 Welcome to my talk on lumbar spine adaptation in cricket fast bowlers and risk factors to lumbar bone stress injury, part of the science in cricket series. I'm Dr Pete Allway, research associate at the University of Suffolk, and I've been researching with the England and Wales cricket boards over the last five years. Today, we're going to explore how bone adapts to physical activity, what the specific adaptations of bone are in cricket fast bowlers, and also explore some of their risk factors to lumbar brain stress injuries. If you've got any questions or comments, please feel free to drop them down below, or if you want to, also message me on Twitter. So bone itself, the main aim of bone is to provide a section from fracture and how bone does this is it tries to optimize bone mass, but also doing this in the most minimal way possible. So it doesn't incur a large metabolic cost on the body. Basically, it doesn't need much, much energy to function. Bone itself is comprised of mainly inorganic material and its main mechanical function is to provide rigid levers for muscle to put against, which allows us to move, which is pretty important. The macrostructure of bone is typically like this where there's a cortical shell with a trabecular filling. The cortical bone itself is really dense, really brittle, really, really hard, whereas trabecular bone is quite soft. It's spongy. It's not very dense, but the rods and struts of this type of bone can orient themselves in any direction against the typical loading patterns. If we zoom in further into the macrostructure, what we find in the cortical bone is it's full of these cylindrical osteons, which contain bone cells and also the blood vessels themselves, which can deliver and take away minerals, which is really important in understanding how bone adapts to physical activity. If we look at bone cells themselves, the most important one arguably is the osteocytes, which make up 85 to 95% of all the cells in bone. So all those little black dots we can see there, those are osteocytes, and their main function is thought to be the ability to sense mechanical strain imposed on it. Typically this may come from physical activity, and it can also communicate with other osteocytes and also with other cells in the body. One of these cells is osteoclasts, and the role of osteoclasts is to remove damaged or disused bone, and another bone cell is osteoplasts, whose role is to deposit bone. Typically an osteocyte will be stimulated either by heightened loading, damage, or lower loading, which will all cause different physiological responses. So bone itself will respond to its mechanical environment to improve its resistance to fracture, and it does this through modelling and remodelling processes, which we'll come to shortly. We know that the adaptation of bone to physical activity is really, really site-specific. So if we look at tennis players, for example, the research shows that the dominant playing arm of players, so the right arm in a right-handed player, has much greater bone and density, content, and structural properties than the non-dominant arm, likely due to the increased load being put on that arm compared with the non-playing arm. We also know that these adaptations are stimulated by a really short number of loading cycles. So you get most physiological adaptation from the first 50 load cycles in a particular bout of exercise, which is demonstrated when you compare weightlifters who have really, really, really strong and big bones compared with marathon runners. Weightlifters are doing a very small number of cycles in their activity, whereas marathon runners with their lower bone density and smaller bones are doing tens of thousands of cycles, and they have very different responses in there. Following a bout of loading, or after around 50 load cycles, the bone cells will desensitise for about six to eight hours, allowing no further adaptation to take place. How does this adaptation happen? So we know that osteocytes can be the stimulated, and from this they can cause four pathways to happen. Two of these occur in an increased strain stimulus environment on the right through formation, modelling, or targeted remodelling. This acts to try to increase the resilience of bone, increase the strength. Whereas in a decreased strain stimulus environment we get resorption modelling and this use mediated remodelling, and this acts to decrease the strength of bone, but to also improve the metabolic costs of bone. So I'm going to take you through this diagram here just to show how these four things, these four pathways work. So firstly at the top we've got formation modelling. So in this situation we're in a mechanical environment where there's height of loading. This height of loading perturbs the osteocytes who send out signals that they need greater bone to be deposited. Because of the signal osteoblasts come to the site of greatest loading and they deposit bone down which over time becomes mineralised and increases bone strength, therefore increases resilience to fracture. In a similar scenario we have height in loading and in this targeted remodelling case what happens here is that the loading is so great that our osteocytes actually die. So there are microcracks in the bone and these go through the osteocytes themselves. At death these osteocytes will release a signal that there is damaged bone in this area and this damaged bone is resorbed by osteoclasts causing temporary resorption of bone. But also there are then signals put out for osteoblasts to come and fill in the hole caused by the resorption. Because of this we end up with greater mineralisation and often greater bone strength properties than previously. Then we move on to this use pathways. So firstly we have this use mediasis remodelling and in this situation where bone isn't being stimulated, again osteocytes die, again osteoclasts take bone away. But this time the osteoblastic response isn't as great as in the targeted remodelling case. This results in less mineralisation and ultimately weaker bones. Finally at the bottom we have resorption modelling and again we go through this use induced osteocyte death and in this case only osteoclasts are signalled for. We get this decrease in mass and there's no osteoblastic activity here and resolving in decreased bone strength. And we can see this happening in in baseball pictures. So this is a cross-section taking through the humerus of the dominant throwing arm versus the non-dominant throwing arm and as well compared with a typical active person. And we can see that there is significantly more bone mass and sheer size in the throwing arm of the of the picture. So this is how bone works, typically really really site-specific response. So now on to fast bowling. So firstly it's probably important to talk about what fast bowling is. So fast bowling is typically characterised by two different things. The first is at front foot contact we have this huge ground reaction force. So at this point we see typically between four to eleven times body weights going through the body. This is coupled with a opposing ciflection and rotation moments following front foot contact in the trunk itself. So as we see here we see the ciflection moving away from the bowling arm while the rotation moves towards the bowling arm in the trunk. You might be wondering why are people using this weird action? Why don't they just throw it like they do in baseball? Well one of the rules in cricket is that you're not allowed to extend your elbow more than 15 degrees. Basically not allowing throwing. Therefore it's a bowl fast. It's important that people run in quite fast and then they do this what might seem like a weird action in order to deliver the ball at speeds in excess of 150 kilometres an hour. So how much do fast bowlers do this weird high loading action? So this is a typical international cricketer and this is that their match volumes taken across their career. So in this near 18 year career I see that this bowler in matches alone has bowled nearly 60,000 deliveries. Therefore if we were to include training overs and balls into this too we'd probably be looking at 100,000 deliveries which is a lot for something which is so high loading. This compares favourably with our cousins in baseball to throw slightly more pitches in matches per year but not by very much. So similar volumes between the two activities. So from this it got us wondering how does the lumbar spine respond to fast bowling given that there is a massive ground reaction force and then you've got this opposing forces being put on the spine during the actual delivery itself. So what we looked at for this is we can bear the group of fast bowlers with our batters with a group of rugby players and a group of physically active controls. We chose the batters because their training volume is going to be similar to the bowlers and we chose the rugby players because the forces in rugby are really bilateral so it should be very different to what we see in the asymmetric fast bowling technique. And what we found in our elite men is that we found that the fast bowlers have high bone bone density in their lumbar spine, much greater than the controls and nearly significantly greater than the batters and the rugby players. And we found a mean Z score in our fast bowlers of about 2.5 which means that they're 2.5 standard deviations above what is normal for their age and their race. So okay we've got some really strong bones here. But then we decided to take it one step further. We suddenly noticing that the patterns of bone was greater on one side than the other. And what we found is that the bone density on the non-dominant or the contralateral side compared to the bowling arm was much greater than on the ipsilateral side or the dominant side. So this build up of bone seemed to increase as well as we moved down from L1 to L4. Where at L4 we have around 25 to 30% greater bone density on that non-dominant side which in a right handed bowler is on the left hand side. So we have this really, really unique adaptation. So our next question was, well, do we see this in our female cohort too? And we know that our female fast bowlers bowl at a slower speed and their match volumes are also low as less. So we're really interested to see if this adaptation persisted regardless of sex. Also in the women's game, there's a much greater prevalence of spin bowlers which allowed us to independently compare spin bowlers with fast bowlers. And again, we also were interested in how our bath is compared. As well as this, we use footballers for this comparison again because of the bilateral characteristics. What we found in this is that between groups there were no differences. So your batters, fast bowlers, spin bowlers and footballers, all of them had high bone marrow density. So it all adapted to their activities. But again, what we found when we looked closer was a similar pattern to the men. We found that there was greater bone marrow density on the contralateral side of the spine. So the opposite side to the bowling arm, we found that there was much greater density and this increased from L1 to L4. What was also interesting, and this was the spin bowlers also had the same pattern, albeit just at L4. So from this information, from in the elite males and females, what we've come to find out is that we have this, this unique adaptation to bowling, not just fast bowling, but spin bowling too, which is independent of sex or bowling type. So anyone who bowls likely has the same unique adaptation, which to date hasn't been seen in any other sport. So basically, fast bowlers have some really weird, interesting adaptations going on. But this only made us want to think further about this. So our next question was trying to understand, well, how does this adaptation change with age? So to do this, we took our elite cohort of players through from academy level through to the elite level. So 14 to 24 year olds. And we wanted to compare them with high performance field sport controls from football, hockey, etc. To try to understand exactly when this awesome adaptation is occurring. And for this, we took scans at the end of the respective seasons in all the sports across a number of times. So I think we had around nearly 300 measurements in these players. And what we found in this is that at age 14, across the whole number of spine, there's really not that much difference at age 14. And it's only really in late adolescence that we start to see this large difference between the fast bowlers and our field sport controls. Particularly from the ages of 14 to 18, we have this rapid acceleration in accrual of bone density. That's likely due to the large forces imposed on the lumbar spine during cricket bowling compared to those in field sports. We notice in our fast bowlers that this seems to plateau at around age 22. So prior to what has been published in the research for typical adaptation in healthy humans. So we have this rapid accelerated adaptation of the whole number spine. Interestingly, when we looked at the site specific adaptation, what we found on the lateral side, the same side as the bowling arm, is that there's no difference in the adaptation patterns between fast bowlers and field sport controls. They are the same. They follow the same pattern and they reach the same peak values. However, on the contractual sides, the opposite side to the bowling arm, what we see is the large differences. Even at age 14, we almost see that there's greater density on this contractual side. And this increases far and beyond the field sport controls. So this adaptation is near localized to the contractual side of the spine. When we were looking at the asymmetry as well, what we find is that even our 14 year olds are asymmetric. So this asymmetric adaptation is already present in 14 year olds. And this almost linearly increases up until age 24, where it likely continues further and throughout the career of a fast bowler. So at age 24, what we typically have around 25% greater bone width density on the contractual side of L4. So this again may just think, well, what actually drives this adaptation? So what we did for this is we used our database from DEXA and we combined it with our database from biomechanics. And what we find drives this adaptation is fat free mass. So unsurprisingly, muscle seems to be the primary driver of bone adaptation in our fast bowlers. And then we find a combination of contralateral thoracic spine rotation with less it's lateral lumbar pelvic rotation coupled with greater contractual pelvic drop. These three factors likely interact together to put a huge torsional load on the spine, which then drives the high asymmetric adaptation scene in fast bowlers. Interestingly, despite being up to 11 times an individual's body weight, we found that there was no significant contribution from ground reaction forces, which suggests that muscle forces alone likely put the greatest strain upon the lumbar spine and they really drive this unique adaptation. Our next question was everyone, well, is this asymmetric adaptation something which is permanent? And to do this, we took two groups. We took one group of players who were undergoing rehab following stress fracture and then a group of players who weren't injured. And we followed them on four different occasions in the subsequent year. And this is what we found. So you see the uninjured players at the top there. We've just had a general increase in their bone density at their whole lumbar spine. Whereas our uninjured players, we see this drastic drop in bone which lasts for around six months post injury and doesn't reach baseline until between nine to 12 months afterwards. This drop of three to four percent of bone in five to six months is basically what astronauts experience when they go to the space station. It's a remarkably quick decrease in bone. And interestingly, when we impose what the players are doing at this time of their rehab, it starts to paint a picture. So, of course, when there's rest, we know that if bones aren't stimulated, they lose bone density. So that was expected. But what we didn't expect so much is that during their SNC phase of their rehab, these players continue to lose bone marrow density. They continue to lose the strength of their bone, which suggests that strength exercises alone are not enough to replicate the strains put on the lumbar spine during fast bowling. It's only when players return to bowl and with such sufficient volume and intensity, the bone marrow density starts to reverse and increase in its density and also mass, and particularly when they return to play. So really getting the volume and intensity up that we see this return of density. You can also use this to understand more about why recurrences of lumbar breastless injuries happen so much. You see players coming back after six to seven months. Their bones are going to be so much weaker and their tolerance to fast bowling is going to be a lot less, make them quite susceptible to injury. We also note that this decrease and increase in density occurs basically across all sites that we see, but greater on the contractual, more adapted site. So we almost have to use it or lose it mentality to bone adaptation. And it means that it means that you need to take care of your fast bowlers during rehab and particularly return to bowling and play. But it also means that the end of the season, it may not be wise to give players a significant break from bowling. We see these large deficits within a month to six weeks of bowling. So perhaps this may provide evidence of the need to not have such long breaks at the end of the season. So to conclude this part, cricket fast bowling is a high lumbar loading, high workload activity. We've seen that fast bowlers have this unique site specific adaptation to their activity with a really high bone density, which is driven by this asymmetric response. This adaptation is already present at 14 years and it increases with chronological age and we know that this adaptation isn't permanent. So into the the second part of this presentation where we're going to go through some of the risk factors to lumbar bone stress injuries. So firstly, we need to understand what are lumbar bone stress injuries. So lumbar bone stress injuries are caused by an imbalance between micro damage and the repair processes of bone. This is what micro damage looks like. You see this white line here basically working its way through bone. And what micro damage does is it decreases the structural properties of bone. So it decreases the the ultimate strength, the stiffness and the amount of work of the failure. Basically, micro damage makes bone more prone to injury. Typically, we can image these using CT or MRI. So you can see here on the right hand side of the image, we can see a clear fracture line through the bone. And these typically occur at the parse or the pedicle in cricket fast bowlers. So what are lumbar bone stress injuries? Well, they're on a continuum, something where there's no bone stress before there's an accumulation of micro damage. This leads into a stress reaction, an incomplete unilateral stress fracture, a complete unilateral stress fracture before we get to the multilevel bilateral stress fractures. Symptoms seem to increase with the severity of the of the injury. As there's time loss, so a stress reaction, you may be looking at a six to 10 weeks off, also known as a hotspot, whereas you're incomplete stress fractures. You're looking at four to six months and then you're complete and you're multilevel. You're looking at at least a season if not more and and possibly surgery if the fracture site remains unstable. From our research, where we looked across seven years of data, we found 57 stress rashes in our professional game. And what we found is that most of them happen at L4 and L5. So about a third of a third at each of these, which differs to other sports with high rates of of lumbar bone stress injuries in other sports, which have high incidence of these such as gymnastics or American football or platform diving. Almost all these injuries are seen at L5, which is that cricket may have a unique etiology of injury. We found that 93% of them were on the non dominant side, so on the contractual side. So as you heard earlier, this site is the most adapted. So it suggests that this site is on the great loads and can fracture. The amount of time loss, which you see per stress fracture is long, is eight months on average. And collectively it costs three to 4000 days per season to the game. And across a career, 67% of all bowlers will have some sort of lumbar bone stress injury. Our typical age of stress fracture is quite young. It's usually in our 18 to 22 year olds and typically in players who are stepping up a level. So if they're going from Academy cricket to second team cricket or second team cricket to first team cricket, and occasionally first team cricket to international cricket is generally when we see players get stress fractures. So younger fast bowlers are generally more at risk of getting stress fractures. So you know that the lumbar spine in cricket is the most prevalent site of injury. It causes the greatest time loss and that is typically driven by lumbar stress fractures. So despite being quite a low incidence injury, the massive time loss makes it extremely prevalent and it's a great cost to the game. So it's really important that we understand more about the risk factors associated with this injury. So we can try to stop them happening. So to explore why risk factors happen or what the risk factors are to lumbar process injury, we need to go through how bone adapts again. So we know that there's a given lumbar load and this interacts with the stiffness properties of bone. And these collectively place a strain within the bone, which is what our bone cells, the osteocytes can detect. So we know that there's this bone cell and activity going on. We also know that bone strains themselves can cause micro damage. And we know that micro damage negatively affects the stiffness of bone and the structural properties. Of course, when you have impaired bone stiffness, when you have this interaction with the same lumbar load, it means that for the same lumbar load, the bone strain is going to be high, which in turn is going to cause more micro damage. So there's almost this negative feedback effect of decreasing bone strain properties causing increased bone strain and this cycle will continue until there's eventually the bone stress injury manifestation. However, in optimal conditions, optimal bone cell activity can occur, which facilitates positive bone adaptation, which will enhance the stiffness of bone, resulting in a comparatively lower bone strain and therefore less likely that micro damage will accumulate. Micro damage isn't all bad though, as we know that with enough rest, we know that this micro damage can actually stimulate positive bone adaptation through its interaction with bone cell activity to again improve bone stiffness. So understand the risk factors. Further, we have to look at what actually contributes to each of these factors independently. So for lumbar load, we know that this is influenced by the technical characteristics a person possesses. So what technique do they borrow with? The muscle properties, so not just the cross-sectional area, but also what's their rate of force development like? How powerful are they? And also the anatomy of the fastballer. So an example of this is that players who have a more lordostatic lumbar spine likely put greater load on their lumbar spine. The factors which affect bone stiffness are typically the things which we can't change. So things like career bowling volume, we can't affect how much we've bowled in their life. Same with genetics, nutritional history and previous physical activity. These are all things which we can't change, and we generally see better bone stiffness in those who have a varied sport. So playing loads of different sports seems to have much better bone outcomes than those who just focus on a single sports. We also know from our work in our injured players that a bout of extended bowling rest has a negative effect on bone stiffness. So if we look into enhanced bone stiffness properties, having a big break from bowling isn't the best idea. There's also a number of factors which we can change that affect bone cell activity. So to optimize the activity of our osteoblasts and osteoclasts, what we want is we want our nutrition to be really good, so making sure we have enough energy to fuel these activities. A lot of the adaptations that we see in bone occurs when we're asleep. Therefore sleep quality is really, really important. The use of painkillers can negatively affect bone cell activity, particularly if taken before physical activity. And then we have our female specific variables. So those with impaired menstrual status may have negative bone cell activity, which affects the ability of bone to adapt. And the same with some contraceptives. I think more research is needed in this area to understand more about the role of different contraceptives on bone cell activity. And then we also know that record damage is likely caused by short-term workloads. So how can we prevent lumbar bone stress injuries? So we have two options based on what we know. We can decrease the amount of lumbar load, or we can enhance the stiffness of the lumbar spine. Both of these have the same effects. They will decrease the bone strain, which is being put in the bone. By doing this, we can decrease the amount of lumbar damage accumulation, and therefore we can increase the capacity an individual has until they can suffer lumbar bone stress injury. So the first thing which we wanted to look at from this was match bone volume, and what we did was we looked at a 7-year period of 1st and 2nd, 11th, Canary Cricut, and we looked at every scorecard of these games collectively. And what we did in this is we took 57 players who got stress fractures, and then we matched them with 57 players who didn't get stress fractures in this time period, and we matched them for age, bowling hands, and career workflows. So we tried to match them as well as possible. We looked at their peak workload in a season, as well as their workflows at injury. So we're looking to see if it's a relationship at any point in a season where there's a big spike in workload, or is it purely laid to the injury itself. And this is what we found. So we found that at injury, we found that 7-day, 28-day, and 90-day workloads, the fast ballers who got injured had significantly greater bowling volumes than those who didn't get injured. We also found this as well when we looked at peak workloads in 7-day, 28-day, and 90-day workloads. And when we ran this data through a regression to find the best predictor of lumbar bone stress injury, what we found is that the bowlers who bowled more than 234 balls in any 7-day period in that season tripled their risk of getting lumbar stress fracture compared to those who bowled less than 210 balls. So this spike in workload at any point in the season seems to massively increase the risk of an individual getting a lumbar stress fracture. And this is regardless of age. And we dug further into this data to look at age-specific thresholds for what we think will foster the best bone adaptation possible without taking players into a zone where they're likely to get injured. So we've released these garlands to all of our professional teams in England. What we are also curious about as well was that there was this delay between the spike in workloads and the injury actually manifesting. So there's typically a three to six-week delay between a spike in workloads and the injury actually manifesting, which maybe gives us a window of opportunities for working to prevent the injury from happening. So to do this, we were also curious about this group of players who didn't get injured despite having really, really high peak 7-day workloads. And when we looked at injured players who bowled more than 234 balls compared to those who bowled more than 234 balls, what we found is that their workloads, their bowling volumes didn't really differ. So they spent as much time above 234 balls as the injured players. The average balls they bowled after their spike in workload was also the same. But what differed was our rest values. So within three weeks of the spike in workload, our uninjured players embarked in a much longer rest than those who did get injured. So uninjured players, they typically would rest. They'd have an unbroken rest of around 15 days compared to cases whose longest rest was around 10 days. And this started in that three-week period. You also note that the bowling volume is a lot less in those players who don't get injured in the two weeks following a spike in workload. So it seems that a reduced bowling volume and a sustained period of rest following a spike in workload may improve the dummy structural properties of bone and can prevent stress fractures. This has to occur in this first three to six weeks following a spike in workload. We've included this in our recommendations to coaches to try to get this rest and decreased volume in. We also know that fast bowling technique likely has an effect on stress fracture. So to this we'll just have a quick recap on what fast bowling is. So typically fast bowlers will run in before bounding into a jump and gather. So before back foot contact, front foot contact, ball release and the follow-through. While the rules of fast bowling say that fast bars cannot extend their elbow by more than 15 degrees during the delivery stride, this also permits a lot of different techniques to survive in cricket. Those who know cricket will see people who like to sling the ball down with a very round arm action and those who like to be really upright when they ball. And it's this possibility to have many different techniques to have the same outcome, which is one of the reasons why fast bowling is so exciting. So the goal of this study here was to look at our historical database of MRI based lumbar bone stress injuries and compare it with our biomechanics database. And what we had for this was at the start we had 50 fast bowlers with no known history of lumbar bone stress injury and 39 of these went on to get lumbar bone stress injuries within two years of their biomechanical testing. Only 11 players did not sustain lumbar bone stress injury in this period and also had 150 match days of unprofessional cricket under their belts suggesting that they've probably survived the high risk region for lumbar stress fractures. And we want you to compare that techniques between the two groups. So what we found is that back foot contact, there was a number of differences between groups with our injured players having greater rear knee flexion, greater rear hip flexion and also greater contralateral thoracic spine rotation but also greater thoracic spine ipsilateral sci-flexion than our uninjured players. So essentially realize that back foot contact is quite important for injury. We also found differences between groups at front foot contact. So we found greater hip flexion at front foot contact in our injured players and more anteriorly tilted pelvis at front foot contact, greater lumbar pelvic extension at front foot contact. And finally at ball release what we find is that our injured players they actually have less thoracic sci-flexion than the uninjured players and while sci-flexion has long been looked at as a risk factor to lumbar stress fracture I think what this shows is it's important where the sci-flexion comes from. So if the sci-flexion comes from the lumbar spine that's slightly more risky than if the sci-flexion comes from the thoracic spine as we know a degree of sci-flexion is they need to get the arm in the right position to deliver the ball. So we found a number of biomechanical factors that differed between injured and uninjured players and while we put this through a regression we found that two factors predicted 88% of lumbar bone stress injuries. So we found hip flexion and lumbar pelvic extension were the two biggest risk factors with greater rear hip flexion being associated with lumbar bone stress injuries as well as greater lumbar pelvic extension at front foot contact. We also looked at mixed actions but none of the characteristics of mixed actions were associated with injury in this cohort. Next we're also curious about our bone density values and how these are related to players who did and didn't have lumbar bone stress injuries. So cross-sectionally at injury what we found is that our injured group had lower bone across the whole L1 to L4 lumbar spine but also on the contractual side of L3 and L4. So we find that in the sites which we expect there to be the greatest adaptation we find in our injured players that this adaptation hasn't occurred and now the challenge is trying to understand why hasn't this adaptation occurred. Is it a consequence of their bowling action or do they have a nutritional deficit? Are they getting enough vitamin D? There's a number of reasons as to why their bone bone density may be lower. We know that younger players are more susceptible to lumbar bone stress injuries and one of the reasons for this may be because they lack the schedule and resilience to withstand the demands of professional cricket. When we impose the value of the injured players BMD over the top of our age versus BMD graph what we find is that it doesn't really interact until around age 20 and it may be that those who have less bowling volume are going to be under this line for a significant proportion of their lives. Basically young players lack the resilience needed. So to summarize, lumbar bone stress injuries are multifactorial. Seven day spikes in workload likely increase the risk of lumbar bone stress injuries. Rest is probably your best friend following any spike in workload and may prevent lumbar bone stress injuries. The technique factors are the best predictors of any risk factor of future lumbar bone stress injuries in fast bowlers and you should always be aware that young fast bowlers are unlikely to have the skeletal resilience to resist the demands of professional cricket. So please be careful with your young cricketers and develop them carefully so their careers can flourish. Thank you so much for listening. As I said in my intro, drop me a message on Twitter or in the comments down below if you have any comments or questions. I hope you have a great day. Thank you.