Sea slugs and anti-sickness drugs
This month we hear about the animals that turn their dinner into solar panels, the first images of anti-nausea drug molecules engaging with their receptors, and what thousands of you told eLife about the people who support their colleagues at work. Plus, exercise stops cancer cells from growing and how we hold onto bad food memories...
In this episode
00:36 - Exercise stops cancer growing
Exercise stops cancer growing
Randall Johnson, University of Cambridge and Karolinska Institutet
Can exercise cut cancer risk? Various lines of evidence suggest that it can, but how? Randall Johnson has found that the same stuff that makes your muscles burn when you run also stimulates classes of immune cells that can suppress the growth of cancers. Chris Smith spoke with Randall to ask, could the two be connected?
Randall - A number of studies over the years have found that there are links between increased exercise and physical fitness and decreased susceptibility to cancer. And there are animal model links that have shown over the years that you can induce animals to exercise, mice in particular, love to exercise. They love to run on wheels and do it voluntarily, and that they will get fewer tumours and the tumours will grow more slowly.
Chris - Of course, one possible criticism is that individuals who are more prone to cancer are just lazier.
Randall - Yeah. And their lifestyles may be more prone to induce a malignancy as well. And it's one of the things that you do these experiments to try and test.
Chris - And did you get a sort of handle on that?
Randall - What we did is essentially first started out to just, in our own systems, try and determine whether we saw a decrease in tumour growth when animals were allowed to exercise. And these were in all cases, animals who just had a free wheel put inside their cages. And they were just allowed to run as much as they want. And mice will run up to six, seven kilometers a night. And so we found that animals who got a wheel in their cage that was locked, so they couldn't run, had a greater tumour growth than animals who were actually allowed to run every night.
克里斯-这是剂量依赖性关系吗?Because that's one of the other key criteria with cancer causation, isn't it, is it dose-dependent? So if you allow a mouse to run six kilometers, does it get more therapeutic suppression of its cancer than if you restrict it and it's only allowed to do three kilometers?
Randall - Yes. In our study, there were a group of mice that ran much longer than another group of mice. And we segregated them by rough categories, ones that ran around approximately three kilometers a night and ones that ran around six kilometers a night. And we did find a dose relationship in that regard. However, we're now doing experiments where we're much more closely controlling the amount that the mice run, to try and approach that, that very question.
Chris - And putting some numbers on it, how much of a difference did it make to say the volume of tumour in a mouse that exercised versus one that wasn't able to exercise?
Randall - Yeah. We were seeing reductions in tumour growth of quite substantial ones, you know, up to 50%. But of course their cancers weren't being cured. What we seem to see is a link to the role of a specific type of immune cell, the cytotoxic or killer T cell, which in many regards is considered to be a very important controlling element in the immune system to combat cancer. And those cells seem to be much more prevalent in the tumours of animals that exercise
克里斯,你的假设,锻炼我n some way, mobilises a particular population of white blood cells, these cytotoxic T cells that will take down tumours and that because there's more of them, the tumour bulk is lower and the animals live longer compared with the ones that don't exercise.
Randall - I need to be careful. There's not more of them in the animal, but there are more attacking the tumour. So we seem to be potentiating their effect on the tumour. We saw that sort of correlation but we wanted to test it. So we did an experiment, you just simply kill off all the animal's cytotoxic T cells. Then the exercise mediated effect goes away.
Chris - Which points the finger strongly at those cells as being a key part of the process. What about doing the opposite? Where if you collect those T cells and put them into an animal that's not allowed to exercise. So it's a lazy mouse. Does it inherit the protection as though it were exercising by doing that?
Randall - Yes. You hit the nail on the head. That's exactly what we did next. We basically took T cells from trained animals and put them into non-trained animals, to coin a phrase. Could we train the T cells? Would they then be better at reducing tumour growth? And in fact, they were
Chris - That's extraordinary. Does this argue then that there is something specific coming out of muscles when they move, when we exercise, that causes these cells to increase their activity? Do we understand, or do you understand yet what is actually driving the link between physical activity and these T cells that seem to have this anti-cancer or cancer-suppressing activity?
Randall - We think we have a good handle on it. One of the really exciting things we followed up on was the muscle produces lactic acid, which we know is important. You feel that in your muscles when you exercise, and that that lactic acid in the blood could actually have striking effects on T cells - improve their performance in combating tumours.
Chris - And have you actually tested that? Can you stimulate T cells with lactic acid and demonstrate they go into this more enhanced weaponised anticancer mode?
Randall - We could. We injected the animals on a daily basis with a quite substantial dose of lactic acid, but enough that we actually were essentially mimicking what would happen from a big bout of exercise. And we saw that when we did that, the high doses actually did reduce tumour growth.
克里斯,你认为可能有一个solution for people who are couch potatoes? I mean, I'm the worst of them, whereby I can have my cake and eat it quite literally and keep my cancer low by either dosing myself with something that will fool my immune system into thinking I've been a lot fitter and less fat than I am, or stealing someone else's T cells and infusing those?
Randall - There's that! There's always this sort of Count Dracula mechanisms of eternal youth that are out there. And there are cancer therapies that involve reinfusing T cells. And what we hope is that this may help us find ways to treat those T cells to make them better anti-cancer agents when they're put back into patients. I would say, this is pure speculation, of course, there's a lot of lactate in yoghurt. I'm sure you're aware there are these populations in Greece and in the Urals that, you know, the centenarians are a very large proportion of the populations and at least the yoghurt ads they always say it's because of their yoghurt consumption. So it's probably not bad for you to eat more yoghurt.
07:44 - Sea slugs photosynthesise
Sea slugs photosynthesise
Vesa Havurinne, University of Turku
We all know we should eat our greens, but for photosynthetic sea slugs, this takes on a whole other meaning. These small marine creatures feed on algae, and steal the photosynthetic chloroplasts in the algae as they digest, incorporating the chloroplasts into specialized pockets of their digestive system where they can be kept, still photosynthesising, for up to a year in some species. Vesa Havurinne from the University of Turku, has recently found that the sea slugs induce protective changes in the chloroplasts they steal and that this allows the chloroplasts to keep photosynthesising outside of the algae. Eva Higginbotham heard how…
Vesa - The term sea slug - it refers to a large group of animals. They are gastropods just like your regular garden snails and slugs. And they can look quite alien to be frank. But when you're talking about photosynthetic sea slugs, you are referring to a very specific group of slugs and they are called sap-sucking sea slugs, or sacoglossans.
Eva - And you've actually sent me a couple of pictures of some sea slugs. So I'm just looking at them here and they're quite cute!
Vesa - Well, if you're into that sort of thing, but yeah!
Eva - And so they've sort of got a white, or sort of opaque-ish, white-looking body with some parts of them that are green. Where does the green color come from?
Vesa - Yeah, the green color comes from the chloroplasts that they steal from the algae they feed on.
Eva - So what makes the sea slugs photosynthetic?
Vesa - Well, they steal the chloroplasts, which are the organelles inside plant cells or algae cells that utilise light energy to convert it to sugars by fixing CO2 from the atmosphere or the surroundings. So basically these slugs, they are taking that organelle from the algae that they eat. And then they take those foreign organelles chloroplasts inside their own animal cells. And then they basically carry out photosynthesis, just like the algae.
Eva - Why do they do that?
Vesa - Well, usually when people are answering this question, they are stating the obvious - like that the slugs would get a energetic benefit, but it's still debated.
Eva - So what were you trying to find out in this study?
视频电子设备标准协会,我们试图找出如果蛞蝓nduce some protective changes to the chloroplasts they steal from the algae. The thing is that when the chloroplasts are inside the slug cells, they are actually quite isolated. They are, for example, cut off from most of these repair mechanisms that are available to them in their normal environment, meaning the algae cell. So because the photosynthetic machinery of the chloroplasts is actually constantly being damaged by light, even though light is required for photosynthesis basically. So we were trying to figure out if they somehow reduce the damage to the chloroplast in the first place, so that they wouldn't have to fix so much damage.
Eva - And what did you find?
Vesa - We compared photosynthesis in the algae versus the slugs. And we found out that the slugs do actually induce photoprotective changes to the chloroplast. The first thing that we noticed was that the slugs actually maintain the photosynthetic machinery in a so-called 'emptier state', electron wise, than the algae. And this allows for more fluent conversion of light energy into sugars and reduces the risk of this excess energy going into unwanted directions, for example, to oxygen, which can create reactive oxygen species and damage the chloroplasts and the slug for that matter. The second thing that we found was that the slugs actually have a more efficient way of preventing excess light energy actually reaching the photosynthetic machinery than the algae. And the third point was that if all these other measures fail, the slugs can still utilise the same safe energy sinks that the algae actually use. So when they are exposed to a very strong light, for example, they can still deal with that excess energy safely without producing reactive oxygen species,
Eva - Are photosynthetic sea slugs the only sort of animals that eat plants and steal their chloroplasts to use in photosynthesis in this way, or is this a mechanism that other species have too?
Vesa - For a long time it was thought that these sap-sucking sea slugs were the only animals capable of this, but there was a recent paper where they showed that actually there are these marine flatworms that are able to do the same trick. And it would be interesting to get my hands on those as well, to see if there are some common characteristics within these two different animal groups. And if so, if there are some general rules for these like stealing chloroplasts and using them for your own gains.
12:55 - Imaging anti-sickness drugs at work
Imaging anti-sickness drugs at work
Sudha Chakrapani, Case Western Reserve University
A class of drugs called “setrons”, one of the best known of which is “ondansetron”, are potent anti-nausea agents often used in patients with disabling sickness during, for instance, cancer chemotherapy or radiotherapy. This leads to higher than normal blood levels of the signalling molecule serotonin, which can activate a region in the brainstem that triggers vomiting. The setron drug family block one class of serotonin receptors to stop this happening. But their interaction with this receptor has never been visualised directly - it had only ever been inferred. This means we don’t know if we could make modified setron molecules that would work even better. So Sudha Chakrapani, from Case Western Reserve University, set out to capture detailed images, under the electron microscope, of this happening, as she told Chris Smith…
Sudha - Based on the chemical properties of setrons, it was known that it is likely to bind in the same pocket as that of serotonin. And there were indirect studies that showed that it is likely to bind because you make certain perturbations to that pocket, it also not only affects serotonin binding, it also affects setron binding. So these were all indirect indications that setrons binding in the pocket, but it was not shown experimentally. So why this is important is because even subtle changes to the setron molecule can have a huge impact on the efficacy of the drug or the effectiveness of the drug. So this was the information that was not available before the study.
Chris - What did you do then to turn what was indirect evidence into direct visualisation of when these drug molecules go in, where they bind to and how they exert their effect?
Sudha - We used an approach called cryo-electron microscopy. We isolated the receptor. We picked out individual particles and we aligned them and we created a three-dimensional reconstruction of this molecule. And we did this in the absence of setrons and the presence of serotonin, and in the presence of different types of setrons. So we were able to identify the interaction fingerprint, as you may say, between the drug and the receptor.
Chris - So you're literally able to see the molecules themselves and what the molecule looks like when serotonin's in there, when the drugs in there, when nothing's in there, and you can see how the shape of the molecule can be distorted or changed when those interactions occur.
Sudha -没错。
Chris - The crucial question of course must be that when you do this and you can really see for real what was happening when the drug was present, does the direct visualisation tie-up with the indirect evidence of how you thought these drugs were working and what did you learn?
Sudha - Yes, the findings agreed very well with what we knew from findings in the past. And there were a few surprises. We were able to identify certain setron orientations, which ended up being slightly different from what we had predicted in the past. And we were also able to rationalise what could have been the causes for this discrepancy between past findings and what we're finding right now.
Chris - And is that the crucial step that will then enable us to optimise those drugs going forward?
Sudha - Yes, absolutely. Having a much better idea about the basis for the drug-receptor interactions will definitely pave the way for using this information to design better drugs.
Chris - Obviously when we tweak any drug or we try to make a drug, we have to be very cautious about off-target effects. Is there a danger based on your knowledge of these sorts of receptors and these sorts of drugs that in trying to optimise the drug better for that particular receptor, we might end up making it bind better elsewhere as well, and therefore causing more side effects?
Sudha——绝对。这是一个危险,当我们尝试to modify the drug and actually we are only looking at one target at a given time. So we have to tread very carefully. One way is there are many different types of serotonin receptors that are present in the body. They differ in their location, let's say in the brain versus in the gut. So it is important to understand the functioning of each of these types of receptors and a detailed knowledge of those will allow us to eventually design drugs that are specific for one type versus the other.
17:39 - Brain basis of bad food memories
Brain basis of bad food memories
Arianna Maffei, Stonybrook University
Memories of previous bad food experiences that make us ill tend to form fast, and they’re enduring. Going back decades, scientists had shown that two regions of the brain - one concerned with tastes and the other concerned with fear and emotion - are tightly connected and forming these avoidance memories depends upon both, although the exact wiring arrangement wasn’t known. Now Arianna Maffei has found the surprising result that when something makes us sick, the strength of the connections between the two key brain regions loosens. The findings are far-reaching, from helping patients undergoing chemotherapy in hospital to conserving endangered species, as she told Chris Smith…
阿里安娜,我们看着的电路是connection between the gustatory cortex, which is the area of the brain that processes taste - taste is intrinsically good or bad in addition to having its own identity, whether it's sugar or salt, and the amygdala, which is a centre of the brain that is known to process positive and negative emotions. So we know from previous work that these two areas are involved in assigning a positive or negative value to a taste stimulus. And we wanted to know how that assignment happens.
克里斯,所以换句话说,如果我喜欢的东西an ice cream and I had the ice cream and I concluded I liked it versus if I have something that I definitely didn't like, the assignment of niceness or nastiness is bound up in this part of the brain, the gustatory cortex and its connections to the adjacent amygdala?
Arianna - Yes. That's exactly how it would work. So the amygdala would assign a pleasant or unpleasant flag to the taste, to the ice cream.
Chris - But what happens if I overdo the ice cream and I end up being sick, and then afterwards I tend to avoid ice cream because I'm thinking I don't like it anymore because it made me sick. Is that circuit bit the one that's being changed here.
Arianna - So this is exactly what we sought out to find. And our hypothesis was that yes, there is a modification in the connection between the amygdala and the gustatory cortex. So when somebody eats something that makes them sick and this very strong memory known as conditioned taste aversion learning is formed, so we really wanted to know how neurons formed this memory and how this memory gets stuck in this circuit.
Chris - So where did you begin?
Arianna - So we began by inducing this form of learning in laboratory animals. We used rats. So what we did is we offered our rats sugared water that they really, really enjoy to drink. And then we associated this sugared water with an injection of a substance - lithium chloride, that make them have a bellyache. And then the next day we offer them a choice between the sugar water and just plain water. And we wanted to see if their preference for sugar has changed. And in fact, they drank a lot more water than sugared water on testing day when the association had been formed.
Chris - And your conclusion from that part of the experiment would be, right, we've got this connection in the gustatory, the taste area of the brain, which originally was assigned an "I like this" message. And after you make the animals feel unwell for a short while, that "I like this" has been turned into an "I don't like this" signal. And you're presuming it's some kind of connection between the amygdala and the taste centre, the gustatory cortex, has changed.
Arianna - Yes. So we know memory has as formed, and from previous work where people were making small lesions, we started out with the hypothesis that the amygdala and the gustatory cortex are necessary. And we wanted to see what happens in the connection between them.
Chris - And if you go in and sample those two areas of the brain, can you see either electrically or chemically, any kind of difference in the behaviour of those sites after you've changed the way the animals regard the sugar water so that once the animals start to avoid it because they don't like it anymore, does the wiring change?
Arianna - Yes. We went to look into whether the connection had changed and we did find a change. What we did find was a surprising change because the hypothesis typically is that when a memory is formed, the connection between two areas or two neurons strengthens. What we did find instead is that the connection between the amygdala and the gustatory cortex had become weaker. So it was exactly the opposite of what we had predicted.
Chris - Now, if that's the case, is it possible to simulate this adversive response by inhibiting or turning off the connections from the amygdala without any kind of making the animals feel ill? So if you just go in and artificially switch off those connections, can you get the same aversive response?
Arianna - We tried that by using a tool that is called optogenetics. It allows us to activate very selectively only a specific connection in the brain. And we implanted an optic fiber in the gustatory cortex. And we tried to make the association between the sugared water and activity that would decrease the strength of the connection between these two areas directly in the gustatory cortex. And indeed what we found is that we could completely substitute to the bellyache with this stimulation directly in the brain. And the next day, the animals would have learned not to drink the sugar water.
Chris - And why does this matter, the fact that you found this, because going back to the 1950s or so, people had made discreet lesions in brains in these areas, and they demonstrated that there is a loosening of this association if you do that - you can prevent this effect happening. So we had an inkling that this was going on, you've confirmed it and proved that that's what's going on independently and via a different way of doing it. But beyond that, are there other implications?
Arianna - Yes, it is very important to know how this form of memories are formed from the intellectual perspective, just to know what is the signature of learning in the brain. But from the more practical perspective, for example, we have patients that are undergoing chemotherapy that, as chemotherapy gives them a bellyache in many cases, it can actually form an association between the food that they have eaten before and give them a really hard time in being able to self-sustain and eat the food that they previously like because of the therapy. So understanding how this form of memory works, also tells us strategies to avoid these negative associations in patients for example. Another reason for why this interesting is that this form of learning is conserved across many, many species and in conservation biology ideas that are related to conditioned taste aversion have been applied to try to protect endangered species from predators, for example, by including the medication like the lithium chloride in the eggs of the species that they want to preserve so that the predator, will be conditioned not to go eat them sugar or salt, and the amygdala, which is a centre of the brain that is known to process positive and negative emotions. So we know from previous work that these two areas are involved in assigning a positive or negative value to a taste stimulus. And we wanted to know how that assignment happens.
克里斯,所以换句话说,如果我喜欢的东西an ice cream and I had the ice cream and I concluded I liked it versus if I have something that I definitely didn't like, the assignment of niceness or nastiness is bound up in this part of the brain, the gustatory cortex and its connections to the adjacent amygdala?
Arianna - Yes. That's exactly how it would work. So the amygdala would assign a pleasant or unpleasant flag to the taste, to the ice cream.
Chris - But what happens if I overdo the ice cream and I end up being sick, and then afterwards I tend to avoid ice cream because I'm thinking I don't like it anymore because it made me sick. Is that circuit bit the one that's being changed here.
Arianna - So this is exactly what we sought out to find. And our hypothesis was that yes, there is a modification in the connection between the amygdala and the gustatory cortex. So when somebody eats something that makes them sick and this very strong memory known as conditioned taste aversion learning is formed, so we really wanted to know how neurons formed this memory and how this memory gets stuck in this circuit.
Chris - So where did you begin?
Arianna - So we began by inducing this form of learning in laboratory animals. We used rats. So what we did is we offered our rats sugared water that they really, really enjoy to drink. And then we associated this sugared water with an injection of a substance - lithium chloride, that make them have a bellyache. And then the next day we offer them a choice between the sugar water and just plain water. And we wanted to see if their preference for sugar has changed. And in fact, they drank a lot more water than sugared water on testing day when the association had been formed.
Chris - And your conclusion from that part of the experiment would be, right, we've got this connection in the gustatory, the taste area of the brain, which originally was assigned an "I like this" message. And after you make the animals feel unwell for a short while, that "I like this" has been turned into an "I don't like this" signal. And you're presuming it's some kind of connection between the amygdala and the taste centre, the gustatory cortex, has changed.
Arianna - Yes. So we know memory has as formed, and from previous work where people were making small lesions, we started out with the hypothesis that the amygdala and the gustatory cortex are necessary. And we wanted to see what happens in the connection between them.
Chris - And if you go in and sample those two areas of the brain, can you see either electrically or chemically, any kind of difference in the behaviour of those sites after you've changed the way the animals regard the sugar water so that once the animals start to avoid it because they don't like it anymore, does the wiring change?
Arianna - Yes. We went to look into whether the connection had changed and we did find a change. What we did find was a surprising change because the hypothesis typically is that when a memory is formed, the connection between two areas or two neurons strengthens. What we did find instead is that the connection between the amygdala and the gustatory cortex had become weaker. So it was exactly the opposite of what we had predicted.
Chris - Now, if that's the case, is it possible to simulate this adversive response by inhibiting or turning off the connections from the amygdala without any kind of making the animals feel ill? So if you just go in and artificially switch off those connections, can you get the same aversive response?
Arianna - We tried that by using a tool that is called optogenetics. It allows us to activate very selectively only a specific connection in the brain. And we implanted an optic fiber in the gustatory cortex. And we tried to make the association between the sugared water and activity that would decrease the strength of the connection between these two areas directly in the gustatory cortex. And indeed what we found is that we could completely substitute to the bellyache with this stimulation directly in the brain. And the next day, the animals would have learned not to drink the sugar water.
Chris - And why does this matter, the fact that you found this, because going back to the 1950s or so, people had made discreet lesions in brains in these areas, and they demonstrated that there is a loosening of this association if you do that - you can prevent this effect happening. So we had an inkling that this was going on, you've confirmed it and proved that that's what's going on independently and via a different way of doing it. But beyond that, are there other implications?
Arianna - Yes, it is very important to know how this form of memories are formed from the intellectual perspective, just to know what is the signature of learning in the brain. But from the more practical perspective, for example, we have patients that are undergoing chemotherapy that, as chemotherapy gives them a bellyache in many cases, it can actually form an association between the food that they have eaten before and give them a really hard time in being able to self-sustain and eat the food that they previously like because of the therapy. So understanding how this form of memory works, also tells us strategies to avoid these negative associations in patients for example. Another reason for why this interesting is that this form of learning is conserved across many, many species and in conservation biology ideas that are related to conditioned taste aversion have been applied to try to protect endangered species from predators, for example, by including the medication like the lithium chloride in the eggs of the species that they want to preserve so that the predator, will be conditioned not to go eat them.
25:10 - Mental health in academia
Mental health in academia
Elsa Loissel, eLife
An emerging trend in academic settings is mental health. Increasing numbers of researchers up and down the career ladder are disclosing mental health problems. This could be because the situation is worsening, or that the working environment is becoming more receptive and supportive in this area. But one thing not often discussed is the people to whom those who need support turn to. Who are the supporters? And who helps them? Is this an organised system, or an ad hoc one where people are taken under a sympathetic wing? Are these supporters properly equipped to guide their colleagues? And are their efforts recognised? The answers to all of these questions is “we don’t know”, so eLife’s Elsa Loissel decided to set up a survey to try to find out. In her words, she “humbly expected a handful of responses”. She got over two and a half thousand, as she told Chris Smith...
埃尔莎——我们有增加evidence that there is an issue with poor mental health in academic settings, and that supporting relationships are quite important. What we wanted to know, and what is less discussed, is what are the people who are supporting others feeling and what do they need
Chris - When you say we've got evidence that there is a problem, what is that evidence and how extensive is it? And is it getting worse or has it just always been there and people are getting better at talking about it?
Elsa - That's always the question. So there is a lot of sort of anecdotal evidence. There are more studies coming out showing that the rates of mental health issues within graduate students is higher than it is in the general population, or comparable groups in the general population. The amount of stress in staff is comparable to healthcare workers, for example. In terms of getting worse, there's a report that's been published, showing that staff are trying to access counseling services more and more. So in general, it sounds like there is a problem in academia with mental health.
Chris - So what did you actually do here in order to try to find out the extent of the problem and really what the problems are?
Elsa - So we collaborated with researchers to design a survey that would be a snapshot of who these supporters are, what they do, who do they support, how they feel, what do they need. I thought we would get a few hundred answers and we could write a nice little feature article about it. And in the end, we got nearly two thousand five hundred people who started the survey, and the final data set - that's about one thousand nine hundred people in total.
Chris - Of course, any kind of study has limitations, and when it's a self-selecting survey, there are also going to be biases because of who chooses to fill it in. So notwithstanding that, what do you think the strengths and weaknesses of what you've got here are?
Elsa - We have not captured the experiences of all supporters. We cannot say anything about, 'this happens at this rate in the community', or we cannot say anything about 'these people are more likely to be supporters and these people are less likely to be supporters' because it is a self-selecting survey. So the people that took it were people that understood the message, were interested in mental health, had experiences of being supporters that they felt strongly about reporting, strongly enough that they spent 15 minutes filling a survey about it. So this sample is not representative.
Chris - And what did they tell you? When you went through the responses? What were the key findings, the key trends that kept emerging again and again, and again?
Elsa - A lot of the support was taking place between peers or between a senior researcher that was not officially in charge of the junior researcher that they were helping. So it's a lot of potentially invisible work that is being done.
Chris - And that's obviously not being recognised. It's not being rewarded, I presume.
Elsa - No. And that's also one of the messages that really emerge. Many supporters need support themselves and they don't receive it from institutions. I think there is a quote that summarises it brilliantly. Someone that says "institutions love us supporting students, but they don't value it. They don't reward it. They don't take it in consideration when they look at workload models or promotion criteria".
Chris - What other important trends or findings emerge?
Elsa - Women emerged as a population that's faced quite a lot of additional challenges. So they were more likely than men to support more than one person at a time, to feel that more people are coming to them because they were supporters, to feel like being a supporter affected their work and left them stressed, took a lot of their time. Early career group leaders, also were a population that felt they needed support in their role and they felt that their work was affected by being a supporter. There was also a huge overlap between people who were struggling with their own mental health while they were having someone else. The majority of supporters also felt very positive about having helped someone. They found it meaningful, they felt that they made a difference in someone's life. And so I would hate to paint this as a burden or as a chore. This is something that people felt very strongly about doing, and they felt natural doing, and they felt distressed not being able to do it properly
Chris - And to finish. What do we do about this then?
Elsa - I think at the level of just the individual, I think for people who were supported, there was a very strong response from supporters saying that they believe that these people belonged in science, that they believed that they were good scientists regardless of their mental health. And so sort of reassurance that they are worthy of being there and of being helped. And I think for supporters, there was a sense of isolation coming from some of the open answers and feeling that there are others that are going through those potential difficulties of not knowing what to do, and sort of maybe open discussions within the lab saying "my students is having a, you know, not a great time, what do you think it should be doing?" At the higher level for institutions, to understand what is going on within the department. Then they can tailor solutions that would really help the people that are doing the work already. We need to understand those relationships better, and that's why we've made our datasets and our code available because we've barely scratched the surface here and there are people out there who could use this dataset and this code and build on it and explore it even further.
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