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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/liver-hormone-fgf21-may-play-key-role-in-alcohol-use-disorder-study-suggests/" 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;">Liver hormone FGF21 may play key role in alcohol use disorder, study suggests</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 27th 2024, 10:00</div>
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<p><p>A recent study published in the journal <a href="https://www.sciencedirect.com/science/article/pii/S0741832924001125"><em>Alcohol</em></a> suggests that a liver hormone, fibroblast growth factor 21 (FGF21), may play a significant role in alcohol use disorder (AUD). The researchers found that after alcohol consumption, individuals diagnosed with AUD showed a greater increase in FGF21 levels compared to healthy individuals with no family history of AUD. This finding could point to FGF21 being involved in the body’s response to alcohol and its role in the development of AUD, potentially leading to new approaches for treatment.</p>
<p>Alcohol use disorder is a condition that affects millions of people worldwide. Despite a growing understanding of the social and genetic factors involved, scientists still do not fully understand the biological mechanisms that contribute to the development of AUD.</p>
<p>One area of interest in recent years has been the hormone FGF21, which is produced by the liver and has been shown to increase significantly in the bloodstream after alcohol consumption. Previous research in animals suggested that FGF21 might reduce alcohol intake, raising the possibility that it could play a role in regulating how much people drink.</p>
<p>“AUD affects 5% of the global population. Despite its high prevalence, the pathophysiology of AUD remains unknown,” said study author Amalie Rasmussen Lanng of the Center for Clinical Metabolic Research at Gentofte Hospital and the Department for Clinical Pharmacology at Bispebjerg Hospital.</p>
<p>“Fibroblast growth factor 21 (FGF21) has been implicated by recent genome-wide association studies as a regulator of alcohol consumption. Therefore, we hypothesized that it plays a key role in regulating alcohol intake in humans, maybe in a classic negative feedback loop.”</p>
<p>To explore the relationship between FGF21 and alcohol use disorder, the researchers recruited three groups of male participants: 15 individuals diagnosed with AUD, 15 healthy individuals without AUD but with a father who had AUD (referred to as the predisposed group), and 15 healthy individuals with no family history of AUD (the control group). All participants were between 20 and 65 years old, and none had other medical conditions like liver disease or diabetes that could affect the results.</p>
<p>On the day of the study, the participants arrived after an overnight fast and were given a specific amount of alcohol based on their body weight. This controlled amount was consumed over a 10-minute period. Blood samples were collected before the alcohol intake and then every hour for 10 hours afterward. These samples were used to measure FGF21 levels in the bloodstream, as well as blood alcohol levels. Additionally, the participants completed a series of questions about their desire to drink alcohol throughout the testing period.</p>
<p>The researchers also ensured that conditions were controlled during the study. For example, all participants ate a standardized meal three hours after consuming alcohol to prevent any effects from differing nutritional intake.</p>
<p>The results showed that alcohol consumption caused an increase in FGF21 levels in all three groups, confirming earlier studies that this hormone rises in response to alcohol intake. However, individuals diagnosed with AUD had a significantly higher spike in FGF21 levels compared to the control group. The predisposed group, while showing elevated FGF21 levels, did not experience as dramatic a rise as the AUD group, but their levels were still higher than the control group’s.</p>
<p>“In our study, people with AUD had higher FGF21 blood concentrations after alcohol intake compared with healthy people, maybe because people with AUD have FGF21-resistance,” Lanng told PsyPost.</p>
<p>The researchers also found differences in the participants’ desire to drink alcohol. Those in the AUD group reported a higher baseline desire for alcohol before consuming it and continued to express a strong desire throughout the testing period. Interestingly, participants in the predisposed group experienced a stronger urge to drink alcohol shortly after consumption compared to the control group, suggesting that a genetic predisposition to AUD might affect how the body responds to alcohol.</p>
<p>“People genetically predisposed to AUD had a strong desire for alcohol just after alcohol intake, not significantly different from people with AUD but significantly different from the healthy control group,” Lanng said. “This illustrates one of the likely reasons for the higher risk of AUD in people genetically predisposed to AUD.”</p>
<p>Despite these differences, the concentration of alcohol in the bloodstream was similar across all three groups. This indicates that the differences in FGF21 levels and alcohol preference were not due to variations in how the participants metabolized alcohol.</p>
<p>While these findings shed light on the possible role of FGF21 in alcohol use disorder, the study has some limitations. First, the sample size was relatively small, with only 45 participants. This limits the strength of the conclusions that can be drawn, and larger studies will be necessary to confirm the findings. Additionally, the study only included men, which limits its applicability to women. The researchers acknowledged this as a limitation but explained that their goal was to keep the study group as homogeneous as possible to increase the reliability of the results.</p>
<p>This study opens several avenues for future research. One area of interest is whether FGF21 plays a direct role in controlling alcohol intake in humans, as suggested by animal studies. Understanding this could help researchers determine if FGF21 could be a target for new treatments for alcohol use disorder. For example, if FGF21 can reduce the desire to drink alcohol, medications that boost its production or enhance its effects could be developed to help individuals reduce their alcohol consumption.</p>
<p>Another important question is why individuals with alcohol use disorder show such a strong response in FGF21 levels after drinking. The researchers speculate that this could be due to a form of “resistance” to FGF21, meaning that the hormone is less effective at reducing the desire to drink in people with AUD, leading to increased production of the hormone. Further studies could investigate this possibility by exploring how the body’s sensitivity to FGF21 changes in individuals with AUD.</p>
<p>“The long-term goal is to gain a detailed understanding of AUD pathophysiology, which will hopefully lead to better treatment opportunities for people with AUD, which could be FGF21-based/analogs,” Lanng said.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.alcohol.2024.08.001">Alcohol-induced fibroblast growth factor 21 secretion is increased in individuals with alcohol use disorder</a>,” was authored by Amalie R. Lanng, Lærke S. Gasbjerg, Andrea I.F. Sucksdorff, Jens S. Svenningsen, Tina Vilsbøll, Matthew P. Gillum, and Filip K. Knop.</p></p>
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<td><a href="https://www.psypost.org/financial-stress-is-associated-with-increased-risk-of-cardiovascular-diseases/" 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;">Financial stress is associated with increased risk of cardiovascular diseases</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 27th 2024, 08:00</div>
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<p><p>A new meta-analysis has examined the association between financial stress and the risk of cardiovascular diseases. The results showed that individuals experiencing financial stress have around a 19% higher risk of developing a major cardiovascular event, such as a myocardial infarction, stroke, or cardiovascular death. The paper was published in <a href="https://www.sciencedirect.com/science/article/abs/pii/S0146280623005704"><em>Current Problems in Cardiology</em></a>.</p>
<p>Cardiovascular diseases are a group of disorders that affect the heart and blood vessels. They include conditions like coronary artery disease, stroke, heart failure, and hypertension. These diseases are the leading cause of death globally, responsible for millions of deaths every year. Atherosclerosis, the buildup of fatty deposits in the arteries, is a primary cause of many cardiovascular conditions, leading to reduced blood flow and an increased risk of heart attacks or strokes.</p>
<p>However, atherosclerosis is not the only cause. Major risk factors for cardiovascular diseases include high blood pressure, high cholesterol, smoking, obesity, and lack of physical activity. Diabetes and a family history of heart disease also increase the risk. Researchers have reported that certain life events or conditions might be associated with the risk of cardiovascular diseases.</p>
<p>Study author Shiba Sai Swarup and her colleagues sought to examine the relationship between financial stress and the risk of developing cardiovascular diseases. They conducted a meta-analysis, searching the scientific literature for published studies reporting on cardiovascular diseases and stress or worries caused by financial troubles.</p>
<p>The authors searched for studies mentioning terms such as “economic stress,” “financial stress,” “strain,” “hardship,” “burden,” and “vulnerability.” This search resulted in over 2,000 records. However, after screening, only seven studies were identified that fulfilled the criteria for inclusion in the analysis. Two of these studies came from the U.S., two included a large number of countries, while the remaining studies were from Germany, Sweden, and Serbia. The studies were diverse, used different definitions of financial stress, and examined different cardiovascular outcomes.</p>
<p>The results showed that financial stress was associated with a 19% higher risk of experiencing a major cardiac event. These events included myocardial infarction, stroke, or cardiovascular death. The increased risk related to financial stress varied significantly between studies, ranging from a 54% reduced risk in one sample of single women to a 184% higher risk in another sample of single men.</p>
<p>“Our findings strongly advocate for healthcare professionals to incorporate assessments of financial stress into patient care protocols and for the development of health policies designed to alleviate the economic strains associated with cardiovascular conditions. By addressing both traditional and socio-economic risk factors effectively, we can significantly contribute to enhancing cardiovascular health outcomes and overall well-being,” the study authors concluded.</p>
<p>The study makes a valuable contribution to the scientific understanding of the links between financial stress and health. However, it should be noted that the number of studies included in this meta-analysis was very small, all came from Western countries, and the findings were highly varied. It is also possible that the strength of this association is not the same for different demographic groups.</p>
<p>The paper, “<a href="https://doi.org/10.1016/j.cpcardiol.2023.102153">Cardiovascular consequences of financial stress: A systematic review and meta-analysis,</a>” was authored by Shiba Sai Swarup, Asha K. P, Bijaya Kumar Padhi, Prakasini Satapathy , Muhammed Shabil, Ganesh Bushi, Aravind P. Gandhi, Mahalaqua Nazli Khatib, Shilpa Gaidhane, Quazi Syed Zahiruddin, Sarvesh Rustagi, Joshuan J. Barboza, and Ranjit Sah.</p></p>
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<td><a href="https://www.psypost.org/childhood-abuse-predicts-increased-risk-of-post-covid-conditions-new-research-shows/" 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;">Childhood abuse predicts increased risk of post-COVID conditions, new research shows</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 27th 2024, 06:00</div>
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<p><p>A new study published in <a href="https://doi.org/10.1016/j.bbi.2024.08.046"><em>Brain, Behavior, and Immunity</em></a> reveals a significant link between childhood abuse and a higher risk of developing post-COVID-19 conditions, also known as long COVID. The research found that those who experienced severe abuse as children had a 42 percent increased risk of post-COVID-19 conditions compared to those who did not experience abuse. The study highlights the importance of considering a person’s full history, including early life experiences, when assessing long-term health outcomes after COVID-19.</p>
<p>Since the beginning of the COVID-19 pandemic, many individuals who recovered from the virus have reported experiencing ongoing symptoms for weeks or even months after their initial infection. These lingering symptoms, which include fatigue, breathing difficulties, and cognitive issues, have been grouped under the term “long COVID.”</p>
<p>Researchers have been trying to identify the risk factors for long COVID, as understanding these risks may help develop better prevention and treatment strategies. However, one area that has been largely unexplored is the role that early life adversities, such as childhood abuse, may play in increasing susceptibility to long COVID.</p>
<p>Childhood abuse can have long-lasting effects on both mental and physical health. People who experienced abuse early in life are more likely to suffer from chronic health conditions, inflammation, and psychological issues later in life. These factors have also been linked to an increased risk of post-COVID conditions, leading the researchers to wonder whether childhood abuse might contribute to the development of long COVID.</p>
<p>“Childhood abuse—whether physical, emotional, or sexual—has been linked to a range of problems, including chronic illnesses and mental health issues, which affect overall well-being,” said study authors Chirag M. Vyas and <a href="https://www.hsph.harvard.edu/profile/andrea-lynne-roberts/">Andrea L. Roberts</a>, an instructor in psychiatry at Harvard Medical School and a principal research scientist at the Harvard T. H. Chan School of Public Health, respectively.</p>
<p>“Meanwhile, many people are experiencing persistent COVID-19 symptoms or “long COVID”, which is becoming a major public health concern. Although there is substantial research on childhood abuse and COVID-19 separately, we haven’t understood how childhood abuse relates to risk of long COVID.</p>
<p>“By investigating this connection, we can better understand how these issues intersect and identify the specific needs of individuals affected by both childhood trauma and long COVID. Ultimately, this research could help create more effective strategies for those at risk, improving health outcomes for vulnerable individuals dealing with the fallout from both experiences. It is about connecting the dots to help people lead healthier lives.”</p>
<p>The researchers analyzed data from three long-term health studies: the Nurses’ Health Study II, the Nurses’ Health Study 3, and the Growing Up Today Study. These studies, which have been ongoing for decades, provided a large pool of participants who had already shared information about their health history, including any experiences of childhood abuse.</p>
<p>In total, 2,851 participants were included in the final analysis. All of these individuals had tested positive for COVID-19 and provided data on both their experiences of childhood abuse and whether they experienced long-term COVID-19 symptoms. Childhood abuse was assessed using standardized questionnaires, which asked participants about both sexual and physical or emotional abuse they experienced before the age of 18. Based on their responses, the participants were categorized into different levels of abuse severity, ranging from no abuse to severe abuse.</p>
<p>To measure post-COVID conditions, participants were asked whether they had experienced any COVID-related symptoms lasting more than four weeks after their initial infection. If they reported ongoing symptoms, they were classified as having post-COVID conditions. The researchers then analyzed the data to determine whether there was a relationship between childhood abuse and post-COVID conditions, while also considering other factors like lifestyle, health conditions, and psychological well-being.</p>
<p>The study revealed a clear connection between childhood abuse and an increased risk of post-COVID conditions. Moreover, the study identified a dose-dependent relationship. Participants who reported severe childhood abuse were 42 percent more likely to develop post-COVID conditions compared to those who had not experienced abuse.</p>
<p>Interestingly, the study found that both physical and emotional abuse, as well as sexual abuse, were independently associated with post-COVID conditions. This means that any form of childhood abuse, whether physical, emotional, or sexual, could increase the risk of long-term COVID-19 symptoms.</p>
<p>“Our findings suggest that experiencing childhood abuse—whether sexual or physical/emotional—is linked to a greater likelihood of facing long COVID,” Vyas and Roberts told PsyPost. “We also found that the more severe the abuse, the higher the risk of reporting these conditions. In simpler terms, if someone experienced more intense or serious forms of abuse during childhood, they might be more likely to report long COVID symptoms. Ultimately, this research underscores the importance of considering a person’s full history—including experiences of abuse—when evaluating their health outcomes after COVID-19.”</p>
<p>This relationship remained strong even when the researchers took into account other factors, such as participants’ smoking habits, body weight, and history of chronic health conditions like diabetes or asthma. In fact, the researchers found that while these lifestyle and health-related factors did explain part of the connection between childhood abuse and post-COVID conditions, they did not account for all of it. The biological and psychological effects of abuse, such as immune system dysfunction and chronic inflammation, may play a larger role.</p>
<p>“We also looked into whether lifestyle and health-related factors—like smoking and medical comorbidities—play a role in this relationship,” the researchers explained. “However, we found that these factors only explained about 25% of the connection. This suggests that there are likely other important factors at play that we haven’t fully understood yet.”</p>
<p>Despite the important insights this study provides, there are some limitations that should be considered. First, the sample was predominantly composed of white women, most of whom were healthcare professionals. This raises questions about whether the findings would apply to more diverse populations, including men or individuals from different racial or socioeconomic backgrounds. The researchers noted that future studies should aim to include more diverse groups to better understand how childhood abuse might affect different segments of the population.</p>
<p>Additionally, because the study relied on participants’ self-reports of both their abuse experiences and their COVID-19 symptoms, there is a possibility of recall bias.</p>
<p>“We gathered data about childhood abuse and long COVID based on what participants reported in study questionnaires,” Vyas and Roberts noted. “This means that people shared their experiences rather than us measuring or assessing them directly. Self-reporting can provide valuable insights, but it also has some limitations.”</p>
<p>“For example, participants might remember their experiences differently or may not feel comfortable sharing certain details. Because of this, it is important to interpret the results carefully, understanding that they reflect individuals’ perspectives and experiences.”</p>
<p>Looking ahead, the researchers plan to investigate these biological mechanisms in more detail. Additionally, they suggest that future studies could examine whether interventions aimed at reducing the long-term effects of childhood abuse might help lower the risk of long COVID in this vulnerable population.</p>
<p>“The long-term goals of this research are twofold,” the researchers said. “The first goal is to explore the biological mechanisms that connect childhood abuse to long COVID. The focus is on understanding how experiences of abuse might affect the body and brain in ways that could increase risk of post-COVID-19 conditions. This could involve examining factors like stress responses, inflammation, or other physical changes that might occur due to childhood abuse.”</p>
<p>“The second goal is to develop effective strategies for individuals who have experienced both childhood abuse and COVID-19. The intention is to identify ways to improve long-term health and well-being for these individuals. This could include creating targeted therapies, support programs, or health interventions that address their unique needs.”</p>
<p>The study, “<a href="https://www.sciencedirect.com/science/article/abs/pii/S0889159124005695">Association between childhood abuse and risk of post-COVID-19 conditions: Results from three large prospective cohort studies</a>,” was authored by Chirag M. Vyas, Siwen Wang, Anthony M. Menor, Laura D. Kubzansky, Natalie Slopen, Janet Rich-Edwards, Jorge E. Chavarro, Jae H. Kang, and Andrea L. Roberts.</p></p>
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<td><a href="https://www.psypost.org/unlocking-mitochondrial-secrets-new-hope-for-parkinsons-treatment/" 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;">Unlocking mitochondrial secrets: New hope for Parkinson’s treatment</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 26th 2024, 16:00</div>
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<p><p>In 1817, a British physician named James Parkinson published <a href="https://doi.org/10.1176/jnp.14.2.223">An Essay on the Shaking Palsy</a>, describing for the first time cases of a neurodegenerative disorder now known as Parkinson’s disease. Today, Parkinson’s disease is the <a href="https://www.parkinson.org/understanding-parkinsons/statistics">second most common neurodegenerative disease</a> in the U.S. It affects about 1 million Americans and more than 10 million people worldwide.</p>
<p>The signature shaking in patients with the disease is the result of <a href="https://doi.org/10.1017/S0317167100010209">dying brain cells that control movement</a>. To date, there are no treatments available that can stop or slow down the death of those cells.</p>
<p>We are <a href="https://scholar.google.com/citations?user=pJSgt4YAAAAJ&hl=en">researchers who study</a> <a href="https://scholar.google.com/citations?user=0WkCIv0AAAAJ&hl=en">Parkinson’s disease</a>. For over a decade, <a href="https://stempel.fiu.edu/research/labs/parkinsons-disease-research-laboratory/">our lab</a> has been investigating the role that mitochondria – the powerhouses that fuel cells – play in Parkinson’s.</p>
<p>Our research has <a href="https://doi.org/10.1186/s13024-024-00708-w">identified a key protein</a> that could lead to new treatments for Parkinson’s disease and other brain conditions.</p>
<h2>Mitochondrial dynamics and neurodegeneration</h2>
<p>Unlike actual power plants, which are set in size and location, mitochondria are rather dynamic. They constantly shift in size, number and location, traveling between many different parts of the cells to meet different demands. These <a href="https://doi.org/10.1038/s41392-023-01547-9">mitochondrial dynamics</a> are vital to not only the function of mitochondria but also the health of cells overall.</p>
<p>A cell is like a factory. Multiple departments must seamlessly work together for smooth operations. Because many major processes interconnect, impaired mitochondrial dynamics could cause a domino effect across departments and vice versa. <a href="https://doi.org/10.1016/j.cub.2022.07.025">Collective malfunction</a> in different parts of the cell eventually leads to cell death.</p>
<figure class="wp-caption aligncenter"><a href="https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=45&auto=format&w=1000&fit=clip"><img fetchpriority="high" decoding="async" src="https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=45&auto=format&w=754&fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=45&auto=format&w=600&h=266&fit=crop&dpr=1 600w, https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=30&auto=format&w=600&h=266&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=15&auto=format&w=600&h=266&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=45&auto=format&w=754&h=335&fit=crop&dpr=1 754w, https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=30&auto=format&w=754&h=335&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/615894/original/file-20240827-16-7e8rrs.jpg?ixlib=rb-4.1.0&q=15&auto=format&w=754&h=335&fit=crop&dpr=3 2262w" alt="Side-by-side comparison of labeled illustration of cross-section of mitochondria and its micrograph" width="600" height="266"></a><figcaption class="wp-caption-text">Mitochondria produce the energy that fuels cells.<a class="source" href="https://openstax.org/books/anatomy-and-physiology-2e/pages/3-2-the-cytoplasm-and-cellular-organelles">OpenStax</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></figcaption></figure>
<p>Emerging studies have linked imbalances in mitochondrial processes <a href="https://doi.org/10.3390/cells8090961">to different</a> <a href="https://doi.org/10.1038/nrn2417">neurodegenerative diseases</a>, including <a href="https://doi.org/10.3389/fgene.2017.00177">Parkinson’s disease</a>. In many neurodegenerative disorders, certain disease-related factors, such as toxic proteins and environmental neurotoxins, disrupt the harmony of mitochondrial fusion and division.</p>
<p>Impaired mitochondrial dynamics also take down the cell’s <a href="https://doi.org/10.1016/j.tcb.2020.01.008">cleaning and waste recycling processes</a>, leading to a pileup of toxic proteins that form harmful aggregates inside the cell. In Parkinson’s, the presence of these toxic protein aggregates is a <a href="https://doi.org/10.1016/j.cell.2022.12.032">hallmark of the disease</a>.</p>
<h2>Targeting mitochondria to treat Parkinson’s</h2>
<p>Our team hypothesized that restoring mitochondrial function by manipulating its own dynamics could protect against neuronal dysfunction and cell death.</p>
<p>In an effort to restore mitochondrial function in Parkinson’s, we targeted a key protein that controls mitochondrial dynamics called <a href="https://doi.org/10.1091/mbc.12.8.2245">dynamin-related protein 1, or Drp1</a>. Naturally abundant in cells, this protein travels to mitochondria when they divide into smaller sizes for higher mobility and quality control. However, too much Drp1 activity causes excessive division, leading to fragmented mitochondria with impaired function.</p>
<p>Using different lab models of Parkinson’s, <a href="https://doi.org/10.1074/jbc.M109.066662">including neuronal</a> <a href="https://doi.org/10.1186/s40478-019-0821-4">cell cultures</a> <a href="https://doi.org/10.1038/s41598-017-07181-0">and rat</a> <a href="https://doi.org/10.1038/ncomms6244">and mice</a> models, we found that the presence of environmental toxins and toxic proteins linked to Parkinson’s cause mitochondria to become fragmented and dysfunctional. Their presence also coincided with the buildup of those same toxic proteins, worsening the health of neuronal cells until they eventually started dying.</p>
<p>We also observed behavior changes in rats that impaired their movements. By reducing the activity of Drp1, however, we were able to <a href="https://doi.org/10.1038/s41598-017-07181-0">restore mitochondria</a> to their normal activity and function. Their neurons were protected from disease and able to continue functioning.</p>
<p>In our 2024 study, we found an <a href="https://doi.org/10.1186/s13024-024-00708-w">additional benefit</a> of targeting Drp1.</p>
<p>We exposed neuronal cells to <a href="https://doi.org/10.3390/biom13081190">manganese, a heavy metal</a> linked to neurodegeneration and an increased risk of parkinsonism. Surprisingly, we found that manganese was more <a href="https://doi.org/10.1186/s13024-024-00708-w">harmful to the cell’s waste recycling system</a> than to its mitochondria, causing buildup of toxic proteins before mitochondria became dysfunctional. Inhibiting Drp1, however, coaxed the waste recycling system back into action, cleaning up toxic proteins despite the presence of manganese.</p>
<p>Our findings indicate that inhibiting Drp1 from more than one pathway could protect cells from degeneration. Now, we’ve identified some FDA-approved compounds that target Drp1 and are testing them as potential treatments for Parkinson’s.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/235860/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/mitochondria-keep-your-brain-cells-alive-helping-them-run-smoothly-may-protect-against-parkinsons-disease-235860">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/puppy-blues-anxiety-frustration-and-exhaustion-common-among-new-dog-owners-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;">‘Puppy blues’: Anxiety, frustration, and exhaustion common among new dog owners, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 26th 2024, 14:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1038/s44184-024-00072-z" target="_blank" rel="noopener">npj Mental Health Research</a></em> has found that many dog owners experience feelings akin to the postnatal baby blues when caring for a new puppy. These “puppy blues” are characterized by feelings of anxiety, frustration, and exhaustion. The emotional strain can make it difficult for owners to bond with their puppies and leave them questioning their ability to care for their new pet. However, these negative feelings generally fade with time, with memories of puppyhood becoming more positive the longer it has been since the puppy phase.</p>
<p>The researchers set out to investigate a phenomenon that many dog owners report experiencing but that has received little attention in scientific research: the emotional strain that comes with caring for a new puppy. While owning a puppy is generally seen as a joyful time, it can also be stressful and emotionally taxing. Dog owners often face a range of challenges, such as sleep deprivation, fear for the puppy’s health, and frustration over the puppy’s behavior. Although the term “puppy blues” is familiar to many, no prior research had systematically studied this experience.</p>
<p>“A few years ago, I noticed on dog-related social media forums that new puppy owners often reported anxiety, frustration, and a loss of attachment to their puppies, often comparing it to the ‘baby blues’ some parents experience,” said study author Aada Ståhl, a doctoral researcher at the University of Helsinki and Folkhälsan Research Center (Group Lohi).</p>
<p>“As a psychologist, I was intrigued but found no research on the topic at the time. Last year, two qualitative studies about this phenomenon were published: one analyzed online discussions, and the other interviewed 19 puppy owners. Seeing a gap in quantitative research, we decided to investigate the symptoms, prevalence, and duration of puppy blues.”</p>
<p>The researchers first gathered detailed qualitative data from over 100 dog owners who reported experiencing emotional difficulties during their puppy’s early life. These participants were recruited via social media and were asked open-ended questions about their feelings and experiences while caring for a new puppy. The responses were analyzed qualitatively to identify recurring themes of emotional strain, such as anxiety, frustration, exhaustion, and regret.</p>
<p>From these initial responses, the research team generated 15 specific items to be used in a new survey, designed to measure the puppy blues. The goal was to create questions that captured the full range of emotional challenges dog owners face during their puppy’s early stages. For example, questions were focused on owners’ worries about the puppy’s health, doubts about their own ability to care for the puppy, feelings of frustration, and physical and mental exhaustion.</p>
<p>Next, the researchers distributed the newly developed survey to over 2,000 dog owners. Participants were recruited from a larger pool of individuals who had previously taken part in studies related to dog behavior and owner well-being. The sample included a diverse range of dog breeds and ownership experiences, though most participants were from Finland.</p>
<p>The researchers found that nearly half of the dog owners surveyed reported experiencing significant negative emotions during their puppy’s early months, though only about 10 percent experienced these feelings to a severe degree. These emotions manifested primarily in three forms: anxiety, frustration, and weariness.</p>
<p>The anxiety reported by owners was often rooted in concerns about their ability to care for the puppy adequately and fears about the puppy’s well-being and development. Many owners expressed feelings of guilt when things did not go as planned, with some feeling inadequate as caregivers. They worried about whether they were doing enough for their puppy, leading to a constant state of nervousness about the puppy’s future and their own competence as dog owners. This anxiety sometimes overlapped with feelings of guilt, where owners blamed themselves for the puppy’s challenges or setbacks.</p>
<p>The second form of emotional strain was frustration, which stemmed from the unexpected difficulties of caring for a new puppy. Owners described feeling overwhelmed by the puppy’s needs and behaviors, such as housetraining accidents or excessive chewing, which were not always easy to manage. In some cases, this frustration made it difficult for owners to bond emotionally with their new pets.</p>
<p>A few owners even regretted getting the puppy, expressing doubts about their decision and, in some cases, considering giving up their dog entirely. The frustration wasn’t just about the challenges of caring for the puppy but also about the gap between expectations and reality. Many owners had anticipated a joyful experience but were confronted with more difficulties than they had expected.</p>
<p>The third key emotion identified in the study was weariness, reflecting the physical and mental exhaustion that often accompanies the early stages of dog ownership. Many participants reported feeling drained by the constant demands of caring for a puppy, especially when it came to sleep disruption and the need for round-the-clock attention. The strain of balancing puppy care with other responsibilities, such as work and family, left some owners feeling overwhelmed and physically exhausted. For many, the relentless nature of puppy care—feeding, training, supervising, and cleaning up after their new pet—proved to be a significant source of stress.</p>
<p>“The arrival of a puppy is generally seen as a positive life change, yet for some people, it triggers significant negative emotions,” Ståhl told PsyPost. “Similar to the ‘baby blues’ experienced by new parents, new dog owners might be struggling with puppy blues including feelings of anxiety, frustration, and weariness. These symptoms often occur together but may also manifest more prominently in one area.”</p>
<p>“It’s important to remember that these feelings are a normal response to a significant life change and typically pass relatively quickly. The development of these experiences is a combination of several factors, rather than, e.g., a lack of preparation for puppyhood. The emotional turmoil caused by this life change can catch even experienced and thoroughly prepared new puppy owners off guard.”</p>
<p>One interesting finding was the way in which these negative emotions faded over time. The researchers found that the further removed participants were from their puppy’s early stages, the more positively they remembered the experience. This suggests that while the “puppy blues” can be intense in the moment, these feelings generally do not last long. The memories of frustration and exhaustion often give way to more positive recollections of puppyhood as time passes, a phenomenon that echoes the way parents often remember the early months of caring for a newborn baby.</p>
<p>“One interesting finding was that the longer the time had passed since puppyhood, the more positively people remembered it,” Ståhl explained. “In psychology, the phenomenon is called ‘fading affect bias,’ according to which the negative emotional content of memories ‘fades’ over time, and memories do not produce a negative emotional state as strongly as time has passed.”</p>
<p>While the study offers valuable insights into the emotional strain of puppy care, it also has several limitations. One of the key limitations is that the data were collected through self-reported surveys, which may be subject to memory biases.</p>
<p>Another limitation is the homogeneity of the sample. Most of the participants were Finnish and female, so it’s unclear whether the findings apply equally to men or to people in different cultural contexts.</p>
<p>“The lack of diversity in our sample is a key limitation, as most participants were women, and research suggests gender differences in forming attachments to pets,” Ståhl noted. “Women are also at higher risk for affective disorders, and traditional measures may under-report men’s distress. Additionally, data was collected via self-reported online questionnaires, potentially introducing bias from more engaged pet owners. In future studies we aim to collect a more diverse sample to improve generalizability.”</p>
<p>The study is part of a broader research project focused on understanding the relationship between humans and their pets. By developing a tool to measure the puppy blues, the researchers hope to improve support for dog owners and help them navigate the challenges of puppy care. This, in turn, could strengthen the bond between owners and their dogs and promote the well-being of both.</p>
<p>“Our long-term goal is to promote a healthy human-dog relationship and the well-being of both parties,” Ståhl explained. “Supporting the mental well-being of new puppy owners is crucial, as it not only benefits the owners but also may play a key role in the development of the human-canine bond and the dog’s behavior.”</p>
<p>“The owner’s role is especially important during the puppy’s critical socialization period (3-16 weeks). In future studies, we aim to explore the predisposing factors that contribute to puppy blues, coping methods and the role of puppy blues in dog’s behavioral development, and assess the scale’s generalizability across different cultures and genders.”</p>
<p>“We are currently conducting a large-scale survey based study on dog behavior, as well as owner well-being and personality, which also includes an examination of puppy blues,” Ståhl added. “Readers who are dog owners can participate in the survey in English via this link: <a href="https://redcap.link/me_and_my_dog" target="_blank" rel="noopener">https://redcap.link/me_and_my_dog</a>.”</p>
<p>The study, “<a href="https://www.nature.com/articles/s44184-024-00072-z" target="_blank" rel="noopener">Development and validation of the puppy blues scale measuring temporary affective disturbance resembling baby blues</a>,” was authored by Aada Ståhl, Milla Salonen, Emma Hakanen, Salla Mikkola, Sini Sulkama, Jari Lahti, and Hannes Lohi.</p></p>
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<td><a href="https://www.psypost.org/eating-fish-linked-to-lower-risk-of-cognitive-decline-new-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;">Eating fish linked to lower risk of cognitive decline, new study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 26th 2024, 12:00</div>
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<p><p>A recent meta-analysis published in <em><a href="https://doi.org/10.1007/s40520-024-02823-6" target="_blank" rel="noopener">Aging Clinical and Experimental Research</a></em> suggests that eating fish may help protect against cognitive decline, dementia, and Alzheimer’s disease. The study found that people who reported eating the most fish were less likely to experience cognitive impairment or decline compared to those who ate the least. However, the findings were strongest for cognitive decline, while more research is needed to firmly establish the link between fish consumption and dementia or Alzheimer’s disease.</p>
<p>The global population is aging rapidly, with more people living longer than ever before. Unfortunately, this increase in life expectancy also brings a rise in age-related health issues, especially cognitive decline, dementia, and Alzheimer’s disease. Worldwide, cases of dementia and Alzheimer’s are expected to triple by 2050, making cognitive health an urgent area of research. Identifying factors that may protect against cognitive decline is crucial, and diet has emerged as one area of interest.</p>
<p>Fish, which is rich in omega-3 fatty acids and other nutrients, has long been thought to benefit brain health. Omega-3s are known to have anti-inflammatory and antioxidant properties, which may help protect the brain from the damage that contributes to cognitive decline. Previous studies have suggested that eating fish is linked to a lower risk of neurodegenerative diseases, but the evidence has been somewhat inconsistent, particularly regarding specific conditions like dementia and Alzheimer’s disease. This new study aimed to update and clarify the current evidence on the association between fish consumption and cognitive health.</p>
<p>“We all know too well the impact of diet on cardio-metabolic health and and certain types of cancer. The relationship between diet and brain health is far less clear, although there is plenty of evidence suggesting that what and how we eat influences our mental well-being,” said study author Giuseppe Grosso, a professor in human nutrition at the University of Catania.</p>
<p>The researchers conducted a meta-analysis, a type of study that combines data from multiple previous studies to look for overall trends. They reviewed observational studies, which had examined the dietary habits of people over the age of 50 and tracked their cognitive outcomes over time. The researchers focused on studies that assessed fish consumption and its relationship to cognitive impairment, dementia, or Alzheimer’s disease.</p>
<p>They included 35 studies in their analysis, involving more than 849,000 participants from around the world. These studies used a variety of methods to assess how much fish people ate, such as food frequency questionnaires and dietary diaries. They also employed different tools to measure cognitive outcomes, including clinical diagnoses of dementia and Alzheimer’s disease as well as assessments of cognitive decline or impairment.</p>
<p>The researchers divided the participants into groups based on how much fish they ate and compared the highest consumers to the lowest consumers. They then calculated risk ratios, a statistical measure that indicates how likely a certain outcome (in this case, cognitive impairment or dementia) is in one group compared to another.</p>
<p>The study found that people who ate the most fish were significantly less likely to experience cognitive decline or impairment compared to those who ate the least. Specifically, the highest fish consumers had an 18% lower risk of cognitive impairment or decline.</p>
<p>“Individuals consuming fish regularly seem to be at lower risk of cognitive decline,” Grosso told PsyPost. “The average person should just take this into account, since many people simply do not eat fish almost at all.”</p>
<p>The researchers also looked at whether there was a dose-response relationship, meaning whether eating more fish led to progressively greater benefits. They found that higher fish consumption was linked to a reduced risk of cognitive impairment, with the most significant reduction observed in people who ate around 150 grams (about 5.3 ounces) of fish per day.</p>
<p>High levels of fish consumption were also associated with an 18% lower risk of dementia and a 15% lower risk of Alzheimer’s disease. But the results for dementia and Alzheimer’s were less conclusive due to variability across the studies, including differences in diagnostic methods and fewer studies focusing on these conditions.</p>
<p>Alzheimer’s is a complex disease with multiple underlying causes, and fish consumption alone may not be enough to prevent its progression. Additionally, the meta-analysis did not find a clear dose-response relationship for dementia or Alzheimer’s, making it harder to confirm a consistent protective effect.</p>
<p>The researchers also conducted subgroup analyses based on genetic variations, specifically looking at people with different forms of the APOE gene, which is known to influence the risk of Alzheimer’s disease. However, the results were mixed, and there were not enough studies to draw firm conclusions. More research is needed to understand how genetic factors might interact with diet to influence cognitive health.</p>
<p>One of the key strengths of this study is that it pooled data from a large number of participants across multiple countries, increasing the generalizability of the findings. However, the researchers also noted a high degree of variability (or “heterogeneity”) between the studies, which may have influenced the results. Some studies showed stronger effects than others, and the reasons for these differences are not entirely clear.</p>
<p>“We need more robust studies: while evidence exists, the heterogeneity between studies weakens the conclusions; hence, more research is needed,” Grosso explained. “Second, we need to clarify the mechanisms: the brain benefits may depend on fats, proteins, or other currently underrated factors. Having certainty about the mechanisms would strengthen the level of evidence.”</p>
<p>“The effects of diet on human health never depend on isolated components,” he noted. “I expect that the association between fish and cognitive health would be optimal when it occurs within the context of an overall healthy and sustainable diet.”</p>
<p>The study, “<a href="https://link.springer.com/article/10.1007/s40520-024-02823-6" target="_blank" rel="noopener">Fish consumption, cognitive impairment and dementia: an updated dose-response meta-analysis of observational studies</a>,” was authored by Justyna Godos, Agnieszka Micek, Walter Currenti, Carlotta Franchi, Andrea Poli, Maurizio Battino, Alberto Dolci, Cristian Ricci, Zoltan Ungvari, and Giuseppe Grosso.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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