Ep.
28
ADHD Research Recap: Exploring the Genetics of ADHD
Join Skye and Sarah for a research recap and discussion of two research papers on ADHD and genetics. One paper investigates the role of microRNA in ADHD, while the other is a meta-analysis identifying 27 risk loci.
In this podcast episode, Sarah and Skye discuss two research papers, both related to ADHD and genetics. They explore a paper that delves into the role of microRNA in ADHD. The other study they discuss is a meta-analysis of ADHD genetics, which identifies 27 risk loci.
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The ADHD Academy
Unconventional Organisation
Alterations in microRNA of extracellular vesicles associated with major depression, attention-deficit/hyperactivity and anxiety disorders in adolescents.
Genome-wide analyses of ADHD identify 27 risk loci, refine the genetic architecture and implicate several cognitive domains
Hi, we are the ADHD Skills Lab podcast. My name is Skye. And my name is Sarah. And we will be your hosts, chatting to you about practical ADHD strategies you can use, the research behind some of these strategies, as well as interviewing other professionals with ADHD about how they've developed skills and working through struggles in their lives. You might know us from Unconventional Organization, where we talk about this kind of stuff all day long. So we're super excited to have you along and we're going to chat through it together.
So today I am really excited. We're having a very cool episode of ADHD research recap because today we have Abby with us. Abby is one of our unconventional ADHD coaches and she also has an understanding of genetics, both from her professional background and in general. Sarah and I are really excited to have her on the podcast today. We've had some very interesting but hard to. Delved into papers on genetics that we've been holding specifically to chat with Abby about. So yeah, welcome Abby. Great to have you here. Thank you for having me. Yeah. So tell us a little bit about how you came to have an understanding of genetics and what it means and, and your interest in genetics with ADHD. Yeah. Well, I guess like a lot of other people with ADHD, I have studied a lot of things and a lot of those things have been within the science space. I started off in pharmacy and was particularly interested in, I guess, the biochemistry aspects of pharmacy and how we do drug development and drug modeling and all of those sorts of things. I didn't really find that sort of manifested in the job itself, so of course went for something else. I've also always had a really strong interest in human psychology and counseling and the nervous system. So I moved on. to do a master's in genetic counseling, which was a really incredible experience and a beautiful way to blend the sort of counseling and psychology theory with genetics at that sort of level and practiced as a genetic counselor for a while. When you were doing genetic counseling, did you then work with people who had ADHD as part of that counseling? I didn't work directly with. people with ADHD, but when I was working in IVF, so I worked in reproductive genetics for a little while, I had some really interesting conversations, and honestly, some challenging conversations with parents who were looking for ways to prevent, I guess what you would say, the genetic transmission of ADHD from them to their children. Oh, wow. Yeah, or if they had a child with ADHD, Is there anything that I can do to, for my next child, not to have ADHD? Did you know you had ADHD at that point? I did. Wow. That must've been some tough conversations. They were tough conversations. I think the beautiful thing about genetic counseling is, you know, one of the underpinning tenants is non-judgment. And, you know, whilst it is challenging, because I personally think that ADHD is. pathologize in the absence of acknowledging the context that we're living in and the context that kids are living in. You know, the world isn't really built for ADHD brains. And I can understand this, you know, a parent stress and their worry and wanting to create the best life that they can for their kids. Yeah, but at the same time, they're really challenging and complex conversations to have, not the least because there is nothing that we can do at this stage. And we can't, we don't have a crystal ball. Yeah, that's so interesting. I guess that kind of leads us to the articles that we're going to discuss today, because there are articles that have just come out this year that are about different DNA ways that we can profile or, you know, understand ADHD. I don't know if they really discussed it or not in those papers, but a lot of the reasoning behind that is to understand ADHD. And then the conversation becomes, do we? cure, you know, you have that whole cure conversation, which, you know, it's very controversial. So in terms of where you were, because obviously that's what you were doing. And now one of the things you're doing is working with us at Unconventional and we're very lucky and happy to have you. So how has that conversation changed as well from doing that genetic counseling to what you're doing now? I think genetic counseling has really, in a lot of ways, has informed the way that I coach. I think the beauty of genetic counseling. You know, honestly, I wish it was something that was, you know, a role that was distributed more broadly throughout the medical system to have sort of counselors there to help support and interpret medical information for people has really helped with the science communication aspect of what we do and the interpretation of the research. There's a huge focus on interpreting and synthesizing really complex information. in a way that is meaningful and empowering for people. So they feel like they can make the best decisions for themselves. And I think honestly, that translates really well into the coaching space as well. Yeah, no, it's very true. I mean, that is one of the things that we try and do is take information that. That may be complex. I mean, in this case, we're going to discuss two papers that Sarah and I both read multiple times with limited understanding. I'm still like Googling definitions and looking for pieces in the paper. Yeah. So in many ways we are going to ask you today to do that thing that, you know, that you have learned to do, which is to take this complicated information and to help explain it, but in this case. for the purposes of hopefully allowing people who have ADHD to feel more confident in understanding their own diagnosis that then they can use and make their own decisions with. I'm happy to do that for the best of my ability. I also read the papers many times. Yeah. Yeah, I know, right?
So we've got two papers to go through today. The first one is paper from 2023 that is from Nature, which is a pretty well-known journal, looking at alterations in microRNA of the extracellular vesicles associated with major depression, attention deficit, hyperactivity, and anxiety. So they're looking at these three areas in adolescence and basically trying to find out are there differences in this microRNA profile between... ADHD, depression, anxiety, and neurotypicals, and also a little bit of a time discussion, but they do talk about the limitations of that as well. And I mean, let's start at the beginning. What is micro RNA? That's a really good question. So micro RNA, it's interestingly has been thought to be as a lot of parts of. the genome and the epigenome, which I'll explain in a second, have been thought to be sort of junk and not really functional within the human body. And often when we label things as junk, later on we figure out that we were wrong. And this is one of those cases. So in the early 2000s, there was, I guess, renewed interest in micro RNA and what it is essentially a small linear pieces of genetic material that can act on the genome. So they can act on DNA to either increase the expression of something or decrease the expression of something. So they would call it, or I would call it like a genetic modulator. So it can act on our genome, which is all about DNA. Interesting. So, so is that kind of what they're saying is that maybe there is something in this micro RNA that is acting on the genome specifically related to ADHD? Potentially. This paper is really, really interesting because what it's saying to us is in particular as it relates to ADHD that there is a particular micro RNA, so like a particular version of a micro RNA with a specific sequence. that we see in greater quantities in the blood of people with ADHD versus people who don't have ADHD. So there's a higher concentration of this particular microRNA. MicroRNA just like DNA and like proteins are produced somewhere in the body and the source code is our DNA. So what's happening here is that there are cells in the body that are producing this micro RNA to do a job. And what we're seeing with this particular one, and they have some, we can talk about what they think this micro RNA is doing. What that tells us is that there is some mechanism that is up regulating or increasing the expression of this micro RNA in people with ADHD. Not sure why. Okay. At this stage. Okay. Well, before we kind of get into what this means. I wanted to take a step back and talk about how they figured this out. What was the methodology? So, Sarah, do you want to kind of give us a bit of a sense of how they did this? Sure. So I'm going to do my best, but I'm pretty sure this is a contribution I can make. So the data that they took for this study was from the Brazilian High Risk Cohort Study, which I'm... sure we've talked about before or something. It's like this. Yeah, it did ring a bell. Yeah, I'm not sure if it's from when we read this months ago, or like, totally separate study that we read. But anyway, this cohort study is like a large group of data points that other people can just use to like make analyses on. Yes. So anyway, their sample size is 116. They're specifically looking for people with high risk for mental disorders. They Sorry, before you continue. 116, does that include people with ADHD and people without ADHD when they divide it into smaller groups? Yeah, the breakdown is in the next paragraph though, and it gives it for each different group. Because I think it is, it says here that the control is 27. And then the incidence, so people who met criteria for disorder, the second time and not the first time, the first time and not the second time, and then both times. are all in this group, which kind of means it wasn't a huge sample. Yeah. What do you think, Abby, do you have any sense of how big a sample would be in this kind of genetic study? I would agree. This would be considered a small, a small sample size. Yeah. And that's just something we like to flag Abby when we're discussing this kind of research, because the results are really interesting, but it's always good to take a look at how they were developed. And then the diagnosis itself was a self-report survey. Yeah, so Abby, you did flag that as a potential limitation, but then I look up what DAUBA is. It's the Development and Wellbeing Assessment. It's actually a three-pronged survey. There's self-report, the parents get a survey, and the teacher also gets a survey. When I looked it up, it actually seems to be pretty good in terms of self-reports, but it's usually just part. of the thing, but it's probably better than some of the things we've looked at. I was just... So it's a self-report survey, but quite a solid one. Quite a good one. Okay. Awesome. Multiple perspectives. Yeah. No, definitely. Which we, which we love. We love it when it's not just the teacher. Or just themselves. Those ones always make me giggle. Yeah. Especially since we have such a weird view of ourselves sometimes. Distorted is the word I was looking for. Yeah. Abby, we did a podcast a few episodes ago where they asked people in medical school if they thought they had ADHD and it was very, very high. It was like, depending on where you kind of are at. This was also a longitudinal study. However, they also flagged this as a potential limitation because there were only two measurement points. They indicate those as wave one and wave two, but the points were three years apart, so not very long. Yeah, sort of a two-point study for sure. Okay. And then in terms of the results, Sarah, do you want to give us like a overview of the results and then Abby, you can let us know what they mean. I will do my best. I'll do my best. So the first thing is that they didn't find any significant effects in the longitudinal analysis. So when they looked at those two time points, they were pretty much the same. The first data point, this microRNA strand specifically that they were looking for was quote unquote, upregulated in participants with ADHD. Now I had to go to chat GPT to help me understand what this actually means. But when I came to the understanding that upregulated means the microRNA is trying to regulate itself, Abby help me out, but I'm pretty sure that's like. bare minimum explanation? Yeah. So essentially, when we talk about upregulation, it can mean a lot of different things in biochemistry. But in this context, what it means is that there is some sort of mechanism that is increasing the output of this particular microRNA, right? So there is something that is basically signaling to the cell that is producing this microRNA to produce more than someone who doesn't have ADHD. That's so interesting. Do we collective humanity have any idea why that happens? Yeah. I'm curious too. Wow. It's a really good question. I think this brings epigenetics into the discussion, right? Which is, so we've got our, our DNA, right? Which is our genetic code. It is the blueprint for us for how to make a human body. It has all of our little quirks. little differences, all of those sorts of things. And then you've got what we call the epigenome and they are all the, I guess, molecular machinery that acts on the DNA that regulates the expression of our genetic material. So it might be something that switches a gene on or off. It might be something, for example, in your gut, if you've had a glass of milk, that milk might send the signal to some cells in your gut. to upregulate lactose because you've got to digest some milk right now. So that's interesting. Yeah, that's like an epigenetic mechanism, for example. And they are infinitely complex. I wouldn't never say that we have a good solid understanding of broadly how all of this works. But micro RNA is one way that the body acts on our DNA to. control how it's expressed or control what proteins are produced and where. Oh, that's so fascinating. So in terms of what they found, they found that there was something happening with people who are ADHD, but this was distinct from people who had anxiety and depression, which was not what they were expecting to find because often those things get connected together. could mean, what they might be hinting at here? Yeah, it's a difficult one. What it looks like is that there is, and this wasn't part of the study, but what it's suggesting is that there is some mechanism that is going on within people with ADHD that means that more of this microRNA is being produced. And that could be for a number of reasons. It could be because there is something going on in the ADHD person. It could be in their brain. It could be in their nervous system that is sending a signal that goes, okay, we need more of this micro RNA to do its job. And we don't know what that job is. I have to clarify that. We're not quite sure what its job is. Conversely, it could be compensating for something or. could explain part of the features of ADHD in terms of what it is doing in our bodies, which again, not really sure. What they did hypothesize was that it may have something to do with glutamate transmission in the brain, potentially. Okay. I was actually just going to ask you if that's where this comes into play because I see glutamate discussed sort of in our notes a little bit further on. And I had no idea what that was. So really thank you for the definition that you put in here. Yeah, you're a transmitter. But honestly, it only made me wanna like go find out more. And then I was looking up what we know about sort of glutamate and dopamine and how those play together. And I got a lot of like question marks, like we're not really there yet, but actually there might be something here. Abby, does that sound right? Yeah, glutamate is also has been, I think, a topic of this a little bit outside of genetics, but glutamate has been a topic of interest as it pertains to things like neuroinflammation. Glutamate is an excitatory molecule in the brain. So it sort of stimulates the brain. When we have just enough, it's great. When we don't have enough, it can be a problem. And when we have too much, it can be a problem. also a problem. Yeah, so there have been a couple of studies actually that show increased levels of glutamate in the brain can cause neuroinflammation and symptoms like brain fog and difficulty with concentration, all those kinds of things. So interesting that it's sort of come up in this paper. Isn't there also research that shows that glutamate might be partly responsible in the triggering and modulation of dopamine receptors? Yes. So like that, so glutamine is a big neurotransmitter, much less understood than dopamine. We talk about dopamine all the time. So really interesting to see if we can continue this. It'd be very cool. In terms of the practical takeaways from this paper, I mean, the first takeaway sounds like there could be some epigenetic switching going on in our genes that is specific to ADHD. And like you said, it might be compensating for something. It might be for some other reason. We're not sure. It could have something to do with glutamate, which, you know, is a neurotransmitter that we're still learning about. But there might be some way for us to sort of see on a molecular level, I guess, a little bit more about our own ADHD. The most interesting takeaway I thought with regards to this is like, could this potentially be a diagnostic test in future? Yeah, I was thinking that too. I was like, should we talk diagnostic test? We always talk about this, but I agree. I think it's so interesting, especially because this is a little bit less of an intensive diagnostic test than if you went the neuroscience route. Right. 100%. And if they do a bigger study with a larger sample and they get the same sort of results. It could be cheaper, more accessible. I guess the psychosocial impact would be less. Diagnosis is really hard to get at the best of times when you can afford it. I think these sorts of molecular markers, if they're verified, could be so useful for us. Yeah. Especially because they're seeing a difference between depression and anxiety and ADHD, which is often a very complicated... thing to navigate even for psychiatrists who were doing it professionally, that in itself would be so helpful. Good time. And I think it would be really interesting in further research to if they can identify the source gene for where this microRNA is coming from and what the role of that gene is. It might tell us more about the architecture of ADHD as a whole as well. Yeah, no, definitely. Oh, well, that's such an exciting study. I'm very happy that you're here to help us break it down and understand it a little bit better because it's definitely interesting to get into genetics. Once you break it down, it makes a lot more sense. It's just getting through the very long string of numbers and letters that is the micro RNA specifically and all of those kinds of things. Yeah. No, the jargon is unfriendly. It's so hard to cut through. Yeah, I know. I thought neuroscience jargon. Yeah. Especially for people with sort of ADHD, possible dyslexia, dyscalculia, like the whole range of things. It just really does not make it easy. Yeah, no, definitely. So it's pretty awesome to have you go through it. Was there anything else you wanted to say, Sarah, to just finish off this paper? One thing that's really important to remind everyone is that we are starting to find functional differences in. bodies, the brains of ADHD people. And that should come with a little bit of self compassion and like maybe some self acceptance, like when you're ready for it. Just because you know, it's, it's okay to be different. No, but like we're actually finding out what specifically is different. And that's a beautiful thing. Yeah. There's a bunch of us out there. It's okay. Yeah. You might have micro RNA that are different, which is pretty cool and weird thought to have, but yeah, definitely. I didn't think I'd be thinking about that today. Yep.
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So the other paper is from Nature Genetics, and you actually flagged this paper for us, Abby. You were very excited about it, and I'm excited to read it as well. This paper looked at genome-wide analysis of ADHD. They identified 27 risk loci, refined the genetic architecture, and implicate several cognitive domains. Basically, what they were looking at was what are the genetic risk loci associated with ADHD? What role do certain variants have with ADHD risks? What is the relationship between ADHD genetic risks and other psychiatric disorders and how does ADHD affect cognition? So lots of different kinds of questions in this big meta analysis where they had a lot of different cases. They had 38,000 plus individuals with ADHD and 186,000 controls. So lots of people. Yeah. So do you want to take us through a little bit, Abby, of what they found as a whole? And then Sarah, we can jump into the methodology. Sure. Yeah, absolutely. So the study mapped 27 ADHD risk loci. Essentially loci is just the location of a gene or a mutation on a chromosome. Most of us, not all of us, most of us have 23 pairs of chromosomes and they're numbered one to 23. one of each pair we get from mom and one of each pair we get from dad. And all of the genes in our genetic material is organized in what appears to be a random way. I'm sure it isn't because we say things are junk and they're random and they end up not being that way. But we can find particular risk locations on chromosomes that are common to people with ADHD. So variants. that are shared by people with ADHD, for example, might sit on a particular location on chromosome number five, if that makes sense. So it's the idea of like, there's certain locations where you have a higher risk of ADHD, if you have this. Is that the concept? Yeah. So what they've done is they've looked at the whole genome. So every single piece of genetic material in all of the... participants with ADHD and without, and had a look at the common variants that are present in people with ADHD. And what they found is that there are specific genes, so specific stretches of DNA that produce specific proteins that are common to people with ADHD, but also just particular areas on chromosomes. that are rich with what seem to be ADHD specific variants. We don't know if that's true, but that's what it looks like. Interesting. And so what was it about those variants that made them seem ADHD specific? Might be helpful to talk about what a gene variant is. What they would have seen is that in the participants without ADHD, they would have had commonalities with their genetic sequence. And we all have variations in our genetic sequence. That's why we look different, sound different, think different, all those kinds of things. And with people with ADHD, they would have found variations that are common for people with ADHD. So particular sequences that they only saw in the ADHD population. And in this particular study, they found 7,000 of those. Whoa. Right. Wow. They found 7,000 potential candidate genes that are common for people with ADHD. Human beings only have approximately 20, 25,000 coding genes. If you think about that, it's almost a third. Yeah. So, Abby, could you have one? gene variation that is correlated with your ADHD or causing your ADHD? Or is it just one? No, absolutely. So this is another study that supports the idea that ADHD is what we call polygenic, right? Which is another barrier word. But essentially what that means, a polygenic condition is a genetic condition that is caused by the contribution of a number of independently interacting gene variants. And what this is telling us here is that it could potentially be thousands of little cumulative differences in people with ADHD that produce the profile of someone with ADHD, rather than it being, for example, something like a single gene condition. I'm picturing like a mob in Minecraft. Just like... going on. Yeah, exactly. And this is exactly the way things like height work as a trait. It might be the contribution of 40 or 50 different genes that cumulatively mean you're five foot six or whatever. Interesting. That's a good explanation. Yeah, honestly, this is great. So, Sarah, do you want to take us through a little bit then of how they got this amazingly intense? results. Like what was the methodology that they did? This is a meta analysis of a bunch of different papers, obviously, which is why they had so many participants, as I mentioned earlier, over 38,000 individuals with ADHD and over 186,000 controls. That's a ton. Anyway, so they looked through a bunch of different databases on like looking for this information. And then from there, they sort of used statistical models to refine the genetic architecture of ADHD, which Abby also added to her glossary. The genetic architecture is just like the pattern of genetic effects that build and control a given... Phenotypic character. Yeah, yeah. Which is the mob that we discussed. The mob of things that could make... They used the statistical method to clean that up. and then looked at the relationship between ADHD, genetic risk compared to other psychiatric disorders. The study looked at a lot of things because they also had other data points on these people other than just do you have ADHD. They also had stuff on educational attainment, age at first birth, age of first smoking and things like that, so I'm not sure. where specifically that stuff came from, but probably like the 200,000. Yeah, I feel like you're going to do that many. You're going to get a lot of information because this is a meta-analysis, how they define who has ADHD is going to be different for all of the different papers. And that's why we're not going to necessarily know that information here. It is interesting to note that there are that many papers that actually discuss genetics of ADHD. Which is interesting in itself. So clearly this is an area that's, you know, being studied quite heavily. In terms of the results, Abby, you mentioned that they found estimated 7,000 common variants. So this might be a group of things that affect ADHD. What else did they find? Cause I'm looking at the notes here in terms of what this was, like, what is the sort of practical information for those of us with ADHD from these results? Yeah, it's a good question because there's a lot of, pardon the pun, noise when you've got so many participants and so much information. I guess the most exciting part about this is that out of the 27 risk loci that they found, 21 of them are novel, so they haven't been seen before. In addition to looking just directly at the code, so looking at DNA. They also looked at what the DNA is producing in some of the participants. It wasn't all of them. So they had a look at what's, what's actually happening in tissues. So we're not just looking at the DNA. We're looking at how the DNA is being expressed, which is the phenotype. Yes. I remember that one from university. Yeah. So that would be like the red hair or the blue eyes or whatever it is that you're expressing. Exactly. Or the amount of micro RNA in your blood, for example. Yes. Or that one, which is way more complex. Or that one. There were two really interesting things that came out of this. The first one being that they had a look at what is being produced in the prefrontal cortex, which we know is really relevant to ADHD in particular. That's where all our executive functions live. They found 23 distinct ADHD-related genes. in the prefrontal cortex, which were being under expressed. So those gene products, it looks like they're, compared to the neurotypical controls, we are producing less product from those genes in the prefrontal cortex than our neurotypical counterparts. Interesting. Yeah. And the second part in terms of looking at what's happening in tissues and cell specific investigations. So they were sort of looking at what are particular cells doing with these risk genes that we found. And one of the things that excited people the most was that we can see that genes that are involved in embryonic brain development are implicated for people with ADHD. So this starts early. That's like Right from the beginning. Yeah. Right from the beginning. You know, we talk about having different brains and this is some really robust evidence that our brains are different from the very beginning. The other thing that we'd love talking about dopamine is that they saw that the ADHD risk genes were enriched. So there were lots of them in the midbrain where our dopaminergic neurons are. and in particular those that control voluntary movement and from board processing. So it's a really interesting, the first thing that came to mind for me was ADHD paralysis, where you're sitting scrolling on your phone, wishing you should go and fold up the laundry, but you can't move. Yeah. So there might actually be some kind of genetic risk factor for that. Yes. We are. either using or producing dopamine in that particular brain region. So we can see genetic evidence that is true. Wow. This is sort of an addition to the other study where it just brings into light a lot of spaces where we could do some kind of diagnostic or understand a little bit more about exactly how you might be affected with ADHD in your brain. Exactly. it's really interesting that we're talking about these two papers because the first paper that we spoke about was talking about something that appears to be really ADHD specific, but the researchers in this particular paper are suggesting that the way that ADHD might develop in someone might be about the accumulation of different genetic variants that sort of pushes you in an by the size of the effect of those variants rather than there being anything that's actually ADHD specific. Yes, we can't just go and find one thing and be like, look, we found it, like turn on, do other things to it. It's more of a cumulative effect. Yeah, exactly. Robbie, would you say that could also contribute to different individuals' expression of ADHD symptoms? And if we're talking about 7,000 potential risk variants, you know, just a few that is hopefully heartening. And as you said before, Sarah, like hopefully molecular source of self-compassion. I mean, we share a lot of things, but we're also very different and have different experiences and things that work differently for us. And we all have our own type of weird and. It makes sense from this context because it really does look like the future of ADHD genetics is there are going to be a lot of complex interrelated genetic findings that will make up the picture of an individual and it's not going to be the same from person to person. Yeah. Yeah, it's very interesting. Yeah, I think what excited me most about this paper, so thank you for giving it to us, Abby, was that it... holding the concept of like nature versus nurture. Now it doesn't like say that anywhere in the paper, but that's where my ADHD brain went. And it turns out the answer is just kind of yes. You know, it's just a classic. Yeah, it's just a big thing in psychology where it's just like, yeah, it's all the things. But yeah, exactly. As you said, Abby, like that should bring some solace to not only self acceptance, but also like For parents who are out there who are worried if their kid is gonna be born with ADHD or not, there are lots of supports that you can put into play for them, but generally speaking, how you do as a parent is not going to make your child have ADHD, and I think we just need to be constantly reminded of that because even though logically it doesn't make sense, I didn't cause my child's ADHD by being a crazy model. The emotions of like, feeling like that's your fault can sometimes veto the logic. So there's the words black and white. ADHD specific loci. 7,000. Example. And they have, so they have just under 7,000 to map now. They've mapped 27. Well done. Wow. That's going to be interesting. Well, very, very big thank you, Abby, for coming along to chat to us. And It goes without saying, but I hope we can have you on again, because apparently there's a lot more things to map and the genetic conversation is so interesting. But there is that barrier, as you said, to understanding it because the words are a little bit complicated and there's a certain level of information, but it's been so nice to have you on to demystify that so that not only us, but then also all the listeners as well, can feel. a bit more empowered to understand our own brains and be able to contribute or at least understand the conversation about this very interesting and potentially future diagnostic conversation. Oh, it's my pleasure. And I think that one thing we say in, well, I used to say in genetic counseling all the time, which is important and like a jump off from what you were saying, Sarah, is that there is nothing anybody does or doesn't do to either inherit or pass on. the genes that they have or the genes that their children have. Genetics is random and that's just a really important reminder. It's fascinating and as you said, Sarah, it can be emotional as well. These are our families and our histories and how we move through the world in these very inaccessible numbers and letters, but knowledge through the lens of self-compassion is really key here. But yeah, thank you so much for having me. It's been really fun to talk about this. Yeah. It's been wonderful to have you. And for those of you who are interested in knowing more about Abby, you can find her on unconventional organizations website and this little video introduction and other things there as well, as well as I think your favorite dopamine, which we ask all other coaches. Yes. I can't remember what I've wrote. It's probably changed by now. Probably dopamine does. Awesome. Thanks for coming, Abby. Thank you, guys. Thank you for that very illuminating episode. I'm very, very excited to see what everyone else thinks about it as well. If you have any genetic comments, please leave them. Email us, we want to know. I'll do my best. No, not you, the audience. Oh, ah! We'll leave in that bit in. Wait.Â
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