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<td><a href="https://www.psypost.org/new-gut-microbiome-discovery-sodium-valerate-could-be-key-to-reducing-alcohol-abuse/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">New gut microbiome discovery: Sodium valerate could be key to reducing alcohol abuse</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 6th 2024, 10:00</div>
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<p><p>In a groundbreaking study, researchers at The Jackson Laboratory and UConn Health have discovered that sodium valerate, a short-chain fatty acid produced by gut microbes, can significantly reduce binge drinking behavior and blood alcohol levels in mice. This finding, published in the journal <a href="https://doi.org/10.1186/s40168-024-01829-6" target="_blank" rel="noopener">Microbiome</a>, offers new insights into the gut-brain connection and suggests a novel treatment for excessive alcohol consumption.</p>
<p>Alcohol use disorder (AUD) is a chronic condition characterized by an inability to control alcohol consumption despite adverse consequences. It affects millions of individuals worldwide, leading to significant health, social, and economic burdens.</p>
<p>Excessive alcohol consumption can result in liver disease, cardiovascular problems, mental health issues, and increased risk of accidents and injuries. Current treatments for AUD, such as medications and behavioral therapies, are often limited in effectiveness, underscoring the need for new and innovative therapeutic approaches.</p>
<p>Recent research has highlighted the intricate connection between the gut microbiome and various health conditions, including AUD. The gut microbiome consists of trillions of microorganisms living in the digestive tract, playing a crucial role in digestion, immune function, and overall health.</p>
<p>Emerging evidence suggests that the gut microbiome can influence brain function and behavior through the gut-brain axis, a bidirectional communication network linking the gut and the central nervous system. Changes in the composition and activity of gut microbes have been linked to mental health disorders, including anxiety and depression, which are often comorbid with AUD.</p>
<p>Given that alcohol consumption can alter the gut microbiome, leading to a decrease in beneficial bacteria and the production of short-chain fatty acids (SCFAs), the research team, led by Yanjiao Zhou and Jason Bubier, hypothesized that supplementing specific SCFAs could mitigate the effects of alcohol and reduce excessive drinking.</p>
<p>The researchers conducted their investigation using a mouse model of binge drinking. They administered three different SCFAs – sodium valerate, sodium butyrate, and sodium acetate – to evaluate their effects on alcohol consumption. Male C57BL/6J mice were used for the study, housed under controlled conditions, and acclimated before experimentation.</p>
<p>Mice were treated with either sodium valerate, sodium butyrate, sodium acetate, or sodium chloride (as a control) in their drinking water for ten days. Following this supplementation, the mice were subjected to a “drinking in the dark” (DID) paradigm, where they had limited access to a 20% ethanol solution to mimic binge drinking behavior. The volume of ethanol consumed was measured, and blood samples were collected to determine blood ethanol concentration.</p>
<p>Sodium valerate supplementation led to a significant reduction in ethanol consumption and blood ethanol levels compared to control mice. Specifically, mice treated with sodium valerate consumed 40% less alcohol and had 53% lower blood ethanol levels. This effect was not observed with other SCFAs, highlighting sodium valerate’s unique potential.</p>
<p>In addition to reducing alcohol consumption, sodium valerate also influenced anxiety-like behaviors in mice. The study employed an open-field activity test to assess anxiety levels, revealing that mice treated with sodium valerate spent more time and made more entries into the center of the field, indicating reduced anxiety.</p>
<p>This anxiolytic effect was accompanied by elevated levels of gamma-aminobutyric acid (GABA) in the brain, stool, and blood of the mice. GABA is a neurotransmitter implicated in anxiety and alcohol use disorders, suggesting that sodium valerate’s impact on GABA levels may be a key mechanism underlying its effects on behavior.</p>
<p>Further molecular analysis provided additional insights into the mechanisms through which sodium valerate exerts its effects. RNA sequencing of the amygdala, a brain region associated with emotional regulation, revealed significant changes in gene expression related to neuroinflammation, neurotransmission, mitochondrial function, and signaling pathways. These alterations suggest that sodium valerate influences multiple brain signaling pathways, which may collectively mediate its effects on reducing alcohol consumption and anxiety.</p>
<p>The study also highlighted the role of the gut microbiome in these processes. Sodium valerate supplementation led to changes in the composition of the gut microbiota, including an increase in specific bacterial genera. These microbiota changes likely contribute to the observed behavioral and molecular effects.</p>
<p>“The study expands our understanding of the important relationship between the gut microbiome and alcohol consumption,” said Bubier. “There is strong evidence that binge drinking significantly alters the microbiome in ways that accelerate the cycle of addiction via the gut-brain axis. Our findings provide a possible biological explanation for why that occurs and identify a potential therapy for reducing excessive alcohol use.”</p>
<p>While the findings are promising, the study has several limitations. Firstly, it was conducted solely on male mice, so further research is needed to determine if the results apply to females. Additionally, the study focused on alcohol-independent mice, meaning the effects of sodium valerate on alcohol-dependent models remain unknown.</p>
<p>Future research should explore the impact of sodium valerate on alcohol-dependent animals and investigate the long-term effects of its supplementation. Understanding the precise mechanisms through which sodium valerate affects alcohol consumption and anxiety will be crucial in developing targeted therapies.</p>
<p>“The implications of our study are significant,” said Zhou. “By demonstrating how sodium valerate alters gene expression and neurotransmitter levels, we provide a multifaceted explanation for its potential as a treatment for excessive alcohol consumption.”</p>
<p>The study, “<a href="https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-024-01829-6" target="_blank" rel="noopener">Short-chain fatty acid valerate reduces voluntary alcohol intake in male mice</a>,” was authored by Suresh C. Bokoliya, Jordan Russell, Yair Dorsett, Hunter A. Panier, Vijender Singh, Lauren Daddi, Hanshu Yuan, Liv R. Dedon, Zhongmao Liu, Yuqi Zhou, Zefang Min, Jessica R. Barson, Jonathan Covault, Jason A. Bubier, and Yanjiao Zhou.</p></p>
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<td><a href="https://www.psypost.org/scientists-unveil-a-fascinating-new-perspective-on-human-consciousness/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Scientists unveil a fascinating new perspective on human consciousness</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 6th 2024, 08:00</div>
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<p><p>Why did the experience of consciousness evolve from our underlying brain physiology? Despite being a vibrant area of neuroscience, current research on consciousness is characterised by <a href="https://academic.oup.com/nc/article/2022/1/niac001/6523097?login=false">disagreement</a> and <a href="https://www.psychologytoday.com/gb/blog/theory-of-knowledge/202310/a-fight-breaks-out-in-the-science-of-consciousness">controversy</a> – with several rival <a href="https://www.nature.com/articles/s41583-022-00587-4">theories</a> in contention.</p>
<p>A recent <a href="https://pubmed.ncbi.nlm.nih.gov/33923218/">scoping review</a> of over 1,000 articles identified over 20 different theoretical accounts. Philosophers like David Chalmers argue that no single scientific theory can truly explain <a href="https://philpapers.org/rec/CHATCM">consciousness</a>.</p>
<p>We define consciousness as embodied subjective awareness, including self awareness. In a <a href="https://www.interaliamag.org/articles/a-social-evolutionary-purpose-for-consciousness/">recent article</a> published in Interalia (which is not peer reviewed), we argue that one reason for this predicament is the powerful role played by intuition.</p>
<p>We are not alone. Social scientist <a href="https://link.springer.com/chapter/10.1007/978-3-030-96993-6_3">Jacy Reese Anthis</a> writes “much of the debate on the fundamental nature of consciousness takes the form of intuition jousting, in which the different parties each report their own strong intuitions and joust them against each other”.</p>
<h2>Dangers of intuition</h2>
<p>Key intuitive beliefs – for example that our mental processes are distinct from our physical bodies (mind-body dualism) and that our mental processes give rise to and control our decisions and actions (mental causation) – are supported by a lifetime of subjective experiences.</p>
<p>These beliefs are found in <a href="https://onlinelibrary.wiley.com/doi/10.1111/cogs.13380">all human cultures</a>. They are important as they serve as foundational beliefs for most liberal democracies and criminal justice systems. They are resistant to counter evidence. That’s because they are powerfully endorsed by social and cultural concepts such as free will, human rights, democracy, justice and moral responsibility. All these concepts assume that consciousness plays a central controlling influence.</p>
<p><a href="https://www.scientificamerican.com/article/can-we-rely-on-our-intuition/">Intuition</a>, however, is an automatic, cognitive process that evolved to <a href="https://theconversation.com/is-it-rational-to-trust-your-gut-feelings-a-neuroscientist-explains-95086">provide fast trusted explanations and predictions</a>. In fact, it does so without the need for us to know how or why we know it. The outcomes of intuition therefore shape how we perceive and explain our everyday world without the need for extensive reflection or formal analytic explanations.</p>
<p>While helpful and indeed crucial for many <a href="https://thedecisionlab.com/insights/society/thinking-fast-when-intuition-isnt-all-bad-according-to-its-biggest-critic">everyday activities</a>, intuitive beliefs <a href="https://www.taylorfrancis.com/chapters/edit/10.4324/9781003189930-8/navigating-conflict-science-intuition-andrew-shtulman">can be wrong</a>. They can also <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10126148/">interfere with scientific literacy</a>.</p>
<p>Intuitive accounts of consciousness ultimately put us in the driver’s seat as “captain of our own ship”. We think we know what consciousness is and what it does from simply experiencing it. Mental thoughts, intentions and desires are seen as <a href="https://www.sciencedirect.com/science/article/pii/S0732118X15300039">determining</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4471880/#:~:text=Importantly%2C%20on%20this%20understanding%2C%20conscious,dimension%20(or%20along%20both).">controlling our actions</a>.</p>
<p>The widespread acceptance of these tacit intuitive accounts helps explain, in part, why the formal study of consciousness was relegated to the margins of mainstream neuroscience until <a href="https://pubmed.ncbi.nlm.nih.gov/32166164/">late 20th century</a>.</p>
<p>The problem for scientific models of consciousness remains accommodating these intuitive accounts within a materialist framework consistent with the findings of neuroscience. While there is no current scientific explanation for how brain tissue generates or maintains subjective experience, the consensus among (most) neuroscientists is that it is a product of brain processes.</p>
<h2>Social purpose</h2>
<p>If that’s the case, why did consciousness, defined as subjective awareness, evolve?</p>
<p>Consciousness presumably evolved as part of the evolution of the nervous system. According to <a href="https://www.sciencedirect.com/science/article/pii/S0732118X15300039#fn4">several theories</a> the key adaptive function (providing an organism with survival and reproductive benefits) of consciousness is to make volitional movement possible. And volition is something we ultimately associate with will, agency and individuality. It is therefore easy to think that consciousness evolved to benefit us as individuals.</p>
<p>But <a href="https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2021.571460/full">we have argued</a> that consciousness may have evolved to facilitate key social adaptive functions. Rather than helping individuals survive, it evolved to help us broadcast our experienced ideas and feelings into the wider world. And this might benefit the survival and wellbeing of the wider species.</p>
<p>The idea fits with new thinking on genetics. While evolutionary science traditionally focuses on individual genes, there is growing recognition that natural selection among humans operates at <a href="https://pubmed.ncbi.nlm.nih.gov/37036975/">multiple levels</a>. For example, culture and society influence traits passed on between generations – we value some more than others.</p>
<p>Central to our account is the idea that sociality (the tendency of groups and individuals to develop social links and live in communities) is a <a href="https://www.nature.com/articles/s41562-018-0384-6">key survival strategy</a> that influences how the brain and cognition evolve.</p>
<p>Adopting this social evolutionary framework, we propose that subjective awareness <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8121175/">lacks any independent capacity to causally influence</a> other psychological processes or actions. An example would be initiating a course of action. The idea that subjective awareness has a social purpose <a href="https://pubmed.ncbi.nlm.nih.gov/33995166/">has been described previously by other reserachers</a>.</p>
<p>The claim that subjective awareness is without causal influence, however, is not to deny the <a href="https://www.interaliamag.org/articles/a-social-evolutionary-purpose-for-consciousness/">reality of subjective experience </a> or claim that the experience is an illusion.</p>
<p>While our model removes subjective awareness from the traditional driving seat of the mind, it does not imply that we don’t value private internal experiences. Indeed, it is precisely because of the value we place on these experiences that intuitive accounts remain compelling and widespread in social and legal organisation systems and psychology.</p>
<p>While it is counter-intuitive to attribute agency and personal accountability to a biological assembly of nerve cells, it makes sense that highly valued social constructs such as free will, truth, honesty and fairness can be meaningfully attributed to individuals as accountable people in a social community.</p>
<p>Think about it. While we are deeply rooted in our biological nature, our social nature is largely defined by our roles and interactions in society. As such, the mental architecture of the mind should be strongly <a href="https://www.newscientist.com/article/mg22730340-200-consciousness-evolved-for-the-greater-good-not-just-the-self/">adapted for</a> the exchange and reception of information, ideas and feelings. Consequently, while brains as biological organs are incapable of responsibility and agency, legal and social traditions have long held individuals accountable for their behaviour.</p>
<p>Key to achieving a more scientific explanation of subjective awareness requires accepting that biology and culture work collectively to <a href="https://pubmed.ncbi.nlm.nih.gov/36180362/">shape how brains evolve</a>. Subjective awareness comprises only one part of the brain’s much larger mental architecture designed to facilitate species survival and wellbeing.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/232459/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/why-consciousness-may-have-evolved-to-benefit-society-rather-than-individuals-232459">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/brain-connectivity-patterns-linked-to-borderline-personality-traits/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Brain connectivity patterns linked to borderline personality traits</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 6th 2024, 06:00</div>
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<p><p>A new study has uncovered significant associations between patterns of brain connectivity and borderline personality traits in adolescents and young adults. Researchers identified specific brain regions linked to emotion regulation and executive function as being most predictive of these traits. Published in <a href="https://doi.org/10.1016/j.biopsych.2024.02.1016"><em>Biological Psychiatry</em></a>, the findings suggest that borderline personality disorder may have roots in brain development, offering insights for early intervention strategies.</p>
<p>Borderline personality disorder is a severe mental health condition characterized by intense mood swings, unstable relationships, impulsive behavior, and a high risk of suicide. Although borderline personality disorder is typically diagnosed in adulthood, symptoms often emerge during adolescence.</p>
<p>Previous research on borderline personality disorder has primarily focused on adults and yielded inconsistent results due to small sample sizes. This study aimed to address these gaps by using large-scale datasets to explore the developmental neurobiology of borderline personality disorder traits in younger populations.</p>
<p>The researchers utilized data from two large publicly available datasets: the Human Connectome Project Young Adult (HCP-YA) and the Human Connectome Project Development (HCP-D). The HCP-YA included data from 870 young adults, while the HCP-D provided data from 610 adolescents.</p>
<p>Participants underwent resting-state fMRI scans, capturing spontaneous brain activity. The researchers then applied a machine learning technique known as multivariate linear ridge regression. This approach allowed them to predict borderline personality traits based on the connectivity patterns between different brain regions. They used a proxy measure for borderline personality disorder traits derived from the NEO Five-Factor Inventory (NEO-FFI), a widely used personality assessment tool. This measure had been previously validated and provided a reliable estimate of borderline personality disorder traits.</p>
<p>The study found that specific patterns of brain connectivity were significantly associated with borderline personality traits. The predictive models demonstrated that connectivity within certain brain networks, particularly those involved in emotion regulation and executive function, could reliably predict borderline personality disorder traits in young adults. Among these networks, the ventral attention network, which is crucial for emotional response and regulation, showed the strongest predictive power.</p>
<p>In young adults, the predictive models achieved a correlation coefficient of 0.14 between the predicted and actual borderline personality disorder scores, indicating a significant association. The researchers also found that this association was heterogeneous across different brain regions. In simpler terms, not all areas of the brain were equally predictive of borderline personality traits, with the most predictive areas located within the ventral attention and frontoparietal networks. These networks are critical for managing emotional responses and higher-order cognitive functions.</p>
<p>When the researchers applied their models to the adolescent dataset, they found that the patterns of brain connectivity still significantly predicted borderline personality disorder traits, achieving a higher correlation coefficient of 0.24. This result indicates that the relationship between brain connectivity and borderline personality traits is consistent across different developmental stages, from adolescence to early adulthood. It suggests that the neural basis of borderline personality disorder traits can be identified early in development.</p>
<p>The study also revealed that brain regions showing the most substantial developmental changes in connectivity during adolescence were the same regions most predictive of borderline personality disorder traits. This alignment underscores the importance of brain development in understanding the emergence of borderline personality traits. The findings suggest that changes in brain connectivity patterns during adolescence might be critical for the development of these traits.</p>
<p>While the study provides valuable insights, it also has limitations. The research did not include participants diagnosed with BPD, focusing instead on traits in typically developing individuals. The study’s reliance on proxy measures of BPD traits, rather than direct clinical assessments, may limit the specificity of the results. Future studies should apply similar methodologies to clinical populations to validate these findings.</p>
<p>“In sum, we demonstrated that multivariate functional connectivity patterns can successfully predict borderline personality traits in unseen data from young adults and adolescents,” the researchers concluded. “The findings suggested that regions whose functional connectivity develops the most in youth align with those associated with BPD, providing new evidence for understanding BPD as a neurodevelopmental disorder. Linking within-individual neurodevelopmental trajectories of functional connectivity to the emergence of BPD is an important direction for future longitudinal studies. More generally, the current findings suggest a new perspective on potential neurodevelopmental origins of BPD.”</p>
<p>The study, “<a href="https://www.sciencedirect.com/science/article/pii/S0006322324011405" target="_blank" rel="noopener">Generalizable Links Between Borderline Personality Traits and Functional Connectivity</a>,” was authored by Golia Shafiei, Arielle S. Keller, Maxwell Bertolero, Sheila Shanmugan, Dani S. Bassett, Andrew A. Chen, Sydney Covitz, Audrey Houghton, Audrey Luo, Kahini Mehta, Taylor Salo, Russell T. Shinohara, Damien Fair, Michael N. Hallquist, and Theodore D. Satterthwaite.</p></p>
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<td><a href="https://www.psypost.org/long-term-benzodiazepine-use-linked-to-shrinkage-in-two-brain-regions/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Long-term benzodiazepine use linked to shrinkage in two brain regions</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 5th 2024, 14:00</div>
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<p><p>Although the overall use of benzodiazepines does not appear to increase the risk of dementia, long-term use is associated with a reduction in the volume of critical brain areas, such as the hippocampus and the amygdala, according to new research published in <a href="https://doi.org/10.1186/s12916-024-03437-5"><em>BMC Medicine</em></a>. This finding supports current medical guidelines that caution against prolonged benzodiazepine use.</p>
<p>Benzodiazepines are a class of medications commonly prescribed to alleviate anxiety and insomnia. Common benzodiazepines include diazepam (Valium), alprazolam (Xanax), and lorazepam (Ativan). These drugs function by enhancing the effect of a neurotransmitter called gamma-aminobutyric acid (GABA), which promotes relaxation and reduces brain activity.</p>
<p>Due to their calming effects, benzodiazepines are among the most frequently prescribed psychotropic medications in developed countries. However, concerns have been raised about their long-term use, especially among older adults, due to risks of dependence, falls, and potential cognitive decline.</p>
<p>The impetus for this study stemmed from conflicting evidence about the long-term effects of benzodiazepines on cognitive health. While some animal studies suggested that benzodiazepines might protect the brain by reducing inflammation, others indicated they could harm the brain by promoting the buildup of harmful proteins associated with dementia.</p>
<p>Previous human studies also yielded mixed results, with some suggesting an increased dementia risk and others finding no such link. This study aimed to clarify these effects by investigating both the risk of dementia and changes in brain structure over time.</p>
<p>“Our interest in this topic was raised by the observation that benzodiazepines are the most commonly prescribed medications in developed countries, and 30-40% of older adults continues use beyond the recommended period of several weeks, while several recent studies indicated that benzodiazepines might have long-term adverse effects on cognition,” said study author Ilse vom Hofe of the Erasmus University Medical Center.</p>
<p>The researchers conducted their study using data from the Rotterdam Study, a large, ongoing research project initiated in 1990 to explore common diseases among older adults. The study included 5,443 participants aged 60 and above who were free from cognitive impairment at the start. These participants underwent follow-up assessments every four years, which included cognitive tests and brain imaging scans. Information on benzodiazepine use was obtained from pharmacy records, allowing researchers to track the duration and dosage of medication use.</p>
<p>To assess the impact of benzodiazepines on dementia risk, the researchers used statistical models to compare the incidence of dementia among benzodiazepine users and non-users. They accounted for various factors that could influence dementia risk, such as age, sex, education, and health conditions like diabetes and heart disease.</p>
<p>In addition to dementia assessments, the study also focused on brain imaging data from 4,836 participants who had undergone at least one MRI scan. These scans measured the volumes of different brain regions, including the hippocampus and amygdala, which are crucial for memory and emotion.</p>
<p>The study’s findings revealed no significant association between benzodiazepine use and an increased risk of developing dementia. This result contrasts with some earlier studies that suggested a higher risk.</p>
<p>But the researchers observed that benzodiazepine use was linked to a subtle reduction in the volume of the hippocampus and, to a lesser extent, the amygdala over time. These brain regions are known to shrink as part of the aging process, and accelerated shrinkage can be a marker of neurodegeneration.</p>
<p>“People should take away from our study that benzodiazepine use was not associated with increased dementia risk,” vom Hofe told PsyPost. “However, benzodiazepine use was associated with sub-clinical accelerated reduction in hippocampal and to a lesser extent amygdalar volume over time, underlining current guidelines cautioning against prolonged benzodiazepine use.”</p>
<p>One of the strengths of this study is its robust design and long follow-up period, which allowed for a thorough investigation of both dementia risk and brain changes. The researchers also took into account a wide range of factors that could confound the results, such as the presence of anxiety and sleep disorders, which are both common reasons for benzodiazepine prescriptions and potential risk factors for dementia.</p>
<p>However, the study has some limitations. While the exclusion of participants with cognitive impairment at baseline helped reduce the risk of reverse causation—where cognitive decline leads to benzodiazepine use rather than the other way around—it may also have led to an underestimation of the drug’s adverse effects. Additionally, the study population was predominantly white, which may limit the generalizability of the findings to other ethnic groups.</p>
<p>“Our results are based on a cognitively healthy population, possible adverse effects of benzodiazepine use in people with cognitive impairment warrant further investigation,” vom Hofe noted.</p>
<p>Despite these limitations, the study’s findings have important implications for the use of benzodiazepines, particularly among older adults. The observed reduction in hippocampal volume associated with benzodiazepine use, even in the absence of increased dementia risk, underscores the importance of caution when prescribing these medications for extended periods. The hippocampus plays a crucial role in memory formation, and its shrinkage is often seen in neurodegenerative diseases like Alzheimer’s.</p>
<p>The study also suggests several directions for future research. Further investigations could explore whether different types of benzodiazepines have varying impacts on brain health. For instance, this study found that high cumulative doses of anxiolytics, which are benzodiazepines prescribed for anxiety, were associated with a higher risk of dementia compared to sedative-hypnotics, which are prescribed for sleep disorders. Understanding these differences could help guide safer prescribing practices.</p>
<p>“This research is part of a line of research investigating the effects of commonly used medications on dementia risk, with the ultimate goal to prevent or delay the onset of dementia,” vom Hofe said.</p>
<p>The study, “<a href="https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-024-03437-5" target="_blank" rel="noopener">Benzodiazepine use in relation to long-term dementia risk and imaging markers of neurodegeneration: a population-based study</a>,” was authored by Ilse vom Hofe, Bruno H. Stricker, Meike W. Vernooij, M. Kamran Ikram, M. Arfan Ikram, and Frank J. Wolters.</p></p>
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<td><a href="https://www.psypost.org/alarming-study-exposes-major-flaw-in-how-top-health-organizations-describe-depression/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Alarming study exposes major flaw in how top health organizations describe depression</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 5th 2024, 12:00</div>
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<p><p>A recent study reveals a troubling trend in how information about depression is presented to the public. Researchers found that major health organizations frequently provide misleading information, portraying depression as a disorder that causes symptoms rather than a descriptive label for those symptoms.</p>
<p>This inaccuracy makes it harder for individuals to understand the real causes of their distress, potentially hindering effective treatment and emotional regulation. The findings, published in the journal <em><a href="https://doi.org/10.1159/000538458" target="_blank" rel="noopener">Psychopathology</a></em>, emphasize the need for clearer communication about mental health diagnoses.</p>
<p>Depression is a complex mental health condition characterized by persistent feelings of sadness, loss of interest or pleasure in activities, and a range of physical and emotional problems. Unlike many physical illnesses with identifiable causes, depression is diagnosed based on a collection of symptoms rather than a clear underlying cause.</p>
<p>These symptoms can include changes in sleep patterns, appetite, energy levels, concentration, daily behavior, or self-esteem. Despite the lack of a singular cause, depression significantly impacts an individual’s ability to function in daily life and can lead to severe consequences if not properly addressed.</p>
<p>The motivation behind the study stems from a critical issue in how depression and other psychiatric diagnoses are communicated to the public. Many leading health organizations describe depression in a way that suggests it directly causes low mood and other symptoms, a form of circular reasoning that confuses the public.</p>
<p>The researchers at the University of Turku and the University of the Arts Helsinki aimed to investigate how widespread this misconception is among authoritative health sources. They recognized that if major health organizations provide misleading information, it can hinder individuals’ understanding of their mental health, making it harder for them to seek appropriate help and interventions.</p>
<p>The researchers were driven by the potential harm caused by this misunderstanding. When people believe their depressive symptoms are caused by an external, pathological process, they may feel less empowered to address the actual factors contributing to their distress. This can lead to a sense of helplessness and hinder their ability to seek effective coping strategies or make meaningful changes in their lives.</p>
<p>“Depression should be considered as a diagnosis similar to a headache. Both are medical diagnoses, but neither explains what causes the symptoms. Like a headache, depression is a description of a problem that can have many different causes. A diagnosis of depression does not explain the cause of depressed mood any more than a diagnosis of headaches explains the cause of pain in the head,” explained Jani Kajanoja, a postdoctoral researcher and a medical doctor at the University of Turku</p>
<p>To carry out this investigation, the researchers selected the websites of English-language health organizations that are highly influential based on search engine results. These organizations included major entities such as the World Health Organization, the American Psychiatric Association, the National Health Service in the UK, and prestigious universities like Harvard and Johns Hopkins. The selection criteria ensured that the study focused on sources that people are most likely to encounter when seeking information about depression online.</p>
<p>The researchers used a content analysis method to evaluate the information presented on these websites. They classified the descriptions of depression into three categories: causally explanatory, purely descriptive, and unspecified.</p>
<p>The “causally explanatory” category included instances where depression was explicitly described as causing its symptoms, such as low mood and loss of interest. The “purely descriptive” category encompassed instances where depression was presented solely as a description of a cluster of symptoms without implying a causal relationship. The “unspecified” category included cases where the nature of the relationship between the diagnosis and symptoms was left unclear or mixed.</p>
<p>The findings revealed a significant issue in how depression is portrayed by authoritative health organizations. Out of the websites analyzed, none presented depression clearly and explicitly as a purely descriptive diagnosis. Instead, 53% of the websites described depression using causally explanatory language, suggesting that depression directly causes the symptoms it is supposed to describe.</p>
<p>For instance, the World Health Organization’s website stated that depression “can cause the affected person to suffer greatly and function poorly at work, at school, and in the family,” while the American Psychiatric Association’s website claimed that “depression causes feelings of sadness and/or a loss of interest in activities you once enjoyed.”</p>
<p>The remaining 47% of the websites used unspecified language, neither clearly stating that depression causes the symptoms nor highlighting that it is merely a descriptive label. This ambiguity can also contribute to public misunderstanding, as it does not clarify the true nature of the diagnosis.</p>
<p>“Presenting depression as a uniform disorder that causes depressive symptoms is circular reasoning that blurs our understanding of the nature of mental health problems and makes it harder for people to understand their distress,” said Kajanoja.</p>
<p>The researchers propose that the issue might stem from a cognitive bias.</p>
<p>“People seem to have a tendency to think that a diagnosis is an explanation even when it is not. It is important for professionals not to reinforce this misconception with their communication, and instead help people to understand their condition,” said Jussi Valtonen of the University of the Arts Helsinki.</p>
<p>The study has some limitations that should be considered. Firstly, it focused exclusively on English-language websites from leading health organizations, potentially missing nuances in non-English sources and smaller, less prominent institutions. Additionally, the analysis did not cover all possible sources of information on depression, such as social media or patient forums, which can also significantly influence public understanding.</p>
<p>Future research could aim to broaden the scope by including a wider variety of information sources and languages. Furthermore, investigating the direct impact of these misleading descriptions on individuals’ perceptions and behaviors regarding their mental health would provide valuable insights.</p>
<p>The study, “<a href="https://doi.org/10.1159/000538458" target="_blank" rel="noopener">A Descriptive Diagnosis or a Causal Explanation? Accuracy of Depictions of Depression on Authoritative Health Organization Websites</a>,” was authored by Jani Kajanoja and Jussi Valtonen.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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