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<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">PsyPost – Psychology News Daily Digest (Unofficial)</span></td>
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<td><a href="https://www.psypost.org/gut-brain-connection-proinflammatory-bacteria-linked-to-hippocampal-changes-in-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;">Gut-brain connection: Proinflammatory bacteria linked to hippocampal changes in depression</a>
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<p><p>A neuroimaging study of unmedicated patients with major depressive disorder (MDD) has uncovered a link between gut microbiota composition and changes in brain function. Specifically, the study found that individuals with higher levels of certain proinflammatory gut bacteria exhibited altered functional connectivity in the hippocampus, a key brain region implicated in memory and emotion. The research, published in <a href="https://www.nature.com/articles/s41398-024-03012-9"><em>Translational Psychiatry</em></a>, highlights the growing recognition of the gut-brain axis as a potential player in the pathology of depression.</p>
<p>The hippocampus is a small, seahorse-shaped structure located in the brain’s temporal lobe. It plays a crucial role in memory formation, learning, and spatial navigation. It is part of the limbic system, which regulates emotions and connects memories to emotional responses. The hippocampus helps convert short-term memories into long-term ones and is essential for recalling past experiences.</p>
<p>In depression, the hippocampus often exhibits structural and functional changes, such as reduced volume or impaired neurogenesis. Chronic stress and elevated cortisol levels, commonly associated with depression, can damage hippocampal neurons and hinder their growth, leading to memory difficulties and emotional dysregulation. A smaller or less active hippocampus may contribute to the persistence of negative thoughts and difficulty in regulating emotions—hallmarks of depression. Furthermore, reduced hippocampal function can impair the ability to learn and implement coping mechanisms for stress.</p>
<p>Study authors Shu Xiao and colleagues aimed to explore the links between alterations in functional connectivity in subregions of the hippocampus and gut microbiota composition in patients with major depressive disorder.</p>
<p>In recent decades, scientists have discovered a bidirectional communication pathway between the brain and gut microbiota—the community of trillions of microorganisms living in the gut. This pathway, termed the microbiota-gut-brain axis, has been shown to play important roles in various processes within the body, including psychological functioning. It is possible that gut microbiota composition might also play a role in major depressive disorder.</p>
<p>The researchers recruited 49 adults with MDD and 44 healthy individuals as controls. Participants were aged between 18 and 55 and were screened for other medical or psychiatric conditions to ensure homogeneity. None of the MDD participants were on medication at the time of the study. The researchers collected fecal samples to analyze gut microbiota composition and performed resting-state magnetic resonance imaging (MRI) scans to examine hippocampal functional connectivity—a measure of how different brain regions communicate during rest.</p>
<p>The researchers found significant differences in gut microbiota composition between the two groups. Participants with MDD exhibited reduced species richness, indicating a lower variety of gut bacteria. However, the diversity index, which measures not only the number of species but also their relative proportions, did not significantly differ.</p>
<p>Importantly, individuals with MDD had a higher abundance of proinflammatory bacteria, specifically those from the <em>Enterobacteriaceae</em> family, and a lower abundance of beneficial bacteria like <em>Prevotella</em>, which are involved in producing short-chain fatty acids (SCFAs) that support gut health and reduce inflammation.</p>
<p>In terms of brain function, there were no global differences in hippocampal functional connectivity between the MDD and healthy control groups. However, a closer analysis revealed altered connectivity patterns within specific hippocampal subregions. In individuals with MDD, there was increased functional connectivity between the left CA3 and right caudal hippocampus, which correlated with the relative abundance of <em>Enterobacteriaceae</em>. This suggests that the presence of proinflammatory gut bacteria may influence hippocampal connectivity, potentially via systemic inflammation or immune signaling pathways.</p>
<p>The findings support the hypothesis that the microbiota-gut-brain axis plays a role in the development of MDD. Gut dysbiosis (imbalance in gut bacteria) may contribute to hippocampal dysfunction through inflammatory pathways, disrupting processes critical for memory, learning, and emotional regulation. The study also noted that individuals with longer histories of MDD had significantly lower levels of <em>Prevotella</em>, highlighting a potential link between prolonged illness duration and gut microbiota changes.</p>
<p>Interestingly, the researchers combined data on hippocampal functional connectivity and gut microbiota composition to develop a machine-learning model that could distinguish MDD patients from healthy controls with high accuracy. This suggests that these biomarkers could eventually aid in diagnosing MDD or identifying individuals at risk.</p>
<p>The study sheds light on the links between brain function and gut microbiota composition. However, it should be noted that the study’s design does not allow for any cause-and-effect conclusions to be drawn from the findings. Additionally, the number of study participants was relatively small, and all were recruited from a single hospital. Studies involving patients from other regions might not yield identical results.</p>
<p>The paper, “<a href="https://doi.org/10.1038/s41398-024-03012-9">Gut proinflammatory bacteria is associated with abnormal functional connectivity of hippocampus in unmedicated patients with major depressive disorder</a>”, was authored by Shu Xiao, Zibin Yang, Hong Yan, Guanmao Chen, Shuming Zhong, Pan Chen, Hui Zhong, Hengwen Yang, Yanbin Jia, Zhinan Yin, Jiaying Gong, Li Huang, and Ying Wang.</p></p>
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<td><a href="https://www.psypost.org/apoe4-gene-may-influence-brain-barrier-function-in-early-stages-of-alzheimers-disease/" 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;">APOE4 gene may influence brain barrier function in early stages of Alzheimer’s disease</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 26th 2024, 06:00</div>
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<p><p>Could early signs of Alzheimer’s disease be found in the brain’s vascular defenses? New research published in <a href="https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.14302"><em>Alzheimer’s & Dementia</em></a> has found that blood-brain barrier function may differ in individuals with the APOE4 gene, a known genetic risk factor for Alzheimer’s disease. The study found increased permeability in the blood-brain barrier of APOE4 carriers, including those without cognitive symptoms or amyloid beta buildup.</p>
<p>The blood-brain barrier is a critical protective shield that separates the brain from the bloodstream. It regulates the exchange of substances between the brain and the rest of the body, ensuring that harmful toxins, pathogens, and immune cells stay out while essential nutrients and oxygen pass through.</p>
<p>The blood-brain barrier plays a vital role in preserving the brain’s delicate environment, allowing it to function optimally. However, when this barrier becomes more permeable or “leaky,” harmful substances can infiltrate the brain, potentially leading to inflammation, neuronal damage, and the development of neurological diseases.</p>
<p>Alzheimer’s disease is a progressive neurodegenerative disorder that affects memory, cognition, and behavior, eventually leading to severe disability. It is characterized by the accumulation of toxic proteins, such as amyloid beta plaques and tau tangles, which disrupt normal brain function. The blood-brain barrier’s dysfunction has been implicated in the disease’s progression, as it may exacerbate the buildup of these proteins and impair the brain’s ability to clear them.</p>
<p>APOE4 is a genetic variant strongly associated with an increased risk of developing sporadic Alzheimer’s disease. It affects multiple processes in the brain, including lipid metabolism, inflammation, and vascular health. APOE4 has been linked to structural and functional changes in the blood-brain barrier, suggesting that individuals carrying this gene may be particularly vulnerable to barrier dysfunction. However, how APOE4 contributes to blood-brain barrier breakdown and its subsequent effects on Alzheimer’s-related changes has not been fully clarified.</p>
<p>“We now appreciate that there are likely many converging avenues leading towards Alzheimer’s disease,” said study author <a href="https://neurosciences.ucsd.edu/research/labs/reas/index.html">Emilie Reas</a>, an assistant professor of neuroscience at the University of California, San Diego.</p>
<p>“Disruption of the blood-brain barrier is a potential pathway by which factors such as inflammation, environmental toxins, vascular disease, or metabolic dysfunction could all promote neurodegeneration and cognitive decline. This made us interested in understanding what happens to the blood-brain barrier in the very earliest stages of Alzheimer’s disease – before symptoms appear – and how its breakdown might affect brain health.”</p>
<p>The research included 55 participants aged 61 to 90, drawn from the San Diego community and an Alzheimer’s research center. Participants were categorized as cognitively normal or mildly impaired based on cognitive tests.</p>
<p>To evaluate blood-brain barrier function, the team used dynamic contrast-enhanced magnetic resonance imaging, a technique that tracks how a contrast agent moves from blood vessels into surrounding brain tissue. This allowed them to measure blood-brain barrier permeability across different brain regions, including the hippocampus, entorhinal cortex, and broader cortical gray matter. They also assessed brain microstructure using diffusion imaging and measured amyloid beta levels using positron emission tomography or cerebrospinal fluid analysis.</p>
<p>Participants underwent genetic testing to determine APOE4 status. The researchers then analyzed how blood-brain barrier permeability varied by APOE4 presence and amyloid status, and how it related to structural brain changes and cognitive performance.</p>
<p>The researchers found that APOE4 carriers had higher blood-brain barrier permeability across the brain’s gray matter compared to non-carriers. Notably, this difference was observed even in cognitively normal individuals who tested negative for amyloid beta, suggesting that blood-brain barrier dysfunction occurs early, before other Alzheimer’s markers are detectable. Among amyloid-positive individuals, the relationship between blood-brain barrier dysfunction and structural changes in the entorhinal cortex was especially pronounced, with evidence of neuronal loss and increased fluid accumulation in brain tissue.</p>
<p>Blood-brain barrier permeability did not correlate with cognitive test performance, suggesting that dysfunction may precede noticeable cognitive decline. Additionally, no significant association was found between age and blood-brain barrier permeability, supporting the idea that changes observed in APOE4 carriers reflect pathological processes rather than normal aging.</p>
<p>“Other studies have found blood-brain barrier breakdown in adults with Alzheimer’s dementia or memory impairment, but to our surprise, we observed no difference between those with or without memory impairment,” Reas told PsyPost. “The main difference is that our study was enriched with cognitively normal older adults who are at higher risk for Alzheimer’s disease. So we believe these individuals were already showing blood-brain barrier dysfunction because they are already on the trajectory to Alzheimer’s disease.”</p>
<p>Interestingly, the breakdown of the blood-brain barrier in APOE4 carriers was not limited to regions traditionally associated with early Alzheimer’s, such as the hippocampus. Instead, it appeared diffusely across the cortical gray matter. This widespread dysfunction could reflect the APOE4 gene’s influence on vascular health, including its effects on inflammation, tight junctions between cells in the blood-brain barrier, and the brain’s waste-clearing mechanisms.</p>
<p>“Our findings suggest that the blood-brain barrier becomes ‘leaky’ in the very early stages of Alzheimer’s disease,” Reas explained. “We believe it’s an early change because it appears in people at higher genetic risk for Alzheimer’s disease, even before any memory problems or abnormal proteins are detectable. We also found that it is also associated with subtle, or ‘microstructural,’ damage to important memory regions, suggesting that it may be involved in early neurodegenerative changes.”</p>
<p>The study offers valuable insights but also has limitations. Its cross-sectional design means it cannot establish a timeline for when blood-brain barrier dysfunction begins relative to other Alzheimer’s-related changes, such as amyloid beta buildup or tau tangles. The small sample size, especially among participants with cognitive impairment, may have limited the ability to detect certain effects.</p>
<p>“Important limitations of our study are the small number of participants who were mostly non-Hispanic White, and that we were only able to conduct MRI at one time-point,” Reas noted. “We are currently expanding our dataset with a more diverse sample, and hope to conduct longitudinal follow-up imaging in the future.”</p>
<p>“In the future, we hope to monitor changes in blood-brain barrier function across the time-course of Alzheimer’s disease, and to understand how it relates to other key pathological changes during the disease. We also aim to understand how protective or risk factors – including health, lifestyle, or genetics – modify blood-brain barrier function over the final decades of life.”</p>
<p>The study, “<a href="https://doi.org/10.1002/alz.14302">APOE 𝜀4-related blood–brain barrier breakdown is associated with microstructural abnormalities</a>,” was authored by Emilie T. Reas, Seraphina K. Solders, Amaryllis Tsiknia, Curtis Triebswetter, Qian Shen, Charlotte S. Rivera, Murray J. Andrews, Austin Alderson-Myers, and James B. Brewer.</p></p>
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<td><a href="https://www.psypost.org/high-potency-cannabis-use-leaves-a-distinct-mark-on-dna/" 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;">High-potency cannabis use leaves a distinct mark on DNA</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 25th 2024, 14:00</div>
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<p><p>Cannabis is one of the most <a href="https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(22)00205-5/fulltext">commonly used drugs</a> in the world. Yet there’s still much we don’t know about it and what effects it has on the brain – including why cannabis <a href="https://www.sciencedirect.com/topics/neuroscience/cannabis-induced-psychosis">triggers psychosis</a> in some people who use the drug. But our recent study has just brought us closer to understanding the biological impact of high-potency cannabis use.</p>
<p>Published in the journal <em>Molecular Psychiatry</em>, our study demonstrates that high-potency cannabis leaves a <a href="https://doi.org/10.1038/s41380-024-02689-0">distinct mark on DNA</a>. We also found that these DNA changes were different in people experiencing their first episode of psychosis compared to users who’d never experienced psychosis. This suggests looking at how cannabis use modifies DNA could help identify those most at risk of developing psychosis.</p>
<p>The amount of THC (Delta-9_tetrahydrocannabinol), the main ingredient in cannabis that makes people feel “high”, has been <a href="https://www.euda.europa.eu/publications/european-drug-report/2023/cannabis_en">steadily increasing</a> since the 1990s in the UK and US. In Colorado, where the drug is legal, it’s possible to buy <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625695">cannabis with 90% THC</a>. While THC is one of over 144 other chemicals found in the cannabis plant, it’s the primary compound used to estimate the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4611354/">potency of cannabis</a>.</p>
<p>Many studies have shown that the greater the THC concentration, the stronger the effects on the user. For example, research has found that people who use high-potency cannabis (with THC of 10% or more) daily are <a href="https://www.thelancet.com/article/S2215-0366(19)30048-3/fulltext">five times more likely</a> to develop a psychotic disorder compared to people who have never used cannabis.</p>
<p>Psychotic disorders associated with <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8223239/">daily use of high-potency cannabis</a> often manifest through a range of symptoms. These can include <a href="https://www.ncbi.nlm.nih.gov/books/NBK447654/">auditory hallucinations</a> (hearing voices that others cannot hear), <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10919765/">delusions of persecution</a> (feeling the target of a conspiracy without evidence) and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10649488/pdf/bmjment-2023-300880.pdf">paranoia</a> (perceiving the environment as hostile and interpreting interactions suspiciously). These are all very distressing and disabling experiences.</p>
<p>Our study aimed the explore the mark that current cannabis use leaves on the DNA. We also wanted to understand if this mark is specific to high-potency cannabis use – and if this might help to identify those users at greater risk of experiencing psychosis.</p>
<p>To do this, we examined the effects of cannabis use on an molecular process called DNA methylation. DNA methylation is a chemical process that regulates gene activity by turning genes on or off and controlling how genes are expressed without changing the structure of the DNA itself. DNA methylation is just one of the many mechanisms that regulate gene activity and are part of an important biological process known as epigenetics. Epigenetics <a href="https://pubmed.ncbi.nlm.nih.gov/32445090/">underpin the interplay</a> between our environment, the lifestyle choices we make (such as using cannabis or exercising) and our physical and mental health.</p>
<p>While <a href="https://doi.org/10.1002/ajmg.b.32813">previous studies</a> have investigated the impact of lifetime cannabis use on DNA methylation, they haven’t explored what effect regular use of different cannabis potencies has on this process. Nor have they explored how this affects with people who have psychosis.</p>
<p>Our study combined data from two large first case-control studies: the Genetic and Psychosis study, which was conducted in south London, and the EU-GEI study, which included participants from England, France, the Netherlands, Italy, Spain and Brazil. Both of these studies collected data on people experiencing their first episode of psychosis and participants who had no health problems and represented the local population.</p>
<p>In total, we looked at 239 people who were experiencing their first episode of psychosis and 443 healthy volunteers. Around 65% of participants were male. Participants ranged in age 16-72. All participants provided information on their cannabis use, as well as DNA samples from their blood.</p>
<p>Around 38% of participants were using cannabis more than once a week. Of those who had used cannabis, the majority had been using high-potency cannabis more than once a week – and had started when they were around 16 years old.</p>
<p>Analyses of DNA methylation were then performed across multiple parts of the whole genome. The analysis took into account the potential impact of several biological and environmental confounders that may have affected the results – such as age, gender, ethnicity, tobacco smoking and the cellular makeup of each blood sample.</p>
<h2>DNA signature</h2>
<p>Our findings revealed that using high-potency cannabis alters DNA methylation – particularly in genes related to energy and immune system functions. This was true for participants who had used high-potency cannabis. However, people who had experienced psychosis had a different signature of alteration in their DNA.</p>
<p>These epigenetic changes show how external factors (like drug use) can alter how genes work. Very importantly, these changes were not explained by tobacco – which is usually mixed into joints by many cannabis users, and is known to <a href="https://www.thelancet.com/article/S2215-0366(19)30048-3/fulltext">alter DNA methylation</a>.</p>
<p>This finding also highlights epigenetic changes as a potential link between high-potency cannabis and psychosis. DNA methylation, which bridges the gap between genetics and environmental factors, is a key mechanism that allows external influences (such as substance use) to impact gene activity. By studying epigenetic changes, researchers may be able to develop a greater understanding on how cannabis use – particularly high-potency types – can influence specific biological pathways. This may in turn help us understand why some cannabis users are at increased risk of psychosis.</p>
<p>We hope that our findings will help scientists to better understand how cannabis use can affect the body’s biology. Future research should now investigate whether the DNA methylation patterns associated with cannabis use can serve as biomarkers to identify users at higher risk of developing psychosis. This could lead to more targeted prevention strategies and inform safer cannabis use practices.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/241384/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/high-potency-cannabis-use-leaves-a-distinct-mark-on-dna-new-research-241384">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/obesitys-effects-on-relationships-and-health-appear-to-be-reduced-in-areas-with-higher-prevalence/" 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;">Obesity’s effects on relationships and health appear to be reduced in areas with higher prevalence</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 25th 2024, 12:00</div>
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<p><p>Individuals with obesity often encounter challenges in relationships, employment, and health, but a recent study published in <a href="https://doi.org/10.1177/09567976241265037"><em>Psychological Science</em></a> has found that the severity of these issues can depend on where they live. The research found that in regions where obesity is more common, the associated social and health difficulties are less pronounced. These findings suggest that societal attitudes and cultural norms surrounding obesity may play a significant role in shaping its consequences.</p>
<p>Obesity is a global health challenge, with prevalence rates doubling worldwide since 1990. Today, over one in four adults in Europe and one in three adults in the United States live with obesity. Alongside well-documented health risks such as cardiovascular disease and mental health struggles, individuals with obesity often face social stigma, discrimination, and economic disadvantages. They are more likely to experience unstable relationships, unemployment, and social exclusion, compounding the health burdens of the condition.</p>
<p>The researchers aimed to explore whether these consequences vary based on the local prevalence of obesity. The underlying theory suggests that societal biases and stigmatization tend to target traits that deviate from the norm. If obesity is more common in a region, it may be viewed as less unusual, potentially reducing the discrimination and negative stereotypes associated with it.</p>
<p>“Obesity affects many people, particularly in the Western world – and it has severe consequences for those affected. Our project originated from the fact that obesity rates greatly vary between and within countries,” said study author Jana Berkessel, a researcher at the Mannheim Centre for European Social Research at the University of Mannheim.</p>
<p>“For example, in the United States, there are some regions where roughly 50% of the population are living with obesity, while in other regions only about 5% of the population are living with obesity. It is quite easily imaginable that persons with obesity in regions with low obesity rates stick out much more and, therefore, will make very different social experiences on an everyday basis.”</p>
<p>The researchers used data from over 3.4 million individuals across the United States and United Kingdom. The study was divided into three parts, examining regional variations in obesity’s consequences and the role of societal attitudes.</p>
<p>Study 1 utilized data from the Behavioral Risk Factor Surveillance System, a large-scale, nationwide survey conducted in the United States. This dataset included responses from 2.8 million participants across more than 2,400 counties. Participants provided self-reported information about their weight, height, relationship status, employment, and general health. By linking these individual responses to regional obesity rates, the researchers could assess how the consequences of obesity differed depending on the local prevalence of the condition.</p>
<p>Study 2 replicated the analysis using data from the BBC Lab in the United Kingdom, a similarly large-scale survey but with notable differences in regional cultural contexts. This dataset included 180,000 participants from 378 districts, offering a cross-national perspective on how regional obesity prevalence impacts personal outcomes.</p>
<p>Study 3 extended the findings by combining U.S. data with insights from Project Implicit, a large-scale initiative measuring explicit weight bias. Explicit weight bias refers to openly expressed stereotypes and prejudices toward individuals with obesity, such as the assumption that they are lazy or undisciplined. This final study aimed to understand whether regional variations in weight bias could explain why the consequences of obesity were less severe in some areas than others.</p>
<p>To measure regional obesity prevalence, the researchers calculated the proportion of individuals with a body mass index (BMI) of 30 or higher within each region. Regional obesity prevalence was then analyzed alongside explicit weight bias scores to determine their influence on the social, economic, and health outcomes reported by participants.</p>
<p>The findings revealed that, across both nations, individuals with obesity generally faced more challenges in relationships, employment, and health compared to their non-obese counterparts. However, the extent of these challenges varied significantly by region.</p>
<p>In regions where obesity prevalence was low, individuals with obesity were more likely to be single compared to those without obesity. For example, in the United States, people with obesity in counties with low obesity prevalence were 1.2 times more likely to be single than their non-obese peers. Conversely, in counties with high obesity prevalence, this disparity disappeared or even reversed, with individuals with obesity slightly less likely to be single than their non-obese counterparts.</p>
<p>Health challenges associated with obesity, such as reporting poor general health, also exhibited regional variation. In low-obesity regions, individuals with obesity were over four times more likely to report poor health compared to their non-obese peers. However, in high-obesity regions, this likelihood was reduced to 1.5 times. While health disparities were still present, their reduced severity in high-obesity areas highlights the potential mitigating effect of cultural norms and societal acceptance on perceived or reported health outcomes.</p>
<p>The researchers found that explicit weight bias was lower in regions where obesity was more prevalent. This reduced bias partially explained why the social and health consequences of obesity were less severe in those areas. For instance, in high-obese regions, the likelihood of being single or reporting poor health was mediated by lower levels of weight bias.</p>
<p>“Across the two datasets we found that obesity has adverse consequences – in the social, economic, and health domain – but that these consequences were less severe in some regions,” Berkessel told PsyPost. “For me, this means, that at least some of the adverse consequences of obesity appear socially construed and, thus, can be reduced. Just to give an example, one way to change society’s views of obesity may be through a more true-to-life representation of different body sizes in the media.”</p>
<p>However, employment outcomes for individuals with obesity were less influenced by regional obesity prevalence. In both the United States and the United Kingdom, individuals with obesity were consistently more likely to be unemployed than those without obesity, regardless of local obesity rates and weight bias. This suggests that factors beyond regional attitudes may contribute to these persistent disparities.</p>
<p>The study highlights important regional variations in the consequences of obesity, but it has limitations. First, the data are primarily from Western countries, and the findings may not generalize to non-Western cultures with different attitudes toward obesity. Second, the study’s cross-sectional design does not establish causality. It is unclear whether living in high-obese regions reduces the impact of obesity or whether individuals with obesity are more likely to remain in such areas. Lastly, while weight bias was identified as a mediator, other factors, such as social comparisons or environmental accommodations, may also contribute to regional differences.</p>
<p>“In my research I am generally interested in how the social context we live in affects our physical and psychological well-being,” Berkessel said. “For example, in a recent study (<a href="https://journals.sagepub.com/doi/full/10.1177/09567976231196145" target="_blank" rel="noopener">Ebert, Berkessel, & Jonsson, 2023, PsychScience</a>) we examined whether the political climate in a state relates to the longevity of political partisans. In another study (<a href="https://www.pnas.org/doi/10.1073/pnas.2103913118" target="_blank" rel="noopener">Berkessel et al., 2021, PNAS</a>) I found that money has a stronger effect on our well-being in countries that are less religious.”</p>
<p>The study, “<a href="https://doi.org/10.1177/09567976241265037">On the Unequal Burden of Obesity: Obesity’s Adverse Consequences Are Contingent on Regional Obesity Prevalence</a>,” was authored by Jana B. Berkessel, Tobias Ebert, Jochen E. Gebauer, and Peter J. Rentfrow.</p></p>
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<td><a href="https://www.psypost.org/parents-are-not-to-blame-for-their-childrens-picky-eating-study-finds/" 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;">Parents are not to blame for their children’s picky eating, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 25th 2024, 10:00</div>
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<p><p>A longitudinal study of British children found that fussy eating is largely determined by genetic factors at all ages. However, it also shows an environmental influence during toddlerhood, suggesting that early interventions to prevent it might achieve some success. The paper was published in the<a href="https://acamh.onlinelibrary.wiley.com/doi/10.1111/jcpp.14053"> <em>Journal of Child Psychology and Psychiatry</em></a>.</p>
<p>Fussy eating, also known as picky eating or food fussiness, is the tendency to eat only a limited range of foods. Individuals with this trait are particular about the flavor or texture of food and are reluctant to try new foods and flavors. While picky eating is commonly observed in young children, it can persist into adulthood. It typically arises in environments where food variety is encouraged, such as at school, social gatherings, or even at home when someone else prepares the food.</p>
<p>Because fussy eaters limit the range of foods they consume, they may experience nutritional deficiencies. When fussy eaters are children, their caregivers often face stress and frustration trying to manage their eating habits. Research suggests that early exposure to a variety of foods and positive mealtime experiences can help reduce food fussiness.</p>
<p>Study author Zeynep Nas and her colleagues aimed to explore the developmental trajectory of fussy eating from toddlerhood to early adolescence and estimate the contribution of genetic and environmental factors to individual differences in this trait.</p>
<p>Participants in the study were drawn from Gemini, a population-based cohort of twin children born in England and Wales in 2007. These children have been followed as part of an ongoing research project for over a decade. At the study’s onset, the children were 16 months old, and there were 3,854 participants. By the time they reached 13 years of age, 970 participants remained in the study.</p>
<p>The researchers analyzed data on fussy eating collected at different time points using the parent-reported Child Eating Behavior Questionnaire, completed when participants were 3, 5, 7, and 13 years old. They also examined data on whether the children were monozygotic or dizygotic twins, as well as their age and sex.</p>
<p>The results showed that children whose food fussiness was above average at the earliest age tended to become even pickier as they grew older. Children who displayed a stronger increase in food fussiness over time also tended to show steeper decreases in food fussiness between the ages of 7 and 13, although their levels of food fussiness remained above average.</p>
<p>The correlation of food fussiness scores among monozygotic twins (who are genetically identical) was twice as high as that among dizygotic twins, indicating that food fussiness is largely genetically driven. Over the years, food fussiness remained moderately to highly stable throughout childhood and early adolescence.</p>
<p>The total contribution of genetic influences to individual differences in food fussiness ranged from 60% to 84%. The heritability of food fussiness was lower at 16 months than at any other time point analyzed in the study. At the same time, shared environmental factors accounted for 25% of individual differences in food fussiness at 16 months but became negligible and indistinguishable from random variation at later ages.</p>
<p>“This novel longitudinal examination provides evidence of FF [food fussiness] being a highly heritable trait that is relatively stable from toddlerhood into early adolescence, with genetic influences largely responsible for its continuity,” the study authors concluded.</p>
<p>“Parents are not to blame for their children’s innate fussy eating behaviors. Interventions targeting FF could start as early as toddlerhood and may need to be tailored and intensive at different developmental time points.”</p>
<p>The study sheds light on the nature of picky eating. However, the assessments of picky eating were based on parental reports, and parents were aware when their children were monozygotic twins. This awareness might have led parents to evaluate their monozygotic twin children as more similar than they truly were, potentially inflating the observed similarities in food fussiness scores and affecting the study’s results and conclusions. Additionally, as the study progressed, a large proportion of participants dropped out, which may have influenced the findings.</p>
<p>The paper, “<a href="https://doi.org/10.1111/jcpp.14053">Nature and nurture in fussy eating from toddlerhood to early adolescence: findings from the Gemini twin cohort,</a>” was authored by Zeynep Nas, Moritz Herle, Alice R. Kininmonth, Andrea D. Smith, Rachel Bryant-Waugh, Alison Fildes, and Clare H. Llewellyn.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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