new field that approaches mental health from an energy conversion perspective.
Meat and vegetables
In the four-month pilot trial, Sethi’s team followed 21 adult participants who were diagnosed with schizophrenia or bipolar disorder, taking antipsychotic medications, and had a metabolic abnormality – such as weight gain, insulin resistance, hypertriglyceridaemia, dyslipidaemia or impaired glucose tolerance. The participants were instructed to follow a ketogenic diet, with approximately 10% of the calories from carbohydrates, 30% from protein and 60% from fat. They were not told to count calories.
“The focus of eating is on whole non-processed foods including protein and non-starchy vegetables, and not restricting fats,” said Sethi, who shared keto-friendly meal ideas with the participants. They were also given keto cookbooks and access to a health coach.
The research team tracked how well the participants followed the diet through weekly measures of blood ketone levels, which are produced when the body breaks down fat instead of glucose for energy. By the end of the trial, 14 patients had been fully adherent, six were semi-adherent and only one was non-adherent.
Physical and mental improvement
The participants underwent a variety of psychiatric and metabolic assessments throughout the trial.
Before the trial, 29% of the participants met the criteria for metabolic syndrome, defined as having at least three of five conditions: abdominal obesity, elevated triglycerides, low HDL cholesterol, elevated blood pressure and elevated fasting glucose levels. After four months on a ketogenic diet, none of the participants had metabolic syndrome.
On average, the participants lost 10% of their body weight; reduced their waist circumference by 11% percent; and had lower blood pressure, body mass index, triglycerides, blood sugar levels and insulin resistance.
“We’re seeing huge changes,” Sethi said. “Even if you’re on antipsychotic drugs, we can still reverse the obesity, the metabolic syndrome, the insulin resistance. I think that’s very encouraging for patients.”
The psychiatric benefits were also striking. On average, the participants improved 31% on a psychiatrist rating of mental illness known as the clinical global impressions scale, with three-quarters of the group showing clinically meaningful improvement. Overall, the participants also reported better sleep and greater life satisfaction.
“The participants reported improvements in their energy, sleep, mood and quality of life,” Sethi said. “They feel healthier and more hopeful.”
The researchers were impressed that most of the participants stuck with the diet. “We saw more benefit with the adherent group compared with the semi-adherent group, indicating a potential dose-response relationship,” Sethi said.
Alternative fuel for the brain
There is increasing evidence that psychiatric diseases such as schizophrenia and bipolar disorder stem from metabolic deficits in the brain, which affect the excitability of neurons, Sethi said. The researchers hypothesise that just as a ketogenic diet improves the rest of the body’s metabolism, it also improves the brain’s metabolism.
“Anything that improves metabolic health in general is probably going to improve brain health anyway,” Sethi said. “But the ketogenic diet can provide ketones as an alternative fuel to glucose for a brain with energy dysfunction.”
Likely there are multiple mechanisms at work, she added, and the main purpose of the small pilot trial is to help researchers detect signals that will guide the design of larger, more robust studies.
As a physician, Sethi cares for many patients with both serious mental illness and obesity or metabolic syndrome, but few studies have focused on this undertreated population. She is founder and director of the metabolic psychiatry clinic at Stanford Medicine.
“Many of my patients suffer from both illnesses, so my desire was to see if metabolic interventions could help them,” she said. “They are seeking more help. They are looking to just feel better.”
