Podcasts about avon longitudinal study

DOI: 10.13056/acamh.28979 In this Papers Podcast, Dr. Umar Toseeb discusses his JCPP paper ‘Genetic influences on sibling bullying and mental health difficulties' (https://doi.org/10.1111/jcpp.13956). There is an overview of the paper, methodology, key findings, and implications for practice. Discussion points include: Insight into the dataset used in the study (Avon Longitudinal Study of Parents and Children). The reason behind the focus on sibling bullying and the prevalence rates of sibling bullying. Sibling bullying and genetic risk for mental health difficulties as additively associated with mental health difficulties. The lack of moderation effect of genetic risk for mental health difficulties on the relationship between sibling bullying and mental health difficulties. Insight into the ‘Diathesis stress model'. Sibling bullying and mental health difficulties as co-occurring, in part, due to shared genetic influences. Potential implications of the research. In this series, we speak to authors of papers published in one of ACAMH's three journals. These are The Journal of Child Psychology and Psychiatry (JCPP); The Child and Adolescent Mental Health (CAMH) journal; and JCPP Advances. #ListenLearnLike

In this episode, Dr Rob Calder talks to Dr Lindsey Hines about her study using longitudinal data to examine links between cannabis use, cannabis potency and psychotic experiences. Dr Hines talks about using Avon Longitudinal Study of Parents and Children (ALSPAC) data - also known as 'Children of the Nineties' and discusses why psychosis and cannabis potency are important to measure and some of the challenges of doing so with both."In unregulated markets like the UK where it's illegal to use cannabis....better health messaging and better awareness among those using cannabis of those potential outcomes is the way that we can go".Original article: Incident psychotic experiences following self-reported use of high-potency cannabis: Results from a longitudinal cohort study by Lindsey A. Hines and colleagues. Published in Addiction (2024)Also in this podcast: Testing the validity of national drug surveys: comparison between a general population cohort and household surveys by Hannah Charles and colleagues. Published in Addiction (2021)The opinions expressed in this podcast reflect the views of the host and interviewees and do not necessarily represent the opinions or official positions of the SSA or Addiction journal.The SSA does not endorse or guarantee the accuracy of the information in external sources or links and accepts no responsibility or liability for any consequences arising from the use of such information. Hosted on Acast. See acast.com/privacy for more information.

In this podcast, we are joined by Dr. Becca Lacey to discuss her JCPP paper ‘Testing lifecourse theories characterising associations between maternal depression and offspring depression in emerging adulthood: the Avon Longitudinal Study of Parents and Children'. Becca is the first author of the paper.

Professor Jean Golding is an epidemiologist who is best known for founding the Children of the Nineties study - more formally known as the Avon Longitudinal Study of Parents and Children. The most detailed project of its kind anywhere in the world, it has followed the lives of children who were born in Avon during 1991 and 1992 and helped scientists make important discoveries about everything from peanut allergy to the effects of long Covid. Jean was born in Cornwall in 1939. As a toddler she suffered two bouts of tuberculosis and spent several weeks in hospital. Then at 13 she contracted polio, leading to a three-month hospital stay. After graduating in mathematics from Oxford University, her first job involved completing calculations for the 1958 perinatal mortality survey, set up to collect information about the social and obstetric factors associated with stillbirth and death in early infancy. By the time she started designing the Children of the Nineties study, Jean was well used to working with large data-sets, but the new project was bigger than ever. It collected more than 1.5m biological samples including blood, placenta, hair, nails and teeth along with thousands of questionnaires. As well as expanding medical knowledge, the study has influenced government policy. Jean retired from the study in 2005. She was awarded an OBE for services to medical science in 2012 and today is Emeritus Professor of Paediatric and Perinatal Epidemiology at the University of Bristol. DISC ONE: The ‘Trelawny' National Anthem by The Fisherman's Friends DISC TWO: Under Milk Wood (Part 1) read by Richard Burton DISC THREE: Bad Penny Blues by Humphrey Lyttelton DISC FOUR: Dawn Chorus by BBC Sound Effects DISC FIVE: The Hippopotamus Song by Flanders & Swann DISC SIX: A Hymn to Him by Rex Harrison DISC SEVEN: Piano Quintet in A Major, Op. Posth. 114, D. 667 "The Trout": I. Allegro vivace by Melos Ensemble DISC EIGHT: Bring Me Sunshine by Morecambe and Wise BOOK CHOICE: The Oxford Book of Twentieth-century English Verse LUXURY ITEM: A mobility power chair CASTAWAY'S FAVOURITE: Dawn Chorus by BBC Sound Effects Presenter Lauren Laverne Producer Paula McGinley

https://psychiatry.dev/wp-content/uploads/speaker/post-10960.mp3?cb=1669504824.mp3 Playback speed: 0.8x 1x 1.3x 1.6x 2x Download: Childhood Trauma As a Mediator of the Association Between Autistic Traits and Psychotic Experiences: Evidence From the Avon Longitudinal Study ofFull EntryChildhood Trauma As a Mediator of the Association Between Autistic Traits and Psychotic Experiences: Evidence From the Avon Longitudinal Study of Parents and Children Cohort –

This month on Episode 33 of Discover CircRes, host Cynthia St. Hilaire highlights two original research articles featured in the February 4 issue of Circulation Research. In addition, she previews Circulation Research's Compendium on Women and Cardiovascular Health, featured in the February 18th issue. This episode also features a conversation with Dr Alastair Poole and Dr Laura Corbin from the University of Bristol and Dr Stephen White from the Manchester Metropolitan University about their study, Epigenetic Regulation of F2RL3 Associates with Myocardial Infarction and Platelet Function.   Article highlights:   Samargandy, et al. Blood Pressure Trajectories and Menopause   Gilchrist, et al. Research Goes Red Registry   Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's Journal, Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh and today I'm going to be highlighting articles from our February issues of Circulation Research. I'm also going to speak with Dr Alastair Poole and Dr Laura Corbin from the University of Bristol and Dr Stephen White from the Manchester Metropolitan University about their study, Epigenetic Regulation of F2RL3 Associates with Myocardial Infarction and Platelet Function.   Cindy St. Hilaire:        The first article I want to share is titled Trajectories of Blood Pressure in Midlife Women: Does Menopause Matter? The first author is Saad Samargandy, and the corresponding author is Samar El Khoudary from the University of Pittsburgh. Blood pressure increases with age, but after midlife, the rate of increase for women generally exceeds that for men. This observation has led to debate over whether menopause might influence the blood pressure trajectory.   Cindy St. Hilaire:        To find out, this group examined data on over 3300 women of diverse ethnicity enrolled in the Study of Women's Health Across the Nation, or SWAN study. The women began the study between 42 and 52 years old, and they had 17 follow-up visits at roughly one-year intervals. At these visits, blood pressure, hormone levels, weight and other health parameters were measured.   Cindy St. Hilaire:        Analysis of the data revealed women fell largely into three blood pressure trajectory groups. Those with low blood pressure before menopause and accelerated blood pressure after menopause, those with a linear increase linked to age, and those with high blood pressure before and a slower ascent afterwards. White, Chinese and Japanese women were more likely to be in the low to accelerated group, as were those with early menopause, while Latino and Black women were more likely to have high blood pressure in general. Together, the results indicate that for many women, menopause itself does not accelerate age-related blood pressure increase, and that women of menopausal age should be advised of this risk and have their blood pressure monitored regularly.   Cindy St. Hilaire:        The second article I want to highlight is titled Research Goes Red: Early Experience With a Participant-Centric Registry. The first author is Susan Gilchrist and the corresponding author is Jennifer Hall from the American Heart Association. Cardiovascular disease is a leading cause of death for men and women alike, but there are particular factors such as pregnancy and menopause that may specifically influence the genesis, presentation and management of the condition in women.   Cindy St. Hilaire:        With that in mind, for the past two decades, the AHA's Go Red for Women campaign has been raising awareness of and driving research into women's cardiovascular health issues. The latest Go Red initiative, an online platform called Research Goes Red, was launched in 2019 with the aim of empowering women to contribute to health research by, among other things, taking part in health surveys. In the last two years, the platform has garnered 15,000 registered individuals between the ages of 30 and 60. It has deployed six targeted health surveys and prompted two AHA-funded research studies based on participant responses: one on perimenopausal weight gain, and one on the use of social media to engage young women in cardiovascular disease awareness. While Research Goes Red has successfully amassed middle aged participants, the authors say that future goals should include increasing the number and the diversity of the registrants and encouraging researchers to use the registry not just for data, but for identifying potential trial participants.   Cindy St. Hilaire:        I want to now mention the 15 articles that are featured in our Compendium on Women and Cardiovascular Disease that is featured in our February 18th issue of Circulation Research. And this also happens to correspond with February being the American Heart Month. So Susan Cheng and colleagues present A Scientific Imperative As Seen Through a Sharpened Lens: Sex, Gender and the Cardiovascular Condition. Genetic, molecular and cellular determinants of sex-specific cardiovascular traits is discussed by Teemu Niiranen and colleagues. Bonnie Ky et al. describe sex-specific cardiovascular risks of cancer and its therapies. Sex differences and similarities in valvular heart disease is presented by Francis Delling and colleagues. Cecile Lahiri and colleagues wrote about the cardiovascular implications of immune disorders in women. Joshua Smith and colleagues discuss sex differences in cardiac rehabilitation outcomes.   Cindy St. Hilaire:        Pregnancy and reproductive risk factors of cardiovascular disease in women is reviewed by Michael Honigberg and colleagues. The impact of sex and gender on stroke is presented by Kathryn Rexrode and colleagues. Ersilia DeFilippis and colleagues cover heart failure subtypes and cardiomyopathies in women. Demilade Adedinsewo and colleagues wrote about cardiovascular disease screening in women, leveraging artificial intelligence, and digital tools. Sexual dimorphism in cardiovascular biomarkers, clinical research implications, is discussed by Jennifer Ho and colleagues. Connie Hess et al. review sex differences in peripheral artery disease. Janet Wei and colleagues provide an update on coronary arterial function and disease in women with non-obstructive coronary arteries. Sex differences in myocardial and vascular aging is presented by Hongwei Ji and colleagues. And lastly, arrhythmias in female patients, incidence, presentation and management, is reviewed by Andrea Russo and colleagues.   Cindy St. Hilaire:        Today I have with me Drs  Alastair Poole and Laura Corbin from the University of Bristol and Dr Stephen White from the Manchester Metropolitan University. And they're here with me to discuss their study, Epigenetic Regulation of F2RL3 Associates with Myocardial Infarction and Platelet Function. And this article is in our February 4th issue of Circ Res. Well, Drs Corbin, Poole and White, thank you so much for joining me today.   Laura Corbin:             Thank you very much.   Stephen White:            Thank you.   Alastair Poole:            Thanks.   Cindy St. Hilaire:        So this is a really neat study. It's bringing in a couple different fields. It's investigating what I'm calling a Venn diagram of these intersecting topics all related to cardiovascular disease: cigarette smoking, epigenetic modification and platelet activation. So can you maybe give us a little bit of background on the status of the field and how these three topics intersected at the start of your study?   Laura Corbin:             So yeah, our working hypothesis was based on existing literature and it was really to look at whether smoking-induced epigenetic DNA hypermethylation of F2RL3 could increase risk of myocardial infarction and whether the route to that could be through platelet function. So there's quite a lot of literature going back probably to around about 2015 that shown that there are changes to the methylome in response to smoking. And DNA methylation is a way of cells controlling gene expression, but without having to actually make changes in the DNA sequence itself. So this could be a really important way that we know that smoking increases the risk of a number of cardiovascular diseases, but we don't really know how that happens. And one way that that could happen is through changes to methylation.   Cindy St. Hilaire:        What is known about how cigarette smoke impacts the status of DNA methylation? How has that switched or changed? Maybe when someone is actively smoking, when someone quits, is it dynamic? What is known about that relationship?   Laura Corbin:            Okay. So yeah, going back to about 2015, there was a number of studies that looked at methylation across the whole genome. So in a hypothesis-free untargeted manner, developments and technology meant that we could look at many, many sites across the genome at the same time. And so studies were done to look at changes that were associated with smoking. And what was found was those changes, actually quite a lot of changes across the genome in a number of different genes, but not really anything much beyond that. So F2RL3 was one of the first sites to be identified as being associated, methylation at that site associated with smoking. And it was replicated in several studies.   Laura Corbin:            And it was also showing that there was a dose-response relationship. So the more a person smoked, the less methylated that site appeared to be. And then there's been some work done already, but we also did it in our paper to show that those methylation marks actually hang around for quite a long time once somebody quits smoking. But also that there's a lot of variation within an individual, so even if you smoke, it doesn't necessarily mean that you'll definitely have low methylation, there's still variation. So there's other factors that are involved in that.   Cindy St. Hilaire:        So you were looking at a specific population of patients, can you tell us a little bit about that group of patients you were looking at? And you mentioned the variability in the amount of smoke they were exposed to, do you know that information? And I guess one of the base questions I had is I'm in Pittsburgh, which back in the '80s and earlier was a steel mill town that had a lot of pollution. And so I'm wondering if you're able to clearly separate out a cigarette smoker from maybe someone who is a light cigarette smoker, but lives in a more polluted area?   Laura Corbin:             Okay. So there's two parts of the study that were looking at this in a human context, so in a whole person context. One of those was using data from the Copenhagen City Heart Study, and that's the one where we looked at the relationship between smoking and methylation and then between methylation and myocardial infarction. So that study is great because it's been tracking people over time and so we're able to use the samples that were collected before they had their cardiovascular event and look at methylation at that point. So we know that the event occurs after that point, which is important. And so we were able to verify in that population that we did see an association between smoking and methylation. We were able to show that it was a dose-dependent relationship. So if we look at something like in that dataset, we had things like the intensity of which people smoke, so pack years is one of the things that we looked at. And it did appear to correspond in an approximately linear fashion.   Laura Corbin:             So we don't really know, I don't think, at this point, what impact other environmental exposures would have on the methylome and how that would interact with the cigarette smoking. That's actually a really interesting point that we'll probably come onto later about whilst we were looking here at the smoking effect on this methylation site, in the second part of the work, we were able to show that even in non-smokers, there's variability in methylation at this site, and that can still have impacts on the biology downstream. So yeah, it's an interesting point.   Stephen White:            Just to maybe just jump in, there's very good amounts of literature now that show quite a good correlation between changes in air quality and cardiovascular events. So smogs, wildfires and so on, clearly correlate with an increase in cardiovascular events. But actually the opposite's also been observed in the more recent COVID lockdowns, where reduction in air pollution also mirrored a reduction in the number of cardiovascular events. So I think you raise a really interesting point about is it cigarette smoke alone or does air quality in general play an effect? And clearly it does play an effect, although we didn't correlate that within this current dataset.   Cindy St. Hilaire:        Your study looked at DNA methylation patterns at cytosine, phosphate, guanidine or CPG sites in the genome. Can you tell us a little bit more about what these islands are and how they change throughout maybe different cells in the body, but also maybe in the same cell, but throughout the course of life or the course of, in this case, cigarette exposure?   Stephen White:            So if we just want to focus in on our study, what we showed was that exposure to cigarette smoke changes endothelial cell methylation. It also changes megakaryocyte methylation patterns in the same way. And I think one of the surprising things was that only 48 hours of exposure to cigarette smoke significantly changes the methylation pattern of the F2RL3 locus. So it's quite a dynamic event, but it does show that these can be quite rapidly regulated. And Laura's really nice work shows that the methylation on cessation of smoking, that pattern does actually go down, but it's a 20-year process. So it looks like it can be rapidly induced, but may actually remain as a methylation mark for a considerable length of time.   Stephen White:            And I think one of the things we did in our study was actually to triangulate not only the observational data and the association data in patients, but actually start to look at a mechanism of how that might actually relate to changes in gene expression. So we showed that this particular CPG site is right next to a binding site for a transcription factor, and transcription factors are the cell's way of regulating how much of a particular gene is expressed. And we show that changes in methylation changed the binding of this transcription factor and therefore change the amount of this particular gene that was made.   Cindy St. Hilaire:        Yeah. Actually, I want to start to talk about that locus you were interested in. So what was known about the F3RL2 locus? How big is it, but also what genes are there and what did you start to investigate with your in vitro modeling?   Stephen White:            So I think when we started, we had the observation that a change in methylation at the F2RL3 locus was associated with the risk of cardiovascular events. And then it was a detective expedition into the gene using various in silico analyses that identified the methylation site that we are interested in, or most interested in, is right next to a transcription factor binding site.   Stephen White:            So we then went on to show that binding of that transcription factor is sensitive to methylation, that if we would just excise that piece of DNA, we can show that that has the ability to regulate F2RL3 expression or the expression of a reporter gene. And then if you knocked out the transcription factor binding site, you lose that regulation. So it was a series of detective work and experimental steps that allowed us to put a mechanism behind the observation that changes in methylation might truly affect the level of gene expression of the F2RL3, otherwise known as PAR4 to platelet biologists. So get that in there.   Alastair Poole:            I first came across it when another member of our team actually mentioned it to me over a casual conversation actually a few years ago that F2RL3 gene was regulated in this way. To me as a platelet biologist, F2RL3 didn't mean a lot, but when I was told then it was the gene that encodes PAR4, it meant everything. And so platelet biologists, we talk about PAR4, which is of course the protein product of the F2RL3 gene. And PAR4 is one of several really key receptors on a platelet surface that responds to, in this case, to changes in thrombin generation, thrombin activity, which is of course the major effectively end product of the coagulation cascade.   Alastair Poole:            So it's what couples coagulation and platelet biology together, thrombin. And there are two major receptors on platelets that operate in response to changes in thrombin and that's PAR1 and PAR4. And they're both very important genes, but yeah, really interestingly, you have this rather selective effect on PAR4 and the paper actually shows it is indeed a selective effect on PAR4 as opposed to PAR1 in terms of epigenetic regulation of its responsiveness to PAR4 activation.   Cindy St. Hilaire:        So I want to tap back onto something that Laura had mentioned briefly, and that is talking about your platelet assays where you isolated platelets from a specific subset of the patients. And I believe it was figure three, and you looked at patients who in adolescence had exhibited differences in the methylation pattern at the site in the F3RL2 locus. What do we know about that innate or early-age change? And then I would love to hear more about this actual experiment, how you looked at the patients earlier versus current and what the thinking was behind that.   Laura Corbin:            So yeah, this part of the work was done in a birth cohort study called the Avon Longitudinal Study of Parents and Children, which is based at the University of Bristol. And this is a really great study, a great resource that we have, and in fact, it's open to all researchers so anyone could use it, where mothers were recruited during pregnancy, which was in around 1991 to 1992. And then those children that were born from those pregnancies have then been followed up ever since.   Laura Corbin:             So that was the data that we were able to use for this part of the study. And what we wanted to do was to look at how this could work functionally, so look at the platelet function, but we really wanted at this point to step away from the smoking. Because obviously if you're going to look at platelet function in smokers versus non-smokers, it's incredibly difficult then to say that that's coming through a specific pathway, because we know that smoking induces lots and lots of changes in methylation, in proteins, all sorts of things going on. So we couldn't see a way of doing that part of the experiment with a comparison of smokers versus non-smokers. But what we know is that there's natural variation in methylation across all sites, including F2RL3.   Laura Corbin:             So we had historic data from earlier time points, so two earlier time points from when the children were under 20. And we looked at those measures for F2RL3 and then just simply ranked people according to whether they had high or low methylation, and then used those two ranks together to then work out who had a consistently high versus consistently low level. And then we invited participants back into the clinic to have samples taken from those up and lower ends of the distribution. At that point, we were just really hoping that that methylation pattern would continue because this was then, I think they aged about 24 by the time we did this work, so it was some time after. And we restricted our selection just to people who were non-smokers, so never smokers based on the information they provided, but also asking them when they came in for that clinic just to verify that they were non-smokers.   Laura Corbin:             And then we had a look at the methylation again. This time we looked across four sites in the region, which are the sites presented in the paper. And luckily for us, there was still that mean difference between the high group and the low group. But what we were able to then do is to compare people with high and low methylation, but without all of the trouble of isolating that pathway in amongst all the other smoking effects. And also not just the smoking effects, but the other confounding factors that come with smoking. So we know that smoking is correlated with a lot of other lifestyle factors. So if you ever do a smoking versus non-smoking comparison, it's really hard to work out exactly which bits are coming from smoking and which pathways it might be going down. So this was the idea behind this part of the study was to just really zoom in on F2RL3 methylation in the absence of all of the other noise in the other experimental designs.   Laura Corbin:             So yeah, the natural variation we see in the non-smoking healthy participants in this part of the study is actually quite a lot less than we see when we look at smokers compared to non-smokers, but it was still enough to then go on and look at the platelet function. And then the differences we saw in the platelet's responses, there is nothing pathological there. It was just very subtle changes in the response when stimulated in the lab.   Alastair Poole:            The only other thing I could add would be that platelets are very complicated cells. Every cell of the body is very complicated. Platelets are certainly very complicated. PAR4, F2RL3, is just one of very many components of the platelet that modulate its activity. So platelets are controlled by multiple forces sort of thing, at which F2RL3 and PAR4 is just one of them. So biology is very good at compensating for one level going up in one part of a pathway and going down compensatory wise in another part of a pathway. There isn't necessarily a direct relationship between one pathway enhancement and an overall effect because of the compensation.   Cindy St. Hilaire:        Why would it be easy?   Alastair Poole:            Yeah. Yeah. It's just very complex, the biology. So yeah, I completely get what you're saying, Laura, that we obviously don't want to frighten people that maybe they've got a propensity to enhance thrombosis based upon a single gene methylation difference because it will be much more complex than that.   Cindy St. Hilaire:        Yeah. I think that's one of the beautiful things about your study is with the luck of having this sample population, you were able to ask these really precise questions that... You can't just start a study now and ask that sort of question. So it was really elegant in that sense.   Cindy St. Hilaire:        Do we know the mechanism of how cigarette smoke induces these methylation changes, or maybe even the specific components of the smoke? And I guess I'm thinking that in terms of vaping that's becoming more and more popular, obviously the company selling those products want to advertise them as safer, but it comes down to is it all of the mixture of the cigarette smoke or is it one component that we know impacts the methyltransferases and demethyltransferases in this process?   Alastair Poole:            Those are two follow-on routes of our study that I have to say that we discussed previously amongst ourselves and identified those as definitely very important follow-up areas. So do e-cigs have similar effects and that's a study that definitely needs to be done. We have done a little bit of work to try to investigate that initially, but I think that's a very important follow-on study. But yeah, you're also right that one of the key things that we want to understand and is, the missing piece in a way, is how is methylation at a molecular mechanistic level altered by smoking? Steve, I don't know whether you have any further details to add to that.   Stephen White:            I think one of the key molecular pathways seems to be the antioxidant response. And so that's largely controlled by another transcription factor called NRF2. And so if you think about smoking or poor air quality, all of those things do combine through this particular pathway that senses free radical damage, free radical stress. So as Alastair said, it's an area we are going to carry on to look at and it's a big area of my own lab's investigations. But oxygen stress is probably the mediating factor, but the actual nuts and bolts about how the demethylase is targeted to this particular locus is still an area of active investigation.   Cindy St. Hilaire:        All right, well, I will be on the lookout for those future studies because it's a really interesting topic, just the whole interplay of all of this. Are there any translational implications for these findings? Do you think potentially we could screen patients, say, to see their methylation status? I don't know if megakaryocytes are easy to isolate, but is it in a circulating cell, would this possibly be able to be turned into a screening tool or a diagnostic tool to predict thrombic events in patients?   Alastair Poole:            It is possible. I think it would not be possible to isolate megakaryocytes very easily. There are a small number in the peripheral circulation, but the majority are not in the peripheral circulation. But we and others have used other blood cells as proxy measures. So actually, the gene methylation changes that we identified here come from other leukocytes, white blood cells, and those effectively are a cell that are exposed to smoke in the same way, or the smoke products in the same way. So we'd use a proxy cell for that.   Alastair Poole:            Yes, I suppose it is possible. As you say, there's a natural variation in methylation status of that gene and there's, layered on top of that, a smoking induced. And I suppose that it would be an interesting further investigation to understand whether, effectively, your natural methylation status of that gene happened to give you an enhanced risk of a cardiovascular event. The work we've done seems to suggest that that may well be the case and therefore you could imagine possibly a personalized medicine approach that might include understanding the methylation status of F2RL3 as part of that.   Cindy St. Hilaire:        Well, it was a beautiful study. I love these studies that bring in lots of different fields or specialties to ask interesting questions. So Dr Corbin and Dr Poole from the University of Bristol and Dr White from Manchester Metropolitan University, thank you so much joining me today.   Stephen White:            Thank you. Our pleasure.   Alastair Poole:            Thank you.   Laura Corbin:             I'd also just like to acknowledge all of our co-authors as it really was a big team effort, especially the guys who are not represented on the call today, which is the folk from the Copenhagen City Heart Study, and also to all of the participants of that study and the Children of the '90s Study that contributed to the work. Thanks very much.   Cindy St. Hilaire:        That's it for the highlights from our February issues of Circulation Research. Thank you so much for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes and the hashtag #DiscoverCircRes. Thank you to our guests, Drs  Alastair Poole, Laura Corbin and Stephen White.   Cindy St. Hilaire:        This podcast is produced by Ashara Ratnayaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Some of the copy text for highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire, and this is Discoverer CircRes, your on-the-go source for the most exciting discoveries and basic cardiovascular research.   Cindy St. Hilaire:        This program is copyright of the American Heart Association 2022. The opinions expressed by speakers of this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, please visit ahajournals.org.    

The death of a family pet can trigger a sense of grief in children that is profound and prolonged, and can potentially lead to subsequent mental health issues, according to a new study by researchers at Massachusetts General Hospital (MGH). The team found that the strong emotional attachment of youngsters to pets might result in measurable psychological distress that can serve as an indicator of depression in children and adolescents for as long as three years or more after the loss of a beloved pet. "One of the first major losses a child will encounter is likely to be the death of a pet, and the impact can be traumatic, especially when that pet feels like a member of the family," the experience of pet death is often associated with elevated mental health symptoms in children, and that parents and physicians need to recognize and take those symptoms seriously, not simply brush them off." Roughly half of the households in developed countries own at least one pet. And the bonds that children form with pets can resemble secure human relationships in terms of providing affection, protection and reassurance. What's more, previous studies have shown that children often turn to pets for comfort and to voice their fears and emotional experiences. While the increased empathy, self-esteem and social competence that often flow from this interaction are beneficial, the downside is children's exposure to the death of a pet which, is, 63 per cent of children with pets during their first seven years of life. Prior research has focused on the attachment of adults to pets and the consequences of an animal's death. The Massachusetts team is the first to examine mental health responses in children. Their analysis is based on 6,260 children from the Avon Longitudinal Study of Parents and Children (ALSPAC), in Bristol, England. This population-based sample is replete with data collected from mothers and children that enabled researchers to track the experience of pet ownership and pet loss from a child's early age up to eight years. "Thanks to this cohort, we were able to analyse the mental and emotional health of children after examining their experiences with pet death over an extended period," notes Erin Dunn, ScD, MPH, with the MGH Center for Genomic Medicine and Department of Psychiatry, and senior author of the study. "And we observed that the association between exposure to a pet's death and psychopathology symptoms in childhood occurred regardless of the child's socioeconomic status or hardships they had already endured in their young lives." Researchers also learned that the relationship between pet death and increased psychopathology was more pronounced in male than female children -- a finding that surprised them in light of prior research -- and that the strength of the association was independent of when the pet's death occurred during childhood, and how many times or how recently it occurred. According to Dunn, this latter finding speaks to "the durability of the bond with pets that is formed at a very early age, and how it can affect children across their development." The MGH study stressed the importance of parents, caregivers, and paediatricians recognizing and taking seriously children's short- and long-term psychological reactions to the death of a pet – reactions that can mimic a child's response to the loss of other significant family members. "Adults need to pay attention to whether those feelings are deeper and more profound and if they're lasting longer than might have been expected," says Crawford. "They could be signs of complicated grief, and having someone to talk to sympathetically or therapeutically may be extremely helpful for a child who is grieving." Reference:

Cranberry Powder Attenuates Benign Prostatic Hyperplasia University of Suwon (South Korea), June 21, 2021   Cranberry powder (CR) is reported to be effective against lower urinary tract symptoms (LUTS) and recurrent urinary tract infections. Benign prostatic hyperplasia (BPH) in men older than 50 years is a common cause of LUTS. Here, we attempted to evaluate if CR is also effective for treating BPH using a BPH-induced rat model, which was orally administered CR. Male Sprague-Dawley rats weighing 200–250 g were randomly divided into the following six groups (n = 9): noncastration group; castration group; BPH group; BPH and cranberry for 8-week (CR8W) group; BPH and cranberry for 4-week (CR4W) group; and BPH and saw palmetto group (saw palmetto). Compared with the BPH group, the CR8W group showed a significant decrease in prostate weight (by 33%), dihydrotestosterone (DHT) levels (by 18% in serum and 28% in prostate), 5-alpha reductase levels (18% reduction of type 1 and 35% of type 2), and histological changes. These results indicate that CR could attenuate BPH by inhibiting 5-alpha reductase and by reducing other biomarkers such as prostate weight and DHT levels. Thus, CR may be an effective candidate for the development of a functional food for BPH treatment. IACUC (USW-IACUC-R-2015-004).   In our investigation, the administration of CP significantly prevented the progression of BPH by reducing the 5AR levels, and consequently reducing DHT levels in the serum and prostate, along with reduction of the prostate size. This study demonstrated that CR exerts positive effects against BPH, based on biochemical and histological changes in BPH-induced rats. Although further investigation and validation is required, our study provides evidence, for developing a potential treatment for BPH from natural products.     Psychedelic spurs growth of neural connections lost in depression Yale University, July 5, 2021 The psychedelic drug psilocybin, a naturally occurring compound found in some mushrooms, has been studied as a potential treatment for depression for years. But exactly how it works in the brain and how long beneficial results might last is still unclear. In a new study, Yale researchers show that a single dose of psilocybin given to mice prompted an immediate and long-lasting increase in connections between neurons. The findings are published July 5 in the journal Neuron. "We not only saw a 10% increase in the number of neuronal connections, but also they were on average about 10% larger, so the connections were stronger as well," said Yale's Alex Kwan, associate professor of psychiatry and of neuroscience and senior author of the paper. Previous laboratory experiments had shown promise that psilocybin, as well as the anesthetic ketamine, can decrease depression. The new Yale research found that these compounds increase the density of dendritic spines, small protrusions found on nerve cells which aid in the transmission of information between neurons. Chronic stress and depression are known to reduce the number of these neuronal connections. Using a laser-scanning microscope, Kwan and first author Ling-Xiao Shao, a postdoctoral associate in the Yale School of Medicine, imaged dendritic spines in high resolution and tracked them for multiple days in living mice. They found increases in the number of dendritic spines and in their size within 24 hours of administration of psilocybin. These changes were still present a month later. Also, mice subjected to stress showed behavioral improvements and increased neurotransmitter activity after being given psilocybin. For some people, psilocybin, an active compound in "magic mushrooms," can produce a profound mystical experience. The psychedelic was a staple of religious ceremonies among indigenous populations of the New World and is also a popular recreational drug. It may be the novel psychological effects of psilocybin itself that spurs the growth of neuronal connections, Kwan said. "It was a real surprise to see such enduring changes from just one dose of psilocybin," he said. "These new connections may be the structural changes the brain uses to store new experiences."   How long can a person live? The 21st century may see a record-breaker University of Washington, July 2, 2021 The number of people who live past the age of 100 has been on the rise for decades, up to nearly half a million people worldwide. There are, however, far fewer "supercentenarians," people who live to age 110 or even longer. The oldest living person, Jeanne Calment of France, was 122 when she died in 1997; currently, the world's oldest person is 118-year-old Kane Tanaka of Japan. Such extreme longevity, according to new research by the University of Washington, likely will continue to rise slowly by the end of this century, and estimates show that a lifespan of 125 years, or even 130 years, is possible. "People are fascinated by the extremes of humanity, whether it's going to the moon, how fast someone can run in the Olympics, or even how long someone can live," said lead author Michael Pearce, a UW doctoral student in statistics. "With this work, we quantify how likely we believe it is that some individual will reach various extreme ages this century." Longevity has ramifications for government and economic policies, as well as individuals' own health care and lifestyle decisions, rendering what's probable, or even possible, relevant at all levels of society. The new study, published June 30 in Demographic Research, uses statistical modeling to examine the extremes of human life. With ongoing research into aging, the prospects of future medical and scientific discoveries and the relatively small number of people to have verifiably reached age 110 or older, experts have debated the possible limits to what is referred to as the maximum reported age at death. While some scientists argue that disease and basic cell deterioration lead to a natural limit on human lifespan, others maintain there is no cap, as evidenced by record-breaking supercentenarians. Pearce and Adrian Raftery, a professor of sociology and of statistics at the UW, took a different approach. They asked what the longest individual human lifespan could be anywhere in the world by the year 2100. Using Bayesian statistics, a common tool in modern statistics, the researchers estimated that the world record of 122 years almost certainly will be broken, with a strong likelihood of at least one person living to anywhere between 125 and 132 years. To calculate the probability of living past 110 -- and to what age -- Raftery and Pearce turned to the most recent iteration of the International Database on Longevity, created by the Max Planck Institute for Demographic Research. That database tracks supercentenarians from 10 European countries, plus Canada, Japan and the United States. Using a Bayesian approach to estimate probability, the UW team created projections for the maximum reported age at death in all 13 countries from 2020 through 2100. Among their findings: Researchers estimated near 100% probability that the current record of maximum reported age at death -- Calment's 122 years, 164 days -- will be broken; The probability remains strong of a person living longer, to 124 years old (99% probability) and even to 127 years old (68% probability); An even longer lifespan is possible but much less likely, with a 13% probability of someone living to age 130; It is "extremely unlikely" that someone would live to 135 in this century. As it is, supercentenarians are outliers, and the likelihood of breaking the current age record increases only if the number of supercentenarians grows significantly. With a continually expanding global population, that's not impossible, researchers say. People who achieve extreme longevity are still rare enough that they represent a select population, Raftery said. Even with population growth and advances in health care, there is a flattening of the mortality rate after a certain age. In other words, someone who lives to be 110 has about the same probability of living another year as, say, someone who lives to 114, which is about one-half. "It doesn't matter how old they are, once they reach 110, they still die at the same rate," Raftery said. "They've gotten past all the various things life throws at you, such as disease. They die for reasons that are somewhat independent of what affects younger people. "This is a very select group of very robust people."     Dried Plum Consumption Improves Total Cholesterol and Antioxidant Capacity and Reduces Inflammation in Healthy Postmenopausal Women San Diego State University, June 27, 2021 Dried plums contain bioactive components that have demonstrated antioxidant and anti-inflammatory effects. The objective of this study was to determine if dried plum consumption reduces the risk factors for cardiovascular disease (CVD) in postmenopausal women, specifically examining lipid profiles, oxidative stress, antioxidant capacity, and inflammation in a dose-dependent manner. We conducted a 6-month, parallel-design controlled clinical trial, where 48 postmenopausal women were randomly assigned to consume 0, 50, or 100 g of dried plum each day. After 6 months of intervention, total cholesterol (TC) in the 100 g/day treatment group (P = .002) and high-density lipoprotein cholesterol in the 50 g/day treatment group (P = .005) improved significantly compared to baseline. Inflammatory biomarkers interleukin-6 (P = .044) and tumor necrosis factor-α (P = .040) were significantly lower after 6 months within the 50 g/day dried plum group compared to baseline. Moreover, total antioxidant capacity increased significantly within the 50 g/day group (P = .046), and superoxide dismutase activity increased significantly within both 50 and 100 g/day groups (P = .044 and P = .027, respectively) after 6 months compared to baseline. In addition, plasma activities of alanine transaminase (P = .046), lactate dehydrogenase (P = .039), and creatine kinase (P = .030) were significantly lower after 6 months in the 50 g/day dried plum group. These findings suggest that daily consumption of 50–100 g dried plum improves CVD risk factors in postmenopausal women as exhibited by lower TC, oxidative stress, and inflammatory markers with no clear dose dependence.     Regular physical activity linked to more 'fit' preteen brains   Childrens Hospital Boston, July 2, 2021 We know exercise has many health benefits. A new study from Boston Children's Hospital adds another benefit: Physical activity appears to help organize children's developing brains. The study, led by Dr. Caterina Stamoulis, analyzed brain imaging data from nearly 6,000 9- and 10-year-olds. It found that physical activity was associated with more efficiently organized, robust, and flexible brain networks. The more physical activity, the more "fit" the brain. "It didn't matter what kind of physical activity children were involved in," says Dr. Stamoulis, who directs the Computational Neuroscience Laboratory at Boston Children's. "It only mattered that they were active." Crunching the data Dr. Stamoulis and her trainees, Skylar Brooks and Sean Parks, tapped brain imaging data from the Adolescent Brain Cognitive Development (ABCD) study, a long-running study sponsored by the National Institutes of Health. They used functional magnetic resonance imaging (fMRI) data to estimate the strength and organizational properties of the children's brain circuits. These measures determine how efficiently the brain functions and how readily it can adapt to changes in the environment. "The preteen years are a very important time in brain development," notes Dr. Stamoulis. "They are associated with a lot of changes in the brain's functional circuits, particularly those supporting higher-level thought processes. Unhealthy changes in these areas can lead to risky behaviors and long-lasting deficits in the skills needed for learning and reasoning." The team combined these data with information on the children's physical activity and sports involvement, supplied by the families, as well as body mass index (BMI). Finally, they adjusted the data for other factors that might affect brain development, such as being born before 40 weeks of gestation, puberty status, sex, and family income. Healthy brain networks Being active multiple times per week for at least 60 minutes had a widespread positive effect on brain circuitry. Children who engaged in high levels of physical activity showed beneficial effects on brain circuits in multiple areas essential to learning and reasoning. These included attention, sensory and motor processing, memory, decision making, and executive control (the ability to plan, coordinate, and control actions and behaviors). In contrast, increased BMI tended to have detrimental effects on the same brain circuitry. However, regular physical activity reduced these negative effects. "We think physical activity affects brain organization directly, but also indirectly by reducing BMI," Dr. Stamoulis says. Analyzing brain effects In the analyses, the brain was represented mathematically as a network of "nodes": a set of brain regions linked by connections of varying strength. Physical activity had two kinds of positive effects: on the efficiency and robustness of the network as a whole, and on more local properties such as the number and clustering of node connections. "Highly connected local brain networks that communicate with each other through relatively few but strong long-range connections optimizes information processing and transmission in the brain," explains Dr. Stamoulis. "In preteens, a number of brain functions are still developing, and they can be altered by a number of risk factors. Our results suggest that physical activity has a positive protective effect across brain regions."   Could Sumac Be Effective on COVID-19 Treatment? Fırat University Medicine Faculty (Turkey), June 11, 2021 Sumac is an herbal product, commonly consumed as a spice and was used for medical treatment for centuries. The phytochemical structure of Sumac was studied extensively, and it was established that the herb contained tannins, polyphenols, flavonoids, organic acids, and essential oils. Various scientific studies demonstrated that Sumac had a free oxygen radical-scavenging effect, a protective effect against liver damage, antihemolytic, leukopenia, and antifibrogenic effects, along with its antiviral, antimicrobial, anti-inflammatory, and antioxidant properties. Recently, several scientific studies described the pathophysiology, clinical course, and the treatment of COVID-19 infection. The examination of the characteristics of COVID-19 infection revealed via the clinical studies suggests that Sumac extract could be useful in the treatment of COVID-19. Given the scientific studies focusing on the beneficial effects of Sumac, the present review aims to provide an encouraging viewpoint to investigate whether Sumac is effective in treating COVID-19 infection. Antiviral Effect SARS-CoV2 virus, which causes COVID-19 infection, is a highly infectious RNA virus. There are no scientific studies on whether Sumac is effective against the SARS-CoV2 virus. On the contrary, the medications currently being used for treatment were directly administered in clinics, without scrutinizing whether they were effective against the novel coronavirus. Subsequently, several medications were identified to be useful during the clinical course of the disease. Yet, there are scientific in vitro and in vivo studies that investigated the antiviral effects of Sumac against several viruses. In a study, bioflavonoids isolated from Sumac were evaluated for their antiviral activities. Sumac presented inhibitory activities against respiratory viruses (influenza A, influenza B, and measles) and herpes viruses (HSV-1, HSV-2, and varicella zoster virus [VZV]).2 Another study found that Sumac extract exhibited significant antiviral activity against fish pathogenic infectious hematopoietic necrosis virus, and viral hemorrhagic septicemia virus. Furthermore, it was considered that Sumac was a potential antiviral therapeutic against fish viral diseases.3 In a study conducted in 2015, it was established that urushiol obtained from Sumac exhibited reverse transcriptase inhibitory activity for human immunodeficiency virus type 1 (HIV-1). It was specified that Sumac could be used as a biological resource due to such inhibitory activity.4 Another study focusing on HIV found that Sumac extracts exhibited anti-HIV activity due to inhibiting the HIV-1 reverse transcriptase and protease activity. It was also demonstrated that Sumac inhibited the viral load in HIV-infected CEM-GFP (a CD4+ T-lymphocytic reporter cell line expressing green fluorescent protein [GFP] under HIV-1 LTR promoter) cells and human peripheral blood lymphocytes.5 Another study reported that Sumac extract presented strong antiviral activity against HSV-1 and HSV-2. The study also revealed that Sumac extract did not only interact with the viral envelope but also interacted with the surface of the host cells of the viruses, thus, disrupted the ability of the virus to adsorb and penetrate the host cells.6 The above-mentioned studies indicated the antiviral effects of Sumac extracts. The review of the viruses, on which Sumac is effective, such as influenza, HSV-1, HSV-2, VZV, and HIV-1 demonstrated that the common point between these viruses was the fact that they are all enveloped viruses, contain dense lipids in their envelopes, and are sensitive to ether.7 Coronaviruses share the same common features.7 Sumac is likely to affect the lipid layer in the virus envelope, disrupting the adsorption to the host cell and preventing the virus from penetrating the host cell, positively contributing to the infection. Naturally, this hypothesis should be evidenced in future studies. However, its effectiveness on the novel coronavirus (SARS-CoV2) should be clarified first through animal testing and subsequently should be tested through human subjects. Conclusion An evaluation of the up to date knowledge, revealed by the clinical studies, on the characteristics of COVID-19 infection, its pathophysiology, clinic, and treatment, suggests that the use of Sumac extracts could be beneficial. Based on the beneficial effects indicated by the scientific studies on Sumac extracts, the present review could be encouraging to investigate its effectiveness for COVID-19 treatment. The authors of the present study believe that the benefits of Sumac extract can be tested by adding the adverse-effect-free Sumac extract to treatment and protecting the existing treatment protocols.   Sugar intake during pregnancy is associated with allergy and allergic asthma in children University of Bristol (UK), July 5, 2021 High maternal sugar intake during pregnancy may increase the risk of allergy and allergic asthma in the offspring, according to an early study led by Queen Mary University of London (QMUL) involving almost 9,000 mother-child pairs. While some research has reported an association between a high consumption of sugar-containing beverages and asthma in children, the relation between maternal sugar intake during pregnancy and allergy and asthma in the offspring has been little studied. The team, which included researchers from University of Bristol, used data from a world-leading birth cohort study, the Avon Longitudinal Study of Parents and Children (ALSPAC), also known as 'Children of the 90s'. The cohort recruited mothers who were pregnant in the 1990s and has been following up their offspring ever since. The current study, which is published in the European Respiratory Journal, analysed associations between maternal intake of free sugars in pregnancy and allergy (defined by positive skin tests to common allergens, namely dust mite, cat and grass) and asthma at seven years of age. While there was only weak evidence for a link between free sugar intake in pregnancy and asthma overall, there were strong positive associations with allergy and allergic asthma (where the child was diagnosed with asthma and had positive skin tests to allergens). When comparing the 20 per cent of mothers with the highest sugar intake versus the 20 per cent of mothers with the lowest sugar intake, there was an increased risk of 38 per cent for allergy in the offspring (73 per cent for allergy to two or more allergens) and 101 per cent for allergic asthma. The team found no association with eczema or hay fever. Lead researcher Professor Seif Shaheen from QMUL said: "We cannot say on the basis of these observations that a high intake of sugar by mothers in pregnancy is definitely causing allergy and allergic asthma in their offspring. However, given the extremely high consumption of sugar in the West, we will certainly be investigating this hypothesis further with some urgency. "The first step is to see whether we can replicate these findings in a different cohort of mothers and children. If we can, then we will design a trial to test whether we can prevent childhood allergy and allergic asthma by reducing the consumption of sugar by mothers during pregnancy. In the meantime, we would recommend that pregnant women follow current guidelines and avoid excessive sugar consumption." The team speculate that the associations may be explained by a high maternal intake of fructose causing a persistent postnatal allergic immune response leading to allergic inflammation in the developing lung. The researchers controlled for numerous potential confounders in their analyses, such as background maternal characteristics, social factors and other aspects of maternal diet, including foods and nutrients that have been previously linked to childhood asthma and allergy. Importantly, the offspring's free sugar intake in early childhood was found to have no association with the outcomes seen in the analysis. As the study is observational, it does not prove a causal link between maternal sugar intake and allergies or asthma. A randomised controlled trial would be needed to definitively test causality.

Amazon indigenous group's lifestyle may hold a key to slowing down aging Tsimane people are unique for their healthy brains that age more slowly   University of Southern California, May 27, 2021 A team of international researchers has found that the Tsimane indigenous people of the Bolivian Amazon experience less brain atrophy than their American and European peers. The decrease in their brain volumes with age is 70% slower than in Western populations. Accelerated brain volume loss can be a sign of dementia.  The study was published May 26, 2021 in the Journal of Gerontology, Series A: Biological Sciences and Medical Sciences.  Although people in industrialized nations have access to modern medical care, they are more sedentary and eat a diet high in saturated fats. In contrast, the Tsimane have little or no access to health care but are extremely physically active and consume a high-fiber diet that includes vegetables, fish and lean meat.  "The Tsimane have provided us with an amazing natural experiment on the potentially detrimental effects of modern lifestyles on our health," said study author Andrei Irimia, an assistant professor of gerontology, neuroscience and biomedical engineering at the USC Leonard Davis School of Gerontology and the USC Viterbi School of Engineering. "These findings suggest that brain atrophy may be slowed substantially by the same lifestyle factors associated with very low risk of heart disease."  The researchers enrolled 746 Tsimane adults, ages 40 to 94, in their study. To acquire brain scans, they provided transportation for the participants from their remote villages to Trinidad, Bolivia, the closest town with CT scanning equipment. That journey could last as long as two full days with travel by river and road.  The team used the scans to calculate brain volumes and then examined their association with age for Tsimane. Next, they compared these results to those in three industrialized populations in the U.S. and Europe.  The scientists found that the difference in brain volumes between middle age and old age is 70% smaller in Tsimane than in Western populations. This suggests that the Tsimane's brains likely experience far less brain atrophy than Westerners as they age; atrophy is correlated with risk of cognitive impairment, functional decline and dementia.  The researchers note that the Tsimane have high levels of inflammation, which is typically associated with brain atrophy in Westerners. But their study suggests that high inflammation does not have a pronounced effect upon Tsimane brains.  According to the study authors, the Tsimane's low cardiovascular risks may outweigh their infection-driven inflammatory risk, raising new questions about the causes of dementia. One possible reason is that, in Westerners, inflammation is associated with obesity and metabolic causes whereas, in the Tsimane, it is driven by respiratory, gastrointestinal, and parasitic infections. Infectious diseases are the most prominent cause of death among the Tsimane.  "Our sedentary lifestyle and diet rich in sugars and fats may be accelerating the loss of brain tissue with age and making us more vulnerable to diseases such as Alzheimer's," said study author Hillard Kaplan, a professor of health economics and anthropology at Chapman University who has studied the Tsimane for nearly two decades. "The Tsimane can serve as a baseline for healthy brain aging."  Healthier hearts and -- new research shows -- healthier brains  The indigenous Tsimane people captured scientists' -- and the world's -- attention when an earlier study found them to have extraordinarily healthy hearts in older age. That prior study, published by the Lancet in 2017, showed that Tsimane have the lowest prevalence of coronary atherosclerosis of any population known to science and that they have few cardiovascular disease risk factors. The very low rate of heart disease among the roughly 16,000 Tsimane is very likely related to their pre-industrial subsistence lifestyle of hunting, gathering, fishing, and farming.  "This study demonstrates that the Tsimane stand out not only in terms of heart health, but brain health as well," Kaplan said. "The findings suggest ample opportunities for interventions to improve brain health, even in populations with high levels of inflammation."   Tai chi about equal to conventional exercise for reducing belly fat in middle aged and older adults University of Hong Kong, May 31, 2021 A randomized controlled trial found that tai chi is about as effective as conventional exercise for reducing waist circumference in middle-aged and older adults with central obesity. Central obesity, or weight carried around the midsection, is a major manifestation of metabolic syndrome and a common health problem in this cohort. The findings are published in Annals of Internal Medicine.  Tai chi is a form of mind-body exercise often described as "meditation in motion." It is practiced in many Asian communities and is becoming increasingly popular in Western countries, with more than 2 million people practicing it in the United States. While it is known to be a suitable activity for older people including those who are not active, there previously has been little evidence on tai chi's health benefits.  Researchers from the University of Hong Kong randomly assigned more than 500 adults over 50 with central obesity to a regimen of tai chi, conventional exercise, or no exercise over 3 months. Participants in the tai chi and exercise groups met for instructor-led workouts for 1 hour 3 times a week for 12 weeks. The tai chi program consisted of the Yang style of tai chi, the most common style adopted in the literature, and the conventional exercise program consisted of brisk walking and strength training activities. Waist circumference and other indicators of metabolic health were measured at baseline, 12 weeks, and 38 weeks. The researchers found that both the tai chi intervention and conventional exercise intervention group had reductions in waist circumference, relative to control. The reduction in waist circumference had a favorable impact on HDL cholesterol, or so-called good cholesterol, but did not translate into detectable differences in fasting glucose or blood pressure.  According to the study authors, their findings are good news for middle-aged and older adults who have central obesity but may be averse to conventional exercise due to preference or limited mobility.   Prenatal exposure to paracetamol associated with ADHD and autism symptoms in childhood Study of more than 70,000 European children bolsters the findings of previous research Barcelona Institute for Global Health (Spain), May 31, 2021 An epidemiological study of more than 70,000 children in six European cohorts has linked symptoms of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum conditions (ASC) to the mothers' use of paracetamol (acetaminophen) during pregnancy. The study, published in the European Journal of Epidemiology, was led by the Barcelona Institute for Global Health (ISGlobal), a centre supported by the "la Caixa" Foundation.  In total, the researchers analysed 73,881 children for whom data were available on prenatal or postnatal exposure to paracetamol, at least one symptom of ASC or ADHD, and main covariates. Depending on the cohort, 14% to 56% of the mothers reported taking paracetamol while pregnant.  The study found that children exposed to paracetamol before birth were 19% more likely to develop ASC symptoms and 21% more likely to develop ADHD symptoms than children who were not exposed.  "Our findings are consistent with previous research," explained ISGlobal researcher Sílvia Alemany, lead author of the study. "We also found that prenatal exposure to paracetamol affects boys and girls in a similar way, as we observed practically no differences."  "Our results address some of the weaknesses of previous meta-analyses," commented Jordi Sunyer, researcher at ISGlobal and last author of the study. "Considering all the evidence on the use of paracetamol and neurological development, we agree with previous recommendations indicating that while paracetamol should not be suppressed in pregnant women or children, it should be used only when necessary."  At some point during pregnancy, an estimated 46%-56% of pregnant women in developed countries use paracetamol, which is considered the safest analgesic/antipyretic for pregnant women and children. However, mounting evidence has linked prenatal paracetamol exposure to poorer cognitive performance, more behavioural problems, and ASC and ADHD symptoms. Those previous studies have been criticised for their heterogeneity. In the new study, therefore, "an effort was made to harmonise the assessment of ADHD and ASC symptoms and the definition of paracetamol exposure," explained Alemany. "The sample is large," she added, "and it includes cohorts from multiple European countries: the United Kingdom, Denmark, the Netherlands, Italy, Greece and Spain. We also used the same criteria for all of the cohorts, thereby reducing the heterogeneity of criteria that has hampered previous studies."  The study also analysed postnatal exposure to paracetamol and found no association between paracetamol use during childhood and ASC symptoms. Nevertheless, the research team concluded that further studies are needed, given the heterogeneity of postnatal paracetamol exposure among the various cohorts, which ranged from 6% to 92.8%. The six cohorts included the study were as follows:   1. Avon Longitudinal Study of Parents and Children (ALSPAC) 2. Danish National Birth Cohort (DNBC)  3. Gene and Environment: Prospective Study on Infancy in Italy (GASPII)  4. Generation R Study 5. INMA (including four subcohorts) 6. Mother-Child Cohort in Crete (RHEA)     Waking just one hour earlier cuts depression risk by double digits University of Colorado, May 28, 2021 Waking up just one hour earlier could reduce a person's risk of major depression by 23%, suggests a sweeping new genetic study published May 26 in the journal JAMA Psychiatry. The study of 840,000 people, by researchers at University of Colorado Boulder and the Broad Institute of MIT and Harvard, represents some of the strongest evidence yet that chronotype--a person's propensity to sleep at a certain time --influences depression risk.  It's also among the first studies to quantify just how much, or little, change is required to influence mental health.  As people emerge, post-pandemic, from working and attending school remotely-- a trend that has led many to shift to a later sleep schedule--the findings could have important implications.  "We have known for some time that there is a relationship between sleep timing and mood, but a question we often hear from clinicians is: How much earlier do we need to shift people to see a benefit?" said senior author Celine Vetter, assistant professor of integrative physiology at CU Boulder. "We found that even one-hour earlier sleep timing is associated with significantly lower risk of depression." Previous observational studies have shown that night owls are as much as twice as likely to suffer from depression as early risers, regardless of how long they sleep. But because mood disorders themselves can disrupt sleep patterns, researchers have had a hard time deciphering what causes what. Other studies have had small sample sizes, relied on questionnaires from a single time point, or didn't account for environmental factors which can influence both sleep timing and mood, potentially confounding results.  In 2018, Vetter published a large, long term study of 32,000 nurses showing that "early risers" were up to 27% less likely to develop depression over the course of four years, but that begged the question: What does it mean to be an early riser? To get a clearer sense of whether shifting sleep time earlier is truly protective, and how much shift is required, lead author Iyas Daghlas, M.D., turned to data from the DNA testing company 23 and Me and the biomedical database UK Biobank. Daghlas then used a method called "Mendelian randomization" that leverages genetic associations to help decipher cause and effect.  "Our genetics are set at birth so some of the biases that affect other kinds of epidemiological research tend not to affect genetic studies," said Daghlas, who graduated in May from Harvard Medical School.  More than 340 common genetic variants, including variants in the so-called "clock gene" PER2, are known to influence a person's chronotype, and genetics collectively explains 12-42% of our sleep timing preference.  The researchers assessed deidentified genetic data on these variants from up to 850,000 individuals, including data from 85,000 who had worn wearable sleep trackers for 7 days and 250,000 who had filled out sleep-preference questionnaires. This gave them a more granular picture, down to the hour, of how variants in genes influence when we sleep and wake up.  In the largest of these samples, about a third of surveyed subjects self-identified as morning larks, 9% were night owls and the rest were in the middle. Overall, the average sleep mid-point was 3 a.m., meaning they went to bed at 11 p.m. and got up at 6 a.m. With this information in hand, the researchers turned to a different sample which included genetic information along with anonymized medical and prescription records and surveys about diagnoses of major depressive disorder.  Using novel statistical techniques, they asked: Do those with genetic variants which predispose them to be early risers also have lower risk of depression? The answer is a firm yes.  Each one-hour earlier sleep midpoint (halfway between bedtime and wake time) corresponded with a 23% lower risk of major depressive disorder. This suggests that if someone who normally goes to bed at 1 a.m. goes to bed at midnight instead and sleeps the same duration, they could cut their risk by 23%; if they go to bed at 11 p.m., they could cut it by about 40%. It's unclear from the study whether those who are already early risers could benefit from getting up even earlier. But for those in the intermediate range or evening range, shifting to an earlier bedtime would likely be helpful. What could explain this effect? Some research suggests that getting greater light exposure during the day, which early-risers tend to get, results in a cascade of hormonal impacts that can influence mood. Others note that having a biological clock, or circadian rhythm, that trends differently than most peoples' can in itself be depressing. "We live in a society that is designed for morning people, and evening people often feel as if they are in a constant state of misalignment with that societal clock," said Daghlas. He stresses that a large randomized clinical trial is necessary to determine definitively whether going to bed early can reduce depression. "But this study definitely shifts the weight of evidence toward supporting a causal effect of sleep timing on depression."  For those wanting to shift themselves to an earlier sleep schedule, Vetter offers this advice: "Keep your days bright and your nights dark," she says. "Have your morning coffee on the porch. Walk or ride your bike to work if you can, and dim those electronics in the evening."     Olive oil nutrient may help prevent brain cancer University of Edinburgh, June 2, 2021 A compound found in olive oil may help to prevent cancer developing in the brain, a study shows. Research into oleic acid – the primary ingredient in olive oil – has shown how it can help prevent cancer-causing genes from functioning in cells. The oily substance – one of a group of nutrients known as fatty acids – stimulates the production of a cell molecule whose function is to prevent cancer-causing proteins from forming. The study team says it is too soon to say whether dietary consumption of olive oil may help prevent brain cancer. Their findings, however, point towards possible therapies based on the oil to prevent brain cancer from occurring. Scientists from the University analysed the effect of oleic acid on a cell molecule, known as miR-7, which is active in the brain and is known to suppress the formation of tumours. They found that oleic acid prevents a cell protein, known as MSI2, from stopping production of miR-7. In this way, the olive oil component supports the production of miR-7, which helps prevent tumours from forming. Researchers made their discoveries in tests on human cell extracts and in living cells in the lab. The study, published in the Journal of Molecular Biology, was funded by the Medical Research Council and the Wellcome Trust. "While we cannot yet say that olive oil in the diet helps prevent brain cancer, our findings do suggest that oleic acid can support the production of tumour-suppressing molecules in cells grown in the lab. Further studies could help determine the role that olive oil might have in brain health," says Dr Gracjan Michlewski.   Study: Boosting selenium intake can help reduce osteoporosis risk Central South University (China), May 29, 2021 Researchers from China have found that increased selenium intake may reduce a person’s risk for osteoporosis. In their report, experts from Central South University in Changsha recruited over 6,200 participants and measured the bone mineral density in the middle phalanges of the second to fourth fingers of their non-dominant hand. The team then assessed the participants’ dietary patterns, particularly their selenium intake, through a validated semi-quantitative food frequency questionnaire which the subjects answered twice within three weeks. After analyzing the participants’ bone mineral density using a compact radiographic absorptiometry system, the team discovered that 9.6 percent of the subjects have osteoporosis. The majority of the cases were reported among women, with 19.7 percent having been diagnosed with the disease. Among men, only 2.3 percent were diagnosed with osteoporosis. The researchers also compared the dietary data of those diagnosed with osteoporosis to those who were not. They found that there are significant differences between the participants in terms of age, gender, smoking and drinking habits, BMI, blood pressure levels, physical activity levels, nutrient supplementation, dietary calcium intake, dietary fiber intake and dietary energy intake. The factors above were measured as they are considered to be vital for the development and prevention of osteoporosis. But most of all, the team observed a significant difference between the subjects with osteoporosis and those who don’t have the disease in terms of dietary selenium intake. The researchers found that those who have osteoporosis also have lower levels of dietary selenium consumption. A person can increase his selenium intake by eating Brazil nuts, fish, shellfish, beef, turkey, chicken, fortified cereals, whole-wheat bread, beans, lentils and eggs. The recommended dietary allowance for selenium is 55 micrograms per day for adult men and women above 19 years old. For pregnant and lactating women, the recommended intake is between 60 to 70 micrograms per day. However, in the study, which involved Chinese citizens, the participants’ selenium intake averaged only 43.5 micrograms per day. This is comparable to the average daily selenium intake of Europeans, which is 40 micrograms per day. The low selenium intake of both populations could be due to the low-selenium content of the soil in both areas. Selenium and thyroid hormones Selenium primarily functions in the body as an essential component of selenoproteins, composed of various enzymes and proteins that help protect the cells from damage and infections. Selenoproteins are also needed in producing DNA and in the metabolism of thyroid hormones. The thyroid glands have the highest concentration of selenium in the body. In connection to thyroid hormones, the researchers postulated that low selenium levels might have increased the level of thyroid hormones in the blood, which may have caused an accelerated bone loss and osteoporosis in the subjects with low dietary selenium intake. Thyroid problems have indirect correlations with osteoporosis and are considered as secondary causes. This means that elevated thyroid hormone levels don’t directly cause osteoporosis, but they can influence how the body maintains a healthy mineral bone density. In addition, hyperthyroidism, a thyroid disorder characterized by too much production of a thyroid hormone thyroxine, is considered as having a close link to the development of osteoporosis. This is because elevated levels of thyroxine accelerate the process of bone degradation, which is conducted by the osteoclasts. Osteoclasts are the cells that dissolvethe bones, initiating new bone production, which is conducted by another cell — the osteoblasts. Excessive thyroxine levels make the osteoclasts work faster than the osteoblasts, causing the bones to be fragile or brittle. However, the researchers in the study did not confirm a causal relationship between dietary selenium intake and osteoporosis, but future studies are underway to provide support to their findings.   Juvenile selenium deficiency impairs cognition and energy homeostasis  University of Hawaii, May 26, 2021 According to news originating from Honolulu, Hawaii, by NewsRx correspondents, research stated, “Selenium (Se) is an essential micronutrient of critical importance to mammalian life.” The news reporters obtained a quote from the research from University of Hawaii: “Its biological effects are primarily mediated via co-translational incorporation into selenoproteins, as the unique amino acid, selenocysteine. These proteins play fundamental roles in redox signaling and includes the glutathione peroxidases and thioredoxin reductases. Environmental distribution of Se varies considerably worldwide, with concomitant effects on Se status in humans and animals. Dietary Se intake within a narrow range optimizes the activity of Se-dependent antioxidant enzymes, whereas both Se-deficiency and Se-excess can adversely impact health. Se-deficiency affects a significant proportion of the world’s population, with hypothyroidism, cardiomyopathy, reduced immunity, and impaired cognition being common symptoms. Although relatively less prevalent, Se-excess can also have detrimental consequences and has been implicated in promoting both metabolic and neurodegenerative disease in humans.” According to the news editors, the research concluded: “Herein, we sought to comprehensively assess the developmental effects of both Se-deficiency and Se-excess on a battery of neurobehavioral and metabolic tests in mice. Se-deficiency elicited deficits in cognition, altered sensorimotor gating, and increased adiposity, while Se-excess was surprisingly beneficial.”

Moderator: BobbieJean Sweitzer, M.D. 
 Participants: Graham J. Walkden, M.B.Ch.B., Hannah Gill, F.R.C.A., Ph.D. and Andrew J. Davidson, M.B.B.S., M.D., F.A.N.Z.C.A., F.A.H.M.S
. Articles Discussed:
 Early Childhood General Anesthesia and Neurodevelopmental Outcomes in the Avon Longitudinal Study of Parents and Children Birth Cohort Anesthesia in Childhood and Neurodevelopmental Outcome: The Ongoing Hunt for a Phenome

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.01.072165v1?rss=1 Authors: Bartsch, U., Corbin, L. J., Hellmich, C., Taylor, M., Easey, K. E., Marston, H. M., Timpson, N. J., Jones, M. W. Abstract: Background: The rs1344706 polymorphism in ZNF804A is robustly associated with schizophrenia (SZ), yet brain and behavioral phenotypes related to this variant have not been extensively characterized. In turn, SZ is associated with abnormal non-rapid eye movement (NREM) sleep neurophysiology. To examine whether rs1344706 is associated with intermediate neurophysiological traits in the absence of disease, we assessed the relationship between genotype, sleep neurophysiology, and sleep-dependent memory consolidation in healthy participants. Methods: We recruited healthy adult males, with no history of psychiatric disorder, from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. Participants were homozygous for either the SZ-associated A allele (N=25) or the alternative C allele (N=22) at rs1344706. Actigraphy, polysomnography (PSG) and a motor sequencing task (MST) were used to characterize daily activity patterns, sleep neurophysiology and sleep-dependent memory consolidation. Results: Average MST learning and sleep-dependent performance improvements were similar across genotype groups, but with increased variability in the AA group. CC participants showed increased slow-wave and spindle amplitudes, plus augmented coupling of slow-wave activity across recording electrodes after learning. Slow-waves and spindles in those with the AA genotype were insensitive to learning, whilst slow-wave coherence decreased following MST training. Conclusion: We describe evidence that rs1344706 polymorphism in ZNF804A is associated with changes in experience- and sleep-dependent, local and distributed neural network activity that supports offline information processing during sleep in a healthy population. These findings highlight the utility of sleep neurophysiology in mapping the impacts of SZ-associated variants on neural circuit oscillations and function. Copy rights belong to original authors. Visit the link for more info

Deu na Revista Crescer: "Kelly Key toma iodo durante gestação para aumentar o QI do bebê - suplementação do mineral gera polêmica entre internautas”. Mas e aí? O que é fato e o que é factóide? Confira no papo entre o leigo curioso, Ken Fujioka, e o cientista PhD, Altay de Souza. OUÇA (23min 14s) Naruhodo! é o podcast pra quem tem fome de aprender. Ciência, senso comum, curiosidades, desafios e muito mais. Com o leigo curioso, Ken Fujioka, e o cientista PhD, Altay de Souza. Edição: Reginaldo Cursino. http://naruhodo.b9.com.br REFERÊNCIAS Podcasts das #Minas: As Mathildas http://cinemacao.com/category/as-mathildas/ Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC) http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)60436-5/fulltext APOIA.SE Você sabia que pode ajudar a manter o Naruhodo no ar? Ao contribuir, você pode ter acesso ao grupo fechado no Facebook e receber conteúdos exclusivos. Acesse: http://apoia.se/naruhodopodcast

Riots started in Tottenham in London on August 6th this year and spread to 35 different locations across the Capital and towns and cities across England, including Birmingham, Bristol, Leeds, Liverpool and Nottingham. Parliament was recalled and there was a rapidly growing consensus among politicians and the media, that the riots were the result of pure criminality. The riots were criminal, the rioters were criminals and their behaviour was motivated by criminality. A popular explanation for the cause came down to "mob mentality", that in the heat of the moment, individuals lose their identity and act emotionally and irrationally, with little sense of self. But three months after the riots, two psychologists of international reputation, Steve Reicher and Clifford Stott, both experts in crowd behaviour and crowd psychology, are challenging that interpretation in a new e-book, "Mad Mobs and Englishmen". They say that not only is the criminality consensus wrong, but it's also dangerous. Claudia speaks to Professor Reicher, about what their research uncovered. "Anchoring" and the Minimum Payments on Credit Cards: The British have the second highest use of credit cards in the world; only Americans make greater use of their flexible friends. And in the UK, our cards are loaded with debt. The minimum payment printed, by law, on the bottom of the monthly bill, is supposed to stop us getting into further debt by ensuring that we always pay off at least some of the balance every month. But new research by Professor Neil Stewart from the University of Warwick has discovered that the minimum payment could be having the opposite effect. Because of the impact of a well-established psychological effect called "anchoring", it appears that simply reading the suggested minimum payment makes us pay off less of the debt that we would otherwise have done. Counterintuitive ? Yes. Bullying and Borderline Personality Disorder: The links between childhood bullying and mental health problems in later life are well established, and new research suggests that the impact could also include increased rates of Borderline Personality Disorder. BPD is quite rare and little is known about its causes, but it's a condition which can feature emotional instability, impulsivity, paranoia and difficulties in relationships. In a huge study over time, 6000 children in all, the Avon Longitudinal Study of Parents and Children (ALSPAC), researchers discovered that children who experienced long term or very severe bullying by their peers are seven times more likely to show symptoms of BPD at the age of 11. Producer: Fiona Hill.

Genetic factors are important determinants of overweight. We examined whether there are differential effect sizes depending on children's body composition. We analysed data of n = 4,837 children recorded in the Avon Longitudinal Study of Parents and Children (ALSPAC), applying quantile regression with sex- and age-specific standard deviation scores (SDS) of body mass index (BMI) or with body fat mass index and fat-free mass index at 9 years as outcome variables and an "obesity-risk-allele score" based on eight genetic variants known to be associated with childhood BMI as the explanatory variable. The quantile regression coefficients increased with increasing child's BMI-SDS and fat mass index percentiles, indicating larger effects of the genetic factors at higher percentiles. While the associations with BMI-SDS were of similar size in medium and high BMI quantiles (40th percentile and above), effect sizes with fat mass index increased over the whole fat mass index distribution. For example, the fat mass index of a normal-weight (50th percentile) child was increased by 0.13 kg/m(2) (95% confidence interval (CI): 0.09, 0.16) per additional allele, compared to 0.24 kg/m(2) per allele (95% CI: 0.15, 0.32) in children at the 90th percentile. The genetic associations with fat-free mass index were weaker and the quantile regression effects less pronounced than those on fat mass index. Genetic risk factors for childhood overweight appear to have greater effects on fatter children. Interaction of known genetic factors with environmental or unknown genetic factors might provide a potential explanation of these findings.

Nicholas Timpson, of the Department of Social Medicine, University of Bristol, gives a talk on Genetics of obesity, and the Avon Longitudinal Study of Parents and Children on the 9th November 2009.