remedy for dengue fever

>> okay, good afternoon. some of you look like i see familiar faces, some of you have been to this series before. it's sort of like a never ending tape because topics change, the speakers change, everything changes, some things are-our topics keep recurring because

they're of major importance. so permit me to spend a couple of minutes for those who may be the first time they've been here. so we started out with a quiz. what's that? don't answer if ue been here before.

it's a bridge. right. what bridge is it? the most famous bridge in the world. what? >> [indiscernible] >> it's also the most wonderful cheapest date in the city of

new york, take a bottle of wine, some cheese, some bread, and it's unbelievable. yeah,--this picture is a side note was actually taken by my grandfather in 1870 something using an old fashioned box camera. now the reason for the bridge is

the reason--reason for the bridge is the reason for this course, and one can wax on and on about this but the point of it is that the major problem is confronted [indiscernible]--scientists have incredible skills, accomplishments in ways in the

most part and those who were on the other side of the bridge, had the cliniciansparticularly out in practice, had great difficulty understanding the first group is talking about and there is some barriers among the first group that don't exactly cause them to get too excited

about what is ing on in the area of bigger health. so the big challenge is not to fill your heads with a lot of sort of medical school facts that you're supposed to memorize, it's to excite. so the purpose of this whole course is to excite your

interest in what a major, major human health problems and where we stand in terms of the linkage with what's going on and i can tell you there have been many examples where people, post docs have gotten so excited about something, they've gone on and pursued it, with some of the

investigators so although this is not intended to be an alternative job market but at this point to a learning thing that your ph ds are not aware of and that is the third major job market in the united states is actually in clinical departments, not like in the old

days where you work for an md, that's gone. now, most schools have changed the rules so you're kind of working with, in other words have you your independence and we'll talk about that at one point along the line but somehow that gets neglected and most

ph.d.s don't realize that's the case. there are 17 full professors of medicine in the united states who do not have an md degree and most of them are in major medical centers. now their story is a very interesting one that we can

address at some time. so, the course is posted on the web site. you just google demystifying medicine, you will see the whole program and we try to get several ahead of time, a brief cv, of who the speakers, a few selected referencesl

field is totally unknown to you but you read about it in the papers or it's exciting, look at some of those papers and you get a little background andthen the power points are there, so you can actually see. usually about a hundred people come onsite which is great

because you get a chance--there's lots of room for questions and discussion. and if somebody says something you really don't understand, speak up. we're not trying to cover--this isn't like a high school curriculum these days where you

have to cover every ubject, that not going to happen, so speak up and we real lye encourage you to do that. what else? if you come to 50% of the sessions and sign-in, at the end we have a not very difficult electronic multiple choice exam

that you can take over and over again and if and whenever you pass it, you will get a certificate from the nih and you attended this course in pathobiology, demystifying medicine, which apparently has some value in the real world. it's not like a ph.d. degree.

let me write that. the last thing i'll mention, most of thetime,we have a live patient who starts out and spends five-10 minutes telling the story of what his or her disease is in their own words, not medical jargon. and it's interesting when we

conducted a little pole amongst people who watch and who attend here, that live patient was a major driving force. puts a human face on the disease as one student put it very well. and then, there's an outstanding clinical investigator, most of the speakers are from nih, which

is a gold mine of this kind of activity. i'm sure you know, we have the world's largest research hospital just up the road there and if you don't know, you should go see it, it's phenomenal. so there are many people who

work there, doing clinical research, bridging the gap and so forth. so those people will speak and then a basic scientist who's also at the cutting edge of what's going on, but their talk is not a research seminar. it's not yesterday's experiment

it's where the issue is today, what do we know, what do we don't know and where are we moving and it's really very exciting because you're going to hear things that won't appear in the published press for a year or more. so at any rate, and if you have

any questions or so, you can contact me, my e-mail address is on my demystifying thing or give me a ring or anything. and i encourage you to sign the sheet, the information is top secret, it doesn't go to the--any security agency or anything, we just use it as a

guide to get a clue as to whose actually here and also on the okay, so enough of the brooklyn bridge. so today we're going to talk about attention deficit hyper-activity disorder and i have been looking forward to this for a long time.

as a physician, i don't see many patients these days, but family, friends and so forth, their kids are taking drugs, not narcotics but stimulates because they have what the door says is adhd. i recently spoke at two high schools, once a very fancy private high school in new york

city, over 40% of the kids in the class i was speaking to were taking drugs because of this. and the other school was a not-so-well-off school in a somewhat different what they might call lower middle class or somethin like that and about 20% of the kids that were there,

these are high school students. so i'm confused, you know? what is this? in the old days in the prebacteriaeriology days, physicians diagnosed pneumonia, and it was only many years later that they, you know could identify probably a hundred

different agents that cause pneumonia. it's syndromes verses symptoms, verses diagnosis, that's one of the huge challenges for the disorders like this. so the symptoms, doesn't mean if a kid is fidgety and can'tit still at the dinner table,

doesn't do his home work, gives awe hard time. and if you're a parent that my son is going to go to harvard, no matter what, is that the setting for adhd. so it sounds like a complicated situation and in my reading i'm not clear how you do diagnose it

and when you do, how do you treat? should all these kids take these drugs, is it good to take these stimlattory drugs for years? i don't know. i suspect you don't know either. but our speakers today know and that's the whole point of the

whole thing, as least i hope they do. okay, so we have--we're very fortunate because again here's a beautiful example of this bridge building taking place here at the nih because, you know you read in the literature who are the names that keep coming up.

[indiscernible]--genetics at yale or geriatrics, associate professor at the university of pennsylvania and then came here to the genome institute to head a unit that is related to bridging genomic analysis with complex diseases and his main work has been on craniofacial

distortion. --took his training inox pord and psychology and he, various places around the world, australia, united states, united kingdom, trained in psychiatry and pediatrics and psychology and filib's approach is completely different and

recently he won of the really highly competitive awards as a steady man investigator gift and he will follow up and speak too much about the genetic aspect of it, but other aspects that deal with how we understand disease. so enough of me. thank you very much for coming.

>> okay, good afternoon everybody, i'm delighted to see this many people here, i frankly thought a few would be coming, i knew win would be coming i am disciplinary lighted you are --at south china lake in main and we were at this wonderful lake and everything is very calm

and we had in the lab--for cloned the gene that has to do with bone growth with how it's shaped and i thought if we can do this, we can do anything, we can tell us a bit of megalow mania in there, and then before we went on vacation, i inquired, i looked at common problem in

geriatrics where the underlying genetic basis is not known and at the time i thought about--i thought about dyslexia. i thought about reading disabilities, i thought about stuttering, i thought about autism and i thought about adhd and after two weeks of staring

at the southlake china lake and i thought adhd is it. and when we got started, start at the [indiscernible], only to find out the problem is o big you can't do it in one lab. it's just huge. and that was the main reason to come to the nih and when i still

remember when i had my interview at the time, our interview director was someone named francis collins, you may have heard of him and he was someone who asked, so what's heritability factor, i tell you what the heritability factor is and i told him, and said, oh

that's higher and there's more genetics to it than to diabetes, which he's studying and that kind of dead it and then i had the position there and then idworking in 1997. so if i can move this forward, i will. i have no conflict if anyone cares to know.

but i will tell you about this, i will tell you and give you an introduction. the introduction today may be slightly longer than the main part just because it's really connecting bridging the clinical part of the basic science part and getting to all onboard here

and tell you about genetic activity, i will tell you about different genetic approaches, some that we have taken, some that others have taken. i will tell you at least focus on one gene, i will focus on a gene cause, and the agent and that's when we talk about the

molecule, just briefly and then we will tell you about pharma co genetic studies in adhd and then how the first studies in the animal model has helped or it's really goal of helping us understand how can we use the medication and other treatments to treat individuals with

adhd better and all of this will be done in 35 minutes and i think my time will probably be done in 30 minutes. so if i'm not done, i stop in the middle of it because i have been only on one panel where we talk about the same session and that is out of all bases in

berlin, germany and i'm looking forward to [indiscernible] so i promise you, i stop with 10 minutes to talk. so most of you know what adhd is you have a child what it real legal is, is some definition there excessive in attention--if a 40 year-old listen to a talk

for 45 minutes, maybe there's some attention issues for the speakers extremely boring. so there's a mighty point criteria, the criteria for each category which i'lltal you about in a moment. adhd is the biggest order between seven and 11% between

the children six to seven ages and you hear of the numbers, for example, the numbers of autism increased over the time and lab and others and can you see it's about 10 times that. what i didn't know when i studied in my lab, is that there are many associated disorders

including opposition of the order and conduct this order and teenagers and adults and something that was called depiction in the older days and the name has changed and the substance use disorder and why it's because of the genetics of adhd and that comes from family

todays of adhd and it comes from the study. so just to very briefly and i will not stay too long on this, so there's an intentive type of adhd, and there's impulsive type of add adhd but the diagnosis altogether is called adhd for attention deficit type disorder

for an inattentive type for them to be, issues such as [indiscernible] there's attentive to the details where it fully appears not to be listening to those who have teenager when is they don't want to listen and they're poorly struggling with obligation, home

work, dislikes or avoids sustained mental effort at the same token or other side of that can sit at a computer game for ours at end. so some of them say my child can't have adhd, they can play this computer game for two hours that's the focus and definitely

part of adhd. so that loses it is objects easily distracted so guess what, any of you hear just lost your key, they had forgotten my power point presentation when i came here, i think that's adhd what i do or not is a different story but you have to have at least

six out of the nine symptomsw72 that are listed here. same thing with adhd and does it cost more in [indiscernible] and restless, loud noisy, and by doing that, sometimes has difficulty in relationships and friendships with other kids. so as i said before, if you feel

you have this setã±o or theother symptoms they make the diagnosis, not like a glucose test, and not 25, that's way too high. the diagnosis of adhd is really made by observation and in an ideal world it's for observation in a different setting, so it's

by observation and eight out of nine symptoms on the hyper active scale, if that person is not impaired by that, by being out there, by being--i will not give you any specific professions here because that could be considered discriminatory, but it has to be

[indiscernible] so some of these symptoms of impairment has to be caused by 12 years of age and after and one other and another condition. actually, i will do this here, just to give you an idea that when this first was described there was a british physician,

150 million years ago, and then the first time that, that stimulate medication was described in 1937 and then really [indiscernible]-- [laughter] and the medication that he gave her was a way to do and she had tennis lessons and she always

was with her opponents and she just made the other day, his wife, he called it sort of the kind form for rita, and that's where the name ridalyn comes from, it is named after his wife. then there are the definitions of adhd, and eventually the

1980s maybe changed to adhd, and then with the dsm-three, 1987, it was a. d. d., so what i'm talking about and showing is adhd. so i still remember in the early 90s was that that's an american disease, we don't have it here, [indiscernible] to the u.s., and

here people say they all go to california, of course, that's not the case. but adhd has been around for a very long time, even pippocrates said patients with kickenned responses to sensory experience, but also less tenaciousness because the soul

moves on quickly to the next impression. i have a heavy german accent, i have to tell you about the story of dr. heinrich hoffmann, a germ pediatrician wrote a back for children with illustrations about inappropriate behaviors, and he had what i called the

bible or whatever your religious affiliation is, for the child psychiatrist and in this book, [indiscernible] you find every single childhood disorder that there is from a child who plays with fire in the german book, and the child life, to ashes, or the child that [indiscernible]

and the treatment of that is just [indiscernible] so you wonder why people in germany, why not everyone needs therapy but maybe they do. so what i wanted to tell you about is the story of [indiscernible] is one of the stories and--sorry phillip.

i wanted to change the story. the reason i want to show this to you, this was a story that in case you didn't know our own mark twain spoke german fluently and he traveled in the 1850s in germany he saw this and as a german school boy raised with this book, it was terrible, i

tell you, and when you read mark twain's version, it's beautiful, you want to read it. it's really good. just google it and you will have all the stories there. so this is an upper class german family and i want to make two points here and i won't read all

of this to you, the mother, father, child as you can see the child has some issues sitting still at the table and the rhymes i won't go through right now and can you imagine what happens next is in essence a nice family dinner is overwith, as you can tell, dad and momma

pretty upset there, probably not a good thing for their marriage either. the point i wanted to make is in germany, it's not common, maybe in france, have you red wine at dinner here, but in german i, that's not common. so i--i may venture to say the

father may have some issues with alcohol here and the other part is the way the dad holds the knife, that's not how you were taught in germany to eat with knives and forks so the dad may have anger management issues as well, i just want to point that out with regard to the genetics

of adhd, so then the next comes and i didn't tell this, so this has ranked eight out of nine in the hyper active state, if you read point by point if you go to the dsm five scale now. so we had an edge up by the name already, and he walks around and bumps into the door here, and

you can tell the point that i want to make here is probably no dog in his right mind was bumped into an employee and i would say that the dog has adhd as well, and even though i won't go into this yesterday, is we found that i will tell you about genes that contribute to adhd, and we found

that genes that contribute to adhd, that some of those are actually the ends performed so that our ancestors would have the genes that contribute to adhd and those who don't have adhd, are the mute ants so people with adhd, typically developing people and we of

course see the slightly different piece and they go off in a separate environment. and here's the other point i want to make and you have the other stories, this boy as saved and it goes together adhd with impairment with lots of home work, you can see his home work

is floating. so sorry for this very long winded introduction, i hope you got your attention to what adhd is, what causes adhd and of course, the short answer is, it's environment and genetics that causes adhd and i would venture to say, that it's just

the environment that causes adhd and not just the genetic but it's also an interaction between the genetics and the environment of course you all know of twin and adoption studies and twin adoption studies are in twin studies and interesting part is twins come in two ways to either

come in, monovie gottic twins where hundred% of the genes are the same and if they're raised together, of course 100% of the environment is the same. if you have dizygotic twins then they're only 50% of genes in common just like siblings that are not born at the same time

but they valid the same home environment. and yes, we are a combination of our genes and our environment and these twin studies are shown here and this is what tells us about heritability and it's something, if you take something away from this lecture, i wanted

you to take away there's some genetics through adhd and we can study the genetics. and you feel like the slate and take a real deep breath, and i guide you through this and in one minute or two minutes, you will understand this, and you can tell your significant other

when you go home, i learned that 70% of genetics is contributed by genetics, 70% of the causes comes from genes and 30% comes from the environment. so the way it works is when we look at each of these, with the blue and the orange, there's one individual study and all of

these studies were done over a period of plus/-20 years, and some were done in other countries, using different criteria and the blue are those where monozygotic twins that had hundred% of the genetics in common. so if one twin had adhd, then if

you have a hundred of those, how many of the other twins have adhd, and even though the number is slightly different, it's anywhere between 70 and 75%, so that if you have 70--if you have a hundred twin pairs, where one twin as adhd, then out of the other twins, about 70 will have

adhd, so what that's telling us is if were all genetics if it were a hundred percent genetics, then of course you would have a hundred twins who would have genetics or would have adhd, and what we only have about 70. and then when you look at--when you look at dizygotic twins, we

look at siblings here, if you see one twin about adhd, then out of the hundreds of twins, one twin has adhd, then it's only 25 of the other twins have adhd, so what that's tell being us is telling us two things, it's telling us that the heritability is more than 70%,

and the genetics of it is 70% and more and the environment is anywhere between 25-30% and what it's also telling us is if in a family, if one sibling was adhd, there's a 25% chance that the next sibling will have adhd as well. i think just to show you where

adhd is here, is it's anywhere i mention between 60-70, 80% here and when you compare this, it says 80%, when you compare this to other factors where genetics contributes to, only height has the higher heritability, schizophrenia has a little bit less heritability and then as

for breast cancer where everyone's seen genetic comes up only to about 30% of genetics and 70% environment. i have this slide here and want to just tell you about the clinical determination of adhd and i mentioned all right, there are just some tough types,

inattentive types, impulsive type and co-morbidity and of the order, conduct disorder, various dependences there and when we were thinking about this, we were actually had learned from others who had studied this, many colleague psychologists and psychiatrist trysts who said not

just the yes or noism but is really important. , and it's important in the severity of each individual symptom and that leads to what's called adhd, comorbid cluster. let me show you what that looks like. and there's a scale on your

y-axis here, if it's at one, the symptom would be very severe, if it's here, you don't have it at all. and it looks for example, it can tell you this questionnaire, everyone and anyone in this room would fit on to this scale somewhere, it's not like it's

them out there, it's not like we don't have adhd, we have nothing to do with it, all of us would fit on the scale somewhere so for example, if there are people who don't have symptoms, each tick marker you see here is one of the questions there, for adhd, i realize i can walk

around with this here. so each of these stick marks means there's impulsive quality to it and it's so the ones on this side here, so for example, this blue line here that would be some people have no problems with inattention, no problems with hyper-activity, not

opposition defied disorder, conduct disorder, in my lab, people cause them the boring and normal here, then there are a little bit here, and have a little bit more here and each of those cluster vs different severitys when you look at it, you can see here, there are

other clusters, there, where individuals for example in yellow have the--have inattentive type and not so much the hyper active type and then there were individuals who have the combined type as you see here and then of course, you find individual who is are quite

seriously effected and many of those individuals could be seriously impaired or they would use what i have and it impairs my daily working. and so there's different ways of looking at this, you cannot determine his [indiscernible] heritability factor to it i hope

with the studies i quoted, i could convince you, yes there's heritability factor to it, and that is a little bit out of fashion now, with candidate genes studies and a particularly good gene that makes perfect sense in studying this and then of course what people have done,

in our institute phillip shaw's group and my group have done genome wide scans and what people have done and they have compared those with the sibling who has adhd and another sibling doesn't have adhd, and they have large payment families and they can look at very large

studies--association studies where you look at thousand people who have adhd and a thousand people who don't have adhd, and my lab and phillip's lab have been involved in any of those three studies. so just a genetic approach that are successful which is an

approach where you look at flawed pedigree, where siblings or large pedigrees with multiple individuals effected and you can tell, this would be difficult here as both mom and dad have adhd, and they could have it for different reasons and this would be caused by linniality and

genetics studies who would exclude that because it really confuses, the issue, because you're not necessarily worth finding the gene that contributes to adhd in this family. so by looking at those approaches, there are

disadvantages, that means that each these small families, there could be heterogeneity and different cause for adhd there. and what that requires trequires large samples and then what we said, we wanted to study large pedigrees in a genetic isolate so the finish would be the

islandic people who have if not for thousands of years but for hundreds of years always be merry among themselves and we try to find a genetic isolate and that was not easy to do and then the problem which is a disadsrabtage, and then here come the advantages, you have a

high statistic of power, and many of those families and then the homogeneity, that means only one gene is responsible for adhd and this could be the two genes that are responsible and those are the genes that are responsible for adhd in one family and within one family you

can already does he fine the pattern of seggregation and that is how is adhd inherited and you can do that from large families and small families, that's actually quite hard to do. so we have combined both and used that to identify adhd genes which i will tell you, and give

you one example over the next short type. just to tell you about a genetic isolate, everyone knows columbia is not a university in new york city, and comes in south america here and here's a larger view of this part and with the mountains here and this is western andies

and eastern andies and the region, and here with the capital, probably you know for a different reason. and that is where we found a genetic isolate and found it with many effected individuals with adhd, and so the rest of columbia, adhd is common as in

the rest of the world about 10% in the area about five million people there. there are adhd, 20% and actually a little--up to a little higher there. so this is what a typical family looks like, and then my laboratory we have had quite a

number of so they call themselves the p a isas, and you look at a number of p a isas in my lab, a number of them have done the work here and we find that there are for example, individuals who have adhd some and possibly effected, some have conduct disorder opposition,

scientist disorder and some are independent and independent, so this is a real pedigree from a real family and they said how often do you see each other? and they said twice a year, once in christmas and another every year one sibling turns tin and the other turns 20 and the next

year someone else. so making a genome wide analysis scan here we found a number of significant linked loci that we found in these families that we found in the p a isas, i will focus only on one of them and that signify region on chromosome four where we

identified the labs [indiscernible]. and there are two things i would like you to take away with this and that is that litroph ilin three worked on a g-protein coupled receptor and a receptor is this molecule, this molecule here that goes from the outside

of the cell to an extra cellular part and then there's a membrane domain part here, seven memory response grain domain here and there's an intracellular part and that is very important for moving forward, the signal from the outside of the cell to the inside of the cell and

this--that is what lampofillin three does. so we did a number of studies so i call it [indiscernible] and without citing every minutia of the brain scan here, i just want to point out of what we did in this study, so what we did is a particular brain scan called

proton magnetic resonance microscopy, long word and what that does is it provides an index of the number of cellsand the metabolism and viability of these cells and what has he known, there's a specific ratio that i practice for many times and what i say here is that it's

decreased in individuals with and what we said we wanted to see in the p a isas where we studied individuals who'o form of this lamp o sillin gene, the susceptibility gene, verses the other form which is the protective gene and we studied here, as you can tell, 15

individual who is had at least one copy of the susceptibility gene, then we studied 10 individuals with at least one copy of the protective gene and then we studied eight individuals who had different haplotypes. so what we find is, we find that

there's a clear cut difference between individuals who are either controls or who have two copies of the protective gene compared to individuals two have two copies of susceptibility gene and what we find, that this specific metabolic brain ratio of n-acetyl aspartate is also

decrease indeed individuals that we had studied when we look at the brain scan and more over we find individuals who have two copies of the suseptibility gene actually have the metabolic changes in the brain going on that correlate with the gene and what this is tells us is that we

have the--our genetic studies show us that the susceptibility allele of this gene that goes together with a metabolic changes that happen in individuals with adhd. so what--i have another two minutes if you can give me three phillip, i would appreciate!u it.

thank you. so what can we do with this here now, with regards to medication, can this tell us anything? and the short answer is that in the future it will, at this very point we have only some glimpse of it, we wanted to just tell you what the cdc in atlanta

found in a study that was done in 2010. it's reported that children when you look at different groups here, and they show how many children have adhd, and then the gray bar next to the other bar of children who are medication. so it's not quite as high as you

heard in the press in new york city where up to 40% of children on adhd medication but if you look at all children in the u.s. the thought of 10-14 year-olds, over six% are on adhd medication, that to me is a huge number. and so just wanted to show you a

study that we did by lookingad individuals with children where we both had the genetic underlying basis and where we found out from the parents, how are your children doing when they're on medication and then some children go off medication, using the off medication time is

during summer break and if you're in winter break and so on. so what you find on the left side, you find children who are off medication and here the "typical range" would be around zero and you see different patterns there where individuals

very high on the adhd are here and then those children do get medication and you find out that those children and some of them are much and the category was a purple line here and the symptoms are doing pretty well, so these are children who respond extremely well to

medication and then you see children who are not doing well at all on medication. adhd medications do not respond well to medication at all, they have more effects than positive effects of it and wouldn't it be wonderful if instead of going from one medication out for

three months, then another medication for three months, the kids get frustrated, the teachers get frustrated and the parents get frustrated if we could do a genetic test and we know, you respond to this medication, you respond by playing soccer by playing soccer

for two years every day. you respond by doing mind space puzzle reduction, and you respond to various kinds of diets if that would work. so what we did was we looked at the susceptibility gene and we found that we can predict a significant p-value for the

prediction of telling who would respond to medication would not respond to medication and just babe steps, but i hope it's in the right direction. i think it's showing that based on--looking at the medications that a child takes and the genotype that a child has that

this will eventually allow us to personalize medicine for every child specifically and i think the last thing i'll have to show you is this paper listed here and i just have to show you about work we did in the zebrafish where we have down regulated the gene for the agent

and then looked at every single zebrafish who either has the down regulated gene or has the normal function of the gene and even though it's hard to see, i can tell you when we did this here, we studied everything of the zebrafish here and we take a thousand pictures per second, so

every milli second, we look at every zebrafish was either down regulated or normal have it, and those who have the zebrafish who have down regulated the lipo fillin three, are harder to determine inattention in the zebrafish. but with the hyper-activity

waorbgsy could so there is a correlation and with that i say thank you very much and show you those individual who is have done the work and the person who are sad to say, not here anymore, but of course at the university at the australian national university and

[indiscernible], from columbia and then individuals who are studying adhd in the lab right now. is martinez here and maria, and many other individuals who are studying this. so thank you for your attention. [ applause ]

and if i'm not mistaken, we do questions at the end? >> i will repeat the question: is anything known about the down regulating signaling pathway and the short answer is, believe it or not, no, very, very little. so if there's an [indiscernible] there must be a one and two

those have been studies in quite length and details and those are one of those understudied genes at this point. possibly. so has a very similar type. i forgot to mention has a very similar structure to other genes that have been shown to be

involved in adhd such as dopamine receptor genes, very similar, these are also g-proteins. so do people outgrow adhd? do you cope with it? how does that work? >> that is a wonderful question, i can give you my 2-cents and

then phil will give you a much more sophisticated answer to that. so what happen system, people as they get older the brain matures and also as people get older, they learn comp pensatory mechanisms that work well for them and the better they can learn those, the better

they can deal, the better they ca deal and that's why, there are mentorship skilly of colleagues get an nih, we have adhd and meet them and you know--yep, have you adhd and they are doing extremely well with it, of course a high iq is a benefit so with that there's

lots of learning as you have noted. and phillip will tell you in more detail why some children are more--why some children seem to outgrow adhd and seem to be doing quite well as other, other children less [indiscernible] and don't do as well.

>> [indiscernible]. >> the cost of medication, i don't know the price, i know what it is on the black market, you may know that ridlin and the stimulus medications are the second most drugs used in college. i won't even go there.

that would be politically incorrect. second common use at campuses, college campuses, one of the tablets between five and $10 it helps keep the study for the exams and they do better. of course one question that you didn't ask but i'm going to tell

you is that if you take the medication, and do better, does that mean have you adhd, no it doesn't mean that, it's just a stimulant medication like a cup of coffee and if you target it just right, if you have just the right [indiscernible] amount of caffeine, quite well, so anyone

benefits from it. >> taking ridlin is analogous to a cup of coffee sthat what you're suggesting? >> i understand from some people anecdoteally, people with a cup of coffee, people with adhd do bet we--we--you a cup of coffee than without a cup of coffee so

caffeine is a stimulate and so is adhd metricsication. have there been other large families like the mediane family, and did they turn up other genes, and [indiscernible] and phillip shaw is studying large families here at nih, but i don't want to

steal his thunder. >> you think this gene is actually increase nothing frequency because of some positive selection? that it's doing something good for the population? >> that's why we have this [indiscernible] my daughter has

to go to harvard but never mind in first grade, she looked out of the window instead of at the black board, i think that--that is certainly one of the issues, but it's based on our studies when we look at higher relative of the primates, all of the primates we get samples from,

have what we--what we would consider susceptibility form of the [indiscernible]. so again humans, the ones who don't have the susceptibility form could be the--what i would call the mutant there were in these--in earlier times, there were individuals there who had

more of the susceptibility. >> so is adhd a disease of a more economically developed society. do you find it in deepest africa? does it correlate with other property and afflu ensel so the longer answer is a little bit

more sophisticated in that, it seems to be something more cultural and i tell will you was why have to close but a colleague of mine from japan, was from a post docker in seattle was his wife and his two boys and they loved u.s., they love consistenter tkpwarten and

came back to japan and something truly unusual happens that never ever happens in japanese schools, the parents were caught in for a teacher parent conference in the middle of the year. and they were severely behaviorial alerts.

and who jim over tables which was like personal freedom in this country at least in consistenter garden. so for this i say thank you very much and look forward to phillip's talk. >> hello, pleasure to be here and thank you for the kind

invitation. i was just at ireland where there's every bacterial infection known to man. hello my young relative so i thought i would start off--this happens a lot because we do clinics every idea and the clinical center in the

pediatrics group and we had a kid with good going adhd in this room, within minutes the child's head would be lodged in the space there and they feet flailing around and they would get the pockets and put those them and they would be chaotic and overwhelming for a child and

so i just described the children in the setting. so one of the kids in our study is called peter, and peter was brought to the clinic by extremely exhausted looking mother who said here, this child really has been doing sommer salts in the womb and he has

never stopped. this child is exhausting. at age three she was called by the prek and said we can't cope with this child so even in prek, there's some minimal requirement of stillness and this child just could not do this n. reading circles he would be up over,

climbing the walls, climbing furniture, unmanageable. this child at the age of six has a high iq that talk of holding him back for a year because he can't complete the basics of learniause he is just so hyper active and so impulsive and cannot pay any attention at

and this has the impact from his learning and peter if you go into the classroom, one thing that's quickly observable is that kids are quite social and they have these networking and peter is isolated and this is not uncommon for kids with adhd, and they are impulsive children

who will get in the space of other kids and have impulsivity, the average five year-old will not get this and will isolate themselves from this, social impairment with it is another key feature of adhd, little peter has social izzoalation and he's doing disasterously at

school bespite his iq and maybe turn to his parents and his mom was honest. she said i love my child, but i'm really not sure if i like him very much. could not get him to do anything. so we spent today, the diagnosis

of adhd, and it is not an easy phenotype so we taught the parents, we taught the schools, and then the diagnosis is clinical skill, it's based on history with those three sets of informants, and we also do lots of psychological testing and then at the end of the day and

get the child to set into [indiscernible] which is always fun getting dna and then we ask the child to lie still in a magnetic resonance scanner while we take pictures of their brain and we've gotten quite good at this and little peter managed to lie still for 25 minutes.

after which his mother offered to by the 1.5 million dollar machine. this is very impulsive notable very impulsive, isolated in the classroom, extremely distractible, sort of child who couldn't complete the simplest of tasks, here and you talk to

her it's like talking to the wall. she hears [indiscernible] the words get in and disasters at school and terribly laid back and really dinner concerned about the future, and during very good at school, coping quite well but there's still

impairment there and she also meets the diagnostic criteria for adhd. see whey will talk about a little bit is--what i will talk about a little bit is what's going on in the brain of these children and then a little bit later i will consider whatalcy

happens to be children as they get older. and what we started looking at is started by judy rappa port and it's an ongoing study, one of the strengths of this and the strengths of the intramural program is the longitudinal study, so a lot of what i'm

talking and kids who emphasis study on the 1990s and followed up to the present day, it gives us a lovely amount of longitudinal data and if you're trying to look at a developmental process, such as adhd, development and longitudinally, it's perfect for

capturing such developmental processes. so briefly talk about three studies that are done, maybe just two. so each of them addresses the question is the brain in anyway a typical adhd and these anomalies are these fixed, do

they remain or do they change. is there difference in the brain in adhd, the50 difference of a trajectory rather than a difference at just one point in time. and the first study i'll talk about is there, this is the human brain, here of course

we're looking at the brain from the side so all the studies i will talk about today actually use an atomic imaging so it's structural brain imaging, there are many, many other ways to look at the brain. i will focus on anatomy here, through the actual structure of

the brain so we can define safely in children using magnetic resonance imaging, don't involve any ionizing radiation and do it on children, year in and year out as they grow up. so we have another one, and here we have the brain of course,

this is the front fit, cognitive control, high order center planning and sensory motor strip, i'll talk about the cortex later but what i will focus on first of all are these bead structures in the bridge. these are the striatum and the reason they're covered the same

is that projections from the frontal lobe and back out again aren't quite organized. there are different parts of the frontal lobes of these different parts, the information processing centers of the brain, these wonderful information processing loops that all talk

to each other so they go from the frontal lobes back out and then to many, many other regions of the brain. so here i'm going to look at the striatum. so here we go, i never understood neuroanatomy in medical school at all and

whenever i got to the class, which way round does this deliver the work and that one, so here you go, these are very nice images where we get mris, the magnetic resonance imaging and you go in and use sophisticated tools which you develop by colleagues in canada

to extract these deep brain structures. the means of the striatum for the processing centers, so to orient you here, we are looking at it from the right side, this is the cotter educational, so we could flip it around. there you go.

oh it's not working anyway, it's a shame, and it was going to spin around and just show you in 3d, the deep striatum of the brain, so what we're asking here is many, many people have looked at the striatum in the adhd, and look at information processing center, and a problem with adhd,

and lots and lots of cross sectional studies and they find that this brain structure is a little bit smaller in kids with adhd, the difference is not enormous, if you go in terms of the sizes, it's a small difference but it's there and it's pretty consistently signed

so if you take kids who have adhd, and compare them to kid who is don't, you will have a bit of a smaller at a group level in the kids with adhd, again i'll overlap, it's enormous, that's why we can't diagnose adhd from the brain scan but at a group level

there's a detectable small difference. so we have these fantastic images of children as they grow up with adhd, and is there more of a difference we can pluck out in hosting it overtime, we are after all thinking of a developmental disorder, is it

the translational research jacketry of different rather than different at one time point. so we have 270 kids with adhd, and 370 kid who is don't have adhd, and most of these are repeated imaging, and you just define the trajectory of growth

of the striatum and we did this for thousands of little surfaces on the striatum, so we use the message to find the change by now the first thing we did, did we find what everyone else finds is the striatum and cross sectional baseline study, is the smaller adhd and indeed it rolls

and here we're looking at the striatum and the front here, this is the containment, and this is looking from the bottom. this is called the ventral striatum here, fit anywhere you see cover there, it means the surface area of that part is reduced significantly reduced in

kids with adhd. so this is just a cross sectional comparison, confirming what i think many people have shown before, perhaps with the higher level of spacial resolution. in terms of the size of this effect, it was small.

there's a big overlap, small effect, but it's very robustly significant. confirm what is we knew. so then we went on to say, well, what about growth? so we have thao*ez kids and sort of interleave from the age of six through the age of 18 when

this study ended and we started the develop--the trajectory of growth. so just to orient, here we're looking at the striatum and each graph here shows surface area change. this is the x-axis which is age from the age 70-17 and the

y-axis is one surface area of one little valid and reliable tex on this striatum and it's just kind of random. so what you can see by and large is look for it specifically looking in blue, the striatum most of the surface gets bigger with age, no great surprise,

many others shown there and they get a bit bigger until you're 16 and then get smaller. what about the kids with adhd in red, while we know there are a bit smaller baseline but would this be from the data wall, they have a reduction in the barrier and it was kind of parallel so

it seemed to be largely a reduction here, so was there anywhere where the stray jectoryot umkc developed differently in the kids with adhd, and anywhere where the trajectory had a different path and indeed there was. and only really one area.

and this is look at the triat umkc from the bottom, this is called the ventral striatum and it was in this region that you had different diagnostic and trajectory. so what happens in that little region there? this is typically developing

[indiscernible] it got a bit bigger that is it did for the rest of the striatum and the kids with adhd, there in red, it got a little bit smaller with age. it contracted. the surface contracted. this is a very interesting

region, it's an interesting region, because the ventral striatum is intimately link wide many, many things that we think might characterize the psychology of kids with adhd, for example, the processing of reward. the kids with adhd as a group

show a marked preference for having a small immediate reward over a longer one that delayed. you go up to a kid and you say, i will give you $10 in 10 minutes or 1 dollar, which would you prefer. lots of typically developing educationals, adhd, and

reasonably reliaisonnably will go for the small immediate reward, this is palpable when you feed them in the classroom. star charts, you do it all week you'll get a reward, you can't do that, you have to do it immediately with them. so it's very important and

regions to the processing of aspects and again there are effective differences in kids with adhd, and by no means they're not all negative. a lot of #keuds have a wonderful exubeerance and brightness to them and this might be this bias, some temperamental

component, again something that has been linked to the ventral striatum, and terms of the psychology of what we know about adhd, this binding made an awful lot of sense. isle also point out that if you do functional studies, and put kids in this scanner and give

them tasks which require them to process rewards this area will be hypoactivated pretty consistently a nice alinement and i'll have a few minutes and then i'll end. so parents decided they would start him on medication, and this happens and the parents

will come in and say what have you done to our child and teachers will go this is the same child, when it works fantastic and it works in the majority of cases of kid who is have severe adhd. has to be monitored carefully for side effects and it's

extremely effective when it works. that was peter. >> and he was able to stool dnaerate them as he grew up. they kept a close eye on his height and weight as you really have to and he's very beautifully treated through

developed and when he got to the age of 12 or 13, symptoms are waning a bit, so the patients started to with bra and then whatever we recently saw him, at the age of 18, he was doing brilliantly. this child no symptoms at all of adhd, went off to college, just

fantastically. peter will be a case of full remission of the disorder which you know happens roughly about 30%. what about susan? susan at baseline looked identical, not identical but in terms of adhd, looked extremely

similar to peter. you could not tell them apart, clinically. so, susan initially reluctant to the medication, and then they waited for a little bit and they tried and actually she didn't respond well to medication as well 20 to 30% well of stimunits

then she start indeed the second and third line medication for adhd, none of which suited here, unfortunately he didn't get the other thicks that could help kids like behaviorial plans at school and educational plans, but that doesn't happen as is often the case sadly and she

really struggled so this is a girl with an iq of 113, 120 who barely graduated high school. she was having a really struggling time. she had symptoms of adhd, very impulsive, very intentive one depressive episode and was beginning to misuse

last when we saw her, she was doing much better and the substances waned but again, this would be a case of persistence, but what are the problems of adhd, and whenever you [indiscernible], when anyone [indiscernible] in the clinic and one parents ask is how will

my child do when they're older. i think i can get through the next year or two but what will they look like when they're 16. and it is very, very difficult to predict the outcome, because many of the usual suspects and childhood psychiatric problems and that would be loads, and

having poor access to healthcare, having severe symptoms, they don't strongly predict outcome in adhd, it is hard to predict outcomes from the typical usual contributors, who were difficult cynical cord for a child. so that turns us to other

sources of information and one of which is the brain the other of which is genetics and i'll talk a little bit about the brain. so in this study, as i said, what are the joys of working here, is you can follow people up this is the 1970s cohort and

this was severe adhd and not one. and then we managed to get back at the age of 24, 112 of them which really isn't bad going at all, given the mobile populations are, and also 112, we scanned everyone and we had this number of good quality

stans and you always lose some for quality reasons and what we're able to do there, if we have brain images acquired on the same scanner, of these individualings, as they grew up from childhood to advesensel, to adulthood, so what we asked is where does the course of your

symptoms, where is that tie to the trajectory of your brain the very broad hypothesis, would actually get better, you will converge more typical dimensions if you get worse or have very perristent symptoms, you will diverge further and further away.

so what he look at first of all is that [indiscernible] of the cerebral cortex and this again is acquired from the images and the thickness is extracted by the computer, it's 80,000 points throughout both cerebral cortexs, so what we're doing here is we're asking words with

the change and thickness of your cortex, it's correlated with or predict if you like, the ultimate outcome of adhd, and the reason for the coupling of trajectory and clinical cords are shown here. as you can see, these are medial uses of the brain, here it was

split in half and opened up, and this region is called the singular cortex here and here, the great trajectory of the cortex change was strongly associated or predicted if you like how many symptoms as an adult of adhd, and particularly in attention and i will note

there's no relationship at all with hyper active impulsiveness, against what we hypothesized but there we go. so what's happening in these regions, i skip that. i'll show you this graph, and then i'll probably end there. so here you go.

this is age, this is the cortex bowls in that region, so blue are typically developing adults, young adolescents adults and the cortex gets a bit thinner in that region and that's been known, the cortex gets thinner during adolescence and what about kids with adhd, who got a

bit better, well they start off a bit thinner and then they converged toward more typical dimension, what about the kids who didn't improve with adhd, they're the ones shown in red here, they essentially--we predicted they would diverge but they didn't, this is a

nonsignificant difference and this is a fixed difference with so just think about those regions, again in the cognitive science of those, the regions make sense, and they're regions very much involved in the control of attention. they're also regions that are

intimately left to something called default network overlapping the brain. this is like you know, the--whenever you're dog nothing, when your mind is wandering, your brain seems to have a stereo typical response. it just lapses into the empty

activity which is spread over different regions of the brain and one of the structural differences here, lapsed into that, this is interesting because one hypothesis of adhd is due to the network or mind wondering, ibt--integrate truing wherever it's can that presents

itself as momentary lapse of attention, and it's an interesting hypothesis. also i think to note is that the picture emerges of the brain and it's richly interconnected and in previous work we find that the trajectories of the frontal cortex growth and alter indeed

kids of adhd, and they're both a bit slower and in some ways a bit delayed in focal regions so there's very stereotype change to a trajectory, in the front at cortex and then also a change of the trajectory in the triat umkc which receives those and from the frontal regions and the

picture emerges and part of the story the disrupgsz of coordinated brain system. and i think actually i'll just skip all of those bits and i'll just--i'll just wepbd that. this is all very good but what can we do with it. and there's still no clinical

row for mri and brain imaging in adhd, and it remain ace clinical diagnosis, will that be the case in the future? and combining different modalities to look at the brain, we will get to a signal which can help at least shift the possibilities that this child

has adhd, and perhaps more ambitiously, can we use the information to predict future outcomes. so this hypothesis, no, this information is all purely observational and descriptive. now what we're doing is taking this description and see figure

we define these trajectories in young kids at three time points one year a part will that project major clinical outcome. so we're taking the observations that aligned and how do we find some sort of neuroimaging marker which can partially and probability of the clinical

course of a child so we can better inform the parents in the clinic and so we can help them in the future. and on that note, i'll end, >> so the question was are there gender differences in the recent diagnose and i guess response to medication.

and there are, there are. the adhd, particularly problems externalizing ones that you see, the ones with behavior and regulation of the behavior is more common in boys. people aren't particular about the portion, i don't think that's diagnoveltyec bias, i

think that it is how it is. is there any difference in response to treatment? not as far i know. i have people that will respond to treatment quite well. >> thank you. >> wow is there any correlation between response to treatment

and likelihood of them having a remission later in life and also, being treated in possibly the cortical thickness later, whether they receive treatment or don't receive treatment? >> yeah, so, it is very hand on heart, it is very difficult to show, if you take them 14 years

how long will they work. so well is one extremely good trial called the mta, the motey modal treatment of adhd, where the double blind up to 18 months which is a phenomenal achievement and it showed up to 18 months, stimulants are very effective they had a good

profile and after that we rely on observational data. that's realry complex to interpret. if you think about it, kids with stimulants who have very severe symptoms might end up being the very ones who need more and more it's hard to make the length

with observation. clinically we think by giving stimulants of kids we give them the opportunity to suck succeed each day in school, that intern should lead to experience of success, and which we hope have long-term outcome. >> so we were told that ridlin

was discovered by serendipity, because a chemist was trying to do something with his wife--k --at any rate, so it turns out that it's a stimulant and yet you describe these children, if anything as being hyper stimulated, i don't understand that.

so what is your thinking about what the mechanism is as to what's going on. i mean a priori, you would think something that would slow them down would be better, what's the basis of--what are you thinking in the neuroifiesio logic cellular basis.

what's the concept of what's going on? >> you want to answer? >> my question sort of relates. could you also commentot benefit of sports in place of treatment? >> so in terms of the theories of how psychostimulants work and they altser dopaminergic hones

in the deep triatal areas and then back to the frontal cortex, they do it by different routes. there are two big classes and the ridlin and the amfetta mine one and the ridlin like ones stops and the dopamine backed up in the presynaptic clamps and the other is to flood the system

with dopamine. one very good [indiscernible], why that makes children more focuses and one way of looking at it is that if you are in a hyper dopaminergic phase then you are sort of creating stimulation around you. if you correct that, that will

be temporarily and it allows you to be much more engage indeed a typical fashion with your environment but that's purly hypothesis, but that's one idea. other one is an inverted use and where are you and where are kids with adhd, so those will be the two ways of dog it.

or for kids, like diet for children, i think the sport, to children who enjoy it and healthy diet for all children are important for all children, regardless of whether they have adhd or not. >> s is it true that half of professional football players

have adhd. >> it's also very true that a lot of successful people have if you think about the genes are common, in some ways particularly if you outgrow adhd, i wonder if some of the intentive styles that are left behind might have an adoptive

role and certainly, you know there's no reason to be pessimistic, i know lottings of incredible highly achieving people [indiscernible]. >> i was just wondering if the mri studies had placebo controls, the controls--where they can--taking pills that they

didn't know were one thing or another? >> so the studies i did are purely structural. they were open observational, there are studies that have been done and i think probably a better way of looking at the effects of medication.

i think a brain's functional study and there's very lifely theories studied which double blinded administration of a stimulant or a placebo and looked at the effect on brain activation during cognitive probe which has to be mean it would be difficult to see, and

temporarily, and it is the underactivation of the brain areas. >> which of the brain areas. >> it depends on the task, certainly the striatum, frontal region and normalization and sort of near normalization, of temporal lobe activity.

so if the cognitive path requires thategession, then requires that region. >> was the striatum always indicated. >> i don't think anyone's done the reward processing on and off. it's an interesting study also

duly. that i don't know of, i know lots of cognitive, or classically cog 95ative probe vs been done. >> is it possible for the drug to structurally help [indiscernible] >> i guess the only way to

answer that would be in the context of the blinded trial which has never been done for brain structures and the structure of impausible thing, there are six or seven good studies which are looked at children with adhd on and off medication and compared them to

the children who had neither adhd or medication, the biggest difference is between having adhd and not having adhd, if there's difference with medication, there's a hint that there is medication have more typical valium. you

--volume. you have to know why they were on medication or not on medication, my take is that there certainly isn't an alarming bad association, would it [indiscernible] i don't know would i expect it to, i would expect to temporarily improve

brain function and then once and these medications only last six or seven hours and then they go back to the function and that's kind of the main story that's coming through. >> i know in a way a politically hot topic. >> the question is, if the

patients have adhd, then what is the percentage of kids in the american school system that are getting [indiscernible] >> i'm not sure if it's the 2010--yeah, that was-- >> --but whey wanted to go along your politically hot topic here is would it be that some

children who don't have adhd, verses other vs adhd, would benefit from the medication and not on medication so what phillip was talking about it's very important to make the diagnosis so if a child has adhd and would benefit from it, from being on medication that

would be wonderful and the [indiscernible] of that child being on medication or property treatment according. >> so the numbers that are that we have more children with adhd, and and less children being medicated? so six% are medicated verses 10%

of adhd. so even though probably most people think otherwise. >> how difficult is it for an adult to be diagnosed with adhd, or is there some sort of attentiveness or-- >> one to two% which goes along with the remission rate you said

and it intentions much more common but you know traditionally, adhd was brought over the childhood problem, and diagnostic criteria, it has been adopted a little bit more recently then trying to make examples of the adults and i think max mentioned a very good

one and restlessness. for adults that's the person has a subjective sense of inner torture when they have sophisticated sit still. most adults will manage to sit but it will be be torture so perhaps a different expression. is it impairing?

not usually. >> do you think there's any cultural differences among the patients that are diagnosed with adhd, so for example, say if a parent is having a lot of trouble with their child, and they simply think that the child needs more discipline as oppose

to the issue where we need to see a physician or say if they did with school, where the teachers aren't as--they don't communicate the issues with the parents as often as if they!4a went to the school. you know where they have a lot of communication or they really

hear more, quote-unquote. >> that's the importance of a good clinical creating an assessment. because you know basically if you do it properly, you would have to be a very unlucky kid to have the world's worst teacher and then meet the child and

they're perfectly good. if that happens and sometimes they will raise your eye brows what you do then then and i coincident make the diagnosis and we have time to make a good diagnosis so it's not unusual to say, we can see how this could thought, let's see if that works

out. if it is a class with the teacher. i'll tell you, you know, sometimes it is, often note so importance of getting multiple good information over time. >> this is talking about the recent diagnosis of adhd, and

it's a complex story so what i can tell you, is recently, sophisticated so, in 1990, there was definitely under diagnosis in black children and the reason can you is there was excellent studies in elementary schools which did [indiscernible] readings of hyper active and

intentive like behaviors and then look at the rate of adhd diagnosis and they were much lower in black kids, that hasn't held with time, so the recent cdc do not so a race or ethnic what they do so is withholding of time and some groups who are really consistently being under

diagnosissed and households in which the language spoken is not english and that speaks to access to the healthcare statistics, and ha is disparity that's overtime and hasn't budged at all. >> my question is the analysis [indiscernible]--since then high

function autistic or some people call it [indiscernible] so how do you differentiate the adhd, verses this problem and some people will treat it literally before they find out they're not >> so the question is merely can you differentiate autistic findings and features in

children or adults from inattention and hyper-activity and i think the short answer is probably yes and that really depends then on not just one person saying but having a healthcare professional who understand the issue, i do think there are differences there, and

i don't mean just genetic differences and i think there are behaviorial differences between autistic and talking about high functioning individuals verses individuals who are high functioning for so yes, even though there is no easy test, no blood test, but i

think between questions there, that are from different, different observers, parents, teachers and when the children can do that themselves and you can differentiate. so can you only trust clinical observations and impressions to a limited degree, but my

clinical impression is, that when i was growing up, although contrary to what you aid, my mother told me, you will never grow up so i am worry body that, but as i was green celling up, i don't remember anything, any classmate, anybody and then suddenly, there was this

epidemic. it almost seems and i'm exaggerating as if everybody has adhd, when 40% of the kids in a very fancy high school are on ridlin, where were they before? did they exist before? to some extent is this something we have created?

now you're taking people that fit the criteria, this is pneumonia due to pneumocockis, you are putting this out there but in society, most people who have the diagnosis i suspect don't fit the criteria, it can't be, can it be that 40% of the kids in school or 20% or even

your figures acss the board? i find that amazing. what do you think? >> you know the school [indiscernible] and we didn't have adhd in northern ireland, i can tell you that. but what we had is that we're naughty children and they had an

awful time and no one liked them and they always sat in the back of the class and then the children would bring them to the black board and they would whack them and i am pretty sure that back then they were adhd, they were just marginalized in the classroom so i think it's a much

more compassionate standing that there's biology to this, and it's a group thing and it's a battle, come through and not throw the baby out with the bath water and there is undoubtedly diagnosis of adhd, and there's undoubtedly the use of stimulants of the cognitive

enhance and relative treatment. that said, both of those said, adhd and very real and very impairing and stimulants to make a huge beneficial on the right diagnosis. >> change you describe in the autistic [indiscernible] that it's now one out of a hundred,

it used to be much, much [indiscernible] so there was a descriptive difference [indiscernible] and i don't know if that's legitimate or not but that's--i don't know what's happening with adhd taorbgs the fact of the matter is, i understand the 40% is different

than the 6 percent of the average in the population. there's someone ought to look into that school. >> yeah, i have a question, what about adults, i saw your study stop at 25, what about the adults and they didn't have if in the old days, i think you had

it in the old days ha is with these people who were born in the 50s and 60s and they still there and they still have adhd, in the check out line in the grocery store and they do this, sometimes i see them, and i see, they stay there, and i know they it's so typical this behavior

and they are grown ups, they are 50, whatever and they still have it so who takes care of them. they still don't have friends, they're still not very liked from other people and you know they're still the same, legally. >> first of all i would say, you know, if there isn't a problem,

a real problem you don't fix it, if you're just wiggling around in the super market, it's fine, whatever, maneuver, you'll get over it. if you're losing your job because you're so impulsive, you can't [indiscernible] you can't hold either job you had, you

know something to choose because you're medicating yourself, you have depressive episodes because you know you just feel like a big old failure and no one has diagnose educational adhd because it's not arrived, it's not impal to diagnose adults and it's a lot more

complicated and you rely on good informants to get a good early, and life long developmental history, which is with the [indiscernible] and so absolutely, so certainly the diagnosis in adults are going up, the rates, they're not startlingly going up, but

they're going up to where mathematically it would be reasonable. so there are instances. >> i couldn't agree more with what you just said, phillip and just to answer your question, i mean those people with the aarp category in the over 50

category, you get the aarp magazine, every five issues there's an article on adhd, and diagnosing adh din the elderly and those who are have it and are impaired by it need to recognize they have a disorder and they have a disorder that can be treated and enough

treatment for disparity and i think the nih, and what the nih is all about. it's not about overmedicating 40% of children of well to do of those kid who is are harvard bound and the likes, but it's really those who have an impairment and i'm always

reminded of our colleagues [indiscernible] who is a child psychologist who says that it's hard to tell like at six, seven, 8:00 in the morning is it night or day? same thing in the evening, getting darks, is it night or day?

but no one will have any problems at one ooh clock, it's day time. of course it's day time or it's 2:00 a.m. in the morning, it's night time. so you yes, can you make the diagnosis of adhd and when you can, i think those children

need-- you can tell adhd from not adhda part, are these individuals, is this a little bit like cholesterol or like blood sugar, like height and the answer is yes and are their great areas there, and the answer is yes but in the most cases, you can tell

the cholesterol of 300 is too a cholesterol of 200 fine, cholesterol of 205 may be border line so the short answer is the research. >> i want to thank both of you for a very, very exciting talk.

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