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Concussion and Addiction

David Baron, DO, MSEd
Concussion and Addiction

Presented by Dave Baron, MSEd, DO, DLFAPA, DFACN

Transcript of Presentation:

Dr. Dan Angres: Welcome to the Positive Sobriety Institute Lunch and Learn. Today is actually a very special presentation. I’m Dr. Dan Angres, the medical director of the Positive Sobriety Institute. We have Dr. David Baron from California, from USC, who is part of our scientific advisory board at RiverMend, our parent corporation for PSI.

Dave came all the way from California late last night and is leaving this afternoon. I mean that’s a long way to come. It’s an honor to have him. I wanted him to see the center but also to be able to give this very important talk. There’s a lot to be said about David. I’ll just mention some of the highlights.

He is currently professor psychiatry at the Keck School of Medicine at USC. Director in global center for exercise psychiatry and sports at USC. An adjunct professor at the USC School of Cinema Television. Dr. Baron is currently working on cutting edge research and traumatic brain injuries funded by the NFL. He is a researcher, teacher, clinician, and has published extensively.

What I can tell you as well is that he has an interest in history. I think this is history that contributed to some of the direction he is in, but he is an Olympic swimmer. And I just found out this morning that he was recently granted to be the full bright scholar distinguished chair representing the western hemisphere including some of the work that will be with United States government and the Canadian government. His work with traumatic brain injury, the NFL sports teams, concussion, ADHD – I could go on and on but I am very honored. We should all be honored to have Dr. Baron here today, especially with the effort that he made today to come here and be with us. David.

Dr. David Baron: First and foremost, I want to thank my good friends Danny and Kathy for inviting me here. I very much appreciate that very flattering introduction but what really matters in doing clinical research is what you learn from your patients, your students, and clinicians who are in the field.

What I want to talk about today is an area that I’ve had a lot of interest in recently. I’ve been involved with concussion research. What we’re really going to be talking about is kind of concussion and substance use disorders.

The big problem that we’ve had in the area of concussion – and that’s where most of my funding is now. So, I’ve got some funding from the NIMH, and as you can see on there, I get some funding from a couple of different sources. A lot in the world of sports. I do some work with the military and some with the NIMH. I get some funding from the CDC. But it’s looking at what is it about concussion? Is it important? One of the things that we see in the area of concussion is many people think we know a lot more about it than we really do. The problem is we know a reasonable amount about traumatic brain injury, TBI. We tend to think that TBI is kind of the same as concussion. It’s not. A lot of the recent work that I’ve done over the years is trying to educate people. So, what is concussion? And kind of how it’s the same but more importantly how is it different?

An analogy I use I called my Baron Sunburn Analogy. So, the question is how much do we learn about a patient who experiences what we call a full thickness burn? They are in a motor vehicle accident. They get caught in the fire. They end up in the burn ICU. How much do we learn about full thickness burn by studying patients who have had multiple sunburns? The answer is zero. Pathophysiology is different. The treatment is different. The outcome is different. This is what I think we need to understand in the area of concussion, because what we see — And I want to share some of the more recent data, some of the stuff that we’re doing in my lab and the lab I’m going to be running up in Canada, is we look at the data on TBI and we assume that’s what’s the same in the area of concussion. It is not.

What do we have to do? We have to study it. Dr. Angres is doing that. We were chatting this morning at breakfast about a longitudinal study of looking at it. I’ve spent a good deal of my time and effort in the world of sports and in the military with concussion. But one of the areas that I am particularly interested in now and I want to collaborate with good centers like this one is to look at what is the role of mild repetitive concussions in things like patients/clients with substance use disorders, domestic violence, and abuse? Kids not necessarily athletes. I’ve done a lot of work with the Egyptians looking at — we filed the entire Egyptian Olympic team looking at the role of ADHD in concussion. What we see is… So how many of the patients that we see will say, “Well, you know I’ve never had a concussion.” You mean you know you never fell down? What if they don’t remember or they don’t report? The key for today, one of the take homes for those of you who kind of zoned out here, play through and I’m sure you’ve had a busy morning. With no lights in here that might happen. We have to remember screening for concussion is an important part of understanding the patient. Is it the whole puzzle? Not at all. But it’s an important piece. It’s just like when we study genetics and genomics.

In the patients that we see there’s not a gene for depression, for substance use, for addiction, for resilience, all the important things we’re looking at. It’s not like the neurologist will have a gene for Tay Sachs or Huntington’s. That’s the difference between our neurology colleagues. What we see in our field as behavioral scientist is a whole bunch of genes, a constellation of genes. Each one may be describing a small amount of variance but that role of genetic influence is very important.

I think this is something so I started working–. My dad was an addiction psychiatrist. Way, way back when I was in high school, he had one of the first early treatment programs. I got very interested in the biology of addiction. What is it? No one comes into this world saying, “My life’s goal is to become the best athlete I can be.” That’s not there. We see that genetic loading where substance abuse runs in families yet for so many years it was viewed as flaw in your moral fiber. We didn’t understand the biology of addiction. Not that biopsychosocial and spiritual issues are unimportant but they are all mixed together just like we see with genomics.

We can identify candidate genes that help us identify a high-risk group. Just like we know — going back to my sunburn analogy — if you’ve got blonde hair and blue eyes you are at the high-risk group for having skin-related sun damage. Does it mean you’re destined to become a melanoma patient? No, but you are in the higher risk. Whereas people who are dark-skinned, dark-eyes are the lower risk but they still can get that. So just like with the sunburn, we know that no one dies with one sunburn. Of course, we all had a mild sunburn at some point. Unless you’re living in a cave somewhere. But what happens? If it goes away you don’t worry about it. It’s only been relatively recently that we’ve understood that there is an additive effect with sunburn. The more sunburns you get, you get the premature aging skin. If you get too many sunburns, you are higher risk for melanoma. But how many are too many? We don’t know. Is there a gene for that? Yeah, probably we are getting some genes but we see the same thing in concussion.

Now, what I’m interested in and what I want us to chat a little bit about today is that role of concussions and what does it mean for treatment. I’m going to try to keep this a bit more clinically oriented. I’m going to share a little bit of animal data just as proof of concept. But one of the things that I think is important that we as providers need to be looking at is what might be that role? Not only acutely but downstream effect.

There are currently 42 descriptions of what a concussion is. This is the one from the CDC. Since they fund some of my trials, I’ll put that in there. So, it’s a type of traumatic brain injury – and this is problem to me because people say, “Well, it’s a TBI – caused by a bump blow or jolt to the head or by a hit to the body that causes the head and brain to move rapidly back and forth. This is kind of distortion effect. This sudden movement can cause the brain to bounce around or twist in the skull stretching and damaging the brain cells and creating chemical changes in the brain.”

Two problems with that: (A) It’s too long. (B) In the beginning it talks about TBI. How do you differentiate that? I put that up there because they funded me and the feds like that, but I think the key here, the take home, is you don’t even have to get hit in the head.

I did an international survey. You could do that now with Google. It’s fairly easy. We looked at 14 countries. And we said, what do people really know about concussion? First of all, people think you have to get hit in the head. They also think you have to have at least some loss of consciousness. You do for a TBI but not for concussion. In fact, it’s fairly rare that you see a loss of consciousness with concussion. People just don’t remember.

I can tell you in the NFL, some of the most significant–So, I take care of the Rams and we do some work with the NFL. Some of the worst concussions we see, there was no hit to the head, but it was a shot to the shoulder and the head jolts. So, if someone’s at the bar and they fall off the stool, they land on their tush, that can cause and does cause a concussion. I take care of the Olympic team. Our pole vaulters. We have a big problem with mild repetitive concussion, not by missing the pit, but the impact of coming down on the head, even when they hit a nice soft landing which they do. I looked at a number of different sports. The key here is I think we as providers have to educate ourselves and people out there that “No. This plays a role in understanding, diagnosing and I believe in treatment.”

I have a slide that I think you’ll find very interesting about timing of treatment. This is one. I’m a member of this international consensus conference. This is a little shorter. I like this a little better. A complex pathophysiologic process affecting the brain induced by traumatic biomechanical forces. Little shorter but that’s what happens. We know now with concussion we can’t use the standard imaging techniques that we’ve used in the past. I can’t tell you how many patients I see – athletes, non-athletes—who say, “Oh, they sent me to the ER. They ran some routine testing and it was normal.” Since it was normal, then nothing happens. I said “Nah, maybe that’s not quite the case.” I live in Los Angeles. If you go out to the Santa Monica pier and look out the Pacific Ocean, you’re not likely to see a whole lot of fish. Does that then mean there are no fish in the Pacific Ocean? Maybe you have to look a little deeper. This is what we see with concussion.

Now, we can measure how the brain communicates. Certainly, in the addiction field, we know that communication is critical. Communicating with our physicians, our providers, our love ones, other people who are involved in addiction. What happens with the brain when you’ve been concussed is that alters that ability, that mechanical ability, to communicate with itself. So we have this white matter tracks kind of on top of this bushy grey matter. And that’s how the brain communicates. When you measure those white matter tracks, how the brain communicates with itself, we can demonstrate it changes.

What we are doing in some of our studies is looking at these higher end white matter tracks and gaining understanding how the brain communicates with other forms of advance imagine spectroscopy, which tells us a little bit about what’s going on as far as the core pathophysiology.

We know that if it’s real, then it’s got to be something that we can measure. Sure enough, we can measure this. We have this regulation of IM pumps in the brain, kind of the way the brain work. It causes this increase in energy demand in the brain so the brain kind of wants more but it’s getting less as a result of the trauma. We call this hypermetabolic state. We can measure this pretty reasonably well with spectroscopy, just the way of imaging the brain that can measure kind of energy requirements. We see this increase blood flow to the brain and we get this energy crisis. And now there’s this big issue and this has been well documented now on this area of the disruption of brain connectivity.

Now, why is this important for a clinician? Because this is going to have a direct impact on how our patients or clients are going to be able to respond to our interventions. Their ability to make good decisions, their reaction time. This is where a lot of research is going on now.

So, when we are dealing with someone who has had an impact on their brain from the use of substances, alcohol or any of them, and you add more on top of that, an individual who has had mild repetitive concussions that they may or not remember. We know there is a cumulative effect. We know that the earlier you have concussions, the younger brain is more sensitive, just like we know with sunburn.

If you talk to our dermatology colleagues, sunburns prior to the age of 8 are probably 2-3 times more significant for long term effects than sunburns after the age of 17, 18, 19, early 20s. The brain is the same way. It remembers. So even though the sunburn goes away, the more we have, we are increasing our risk. That’s the analogy that we need to understand with concussions. The more times people have had a mild concussion – slipped in the shower. And what do you say? I’m a little dazed. That’s a mild concussion.

What we need to work on, one of my primary area of interest going up to Canada, we have a fairly large data set is coming out with a good screener. A good clinical screener. We are not going to be able to send our patients to get this high-end expensive neuroimaging test but what can we as clinicians do to understand how to get data on that piece of information, like how many times has someone been concussed.

We’re working with Lenny Addler who developed the ASRS in the ADHD world. I just talked to Lenny last week. This is what the field needs because we have these huge neuropsychological barriers which are perfectly fine but actually in the concussion world, sometimes they actually induce symptoms. Patient will say “Hey, I got a little headache here.” Because we know cognitive demand can create that even down the road. So, determining return to play in athletes, return to duty in soldiers, return to school as I see a fair amount of NCA athletes get sent to me. These are important issues and these are clinical decisions that we have to make. We can’t rely on high end ivy tower studies. That’s what we’re trying to do. But where the rubber meets the road, how can we as clinicians say, “I think this individual is okay to go back full time or part time.”

I had to throw this in here. I have a whole deck of the different neuroimaging slides. This was done with sports-related concussions but we have DTI. These are beautiful images. The problem is other than being beautiful, what the hell do they mean? What we can say now is I’m smart enough to know I work with really smart high-end neuros from Caltech. Usually MD/PhDs, bioengineers. This is an older one. Now, we have these imaging techniques where you can actually see here’s the disruption.

Now, why I think this is important is because we all know the level of prejudice in our field as behavioral scientists and certainly, in the area of addiction. Is this a real disease? Just choose not to drink as if it is that easy. Maybe one chooses to take that first drink or use the first time, but we know these are diseases that affect the brain with many other factors going on. Many factors. This is why I think psychotherapy is important. Support. We know the importance of long term treatment because treating addiction isn’t like treating an infection. You want to push an antibiotic and you’re fine. No. These are chronic diseases because something has happened in the brain.

I believe it has a lot to do with the brain reward system. So, I’m a big fan of Ken Blum’s work, and Mark Gold. I’ve done a little bit of work with these folks in understanding reward pathways from the brain that then triggers. Because I think this idea of punishment, we all know from Psychology 101, it’s the reward pathway that drives behavior far more than the punishment pathway. Knowing that it might screw up your relationships to lose your job or everything else, that doesn’t really carry the same amount of weight and driving behavior as that reward.

Certainly, Nora Volkow has made a very . . . You know our head of NIDA, a brilliant woman. But driving what is it that makes this feel good. If it feels good, we’re likely to do it again. Whether it’s loving chocolate or being addicted to sex or shopping. That feeling of good. The brain is kind of wired in an interesting way that we go after things that make us feel good. People who get sick when they drink or use in general tend to not do it. I don’t drink. I’ll take a sip to be social for no reason other than I know I’m going to feel worse even with a couple of sips. So, I might have some native American genes or Chinese genes somewhere in me that have some dehydrogenase deficiencies, but there is no reward for it. If there is no reward than likely the behavior goes way down.

What do we do as clinicians? We deal with people to try to give them rewards in other areas. Give them support. Have them understand. Change the way they think. To me, a patient says, “I can’t stop thinking about using.” That’s a patient we all know at very high risk because something is going to happen when they are going to seek that reward. So, what do we say? And that’s why the treatment of the folks that we see has to be longitudinal. It can’t be an index episode. At any program, “Oh, we’ll train for 28 days and then send them out with no follow up.” We know what’s going to happen. We’ve seen it time and again.

So, what are some of the common symptoms now? Interestingly, how many of these symptoms do we see with patients when they come in when they might be intoxicated – a little confusion, a little amnesia? Big thing here we see with the athletes is, “I feel like I’m in a fog.” You’re slipping your form on the ice. We don’t have a whole lot of ice in Los Angeles, but I lived in Wharton, Philadelphia for a long time. We had our share of ice. When you just feel a little daring or you’re a skier. You take a bad fall. You just kind of–Have you ever see that? You just kind of try to shake the cobwebs down. Well, that’s a neurocognitive effect. We can measure it.

John Avendon and I worked on some very simple computer models a number of years ago. That immediate reaction time, it slowed down. People say, “I just can’t.” Now, that post can cause problems and go beyond. When it goes beyond 7-10 days, then we start to worry a little bit. The majority of initial symptoms are resolved within 72 hours, most within a week. When it goes beyond that, then we get in to that what we call post-concussive period. We’ve been able to demonstrate and we’re looking at it now that there are a number of things that dramatically extend that post-concussive period, that time when you’re still experiencing some level of symptoms—substance abuse is one of them, gender affects it, too.

One of the things that I always ask my research colleagues, “With the women you’re seeing, ask the difference between the luteal phase, those two weeks before the onset of the menstrual period versus the follicular phase, that first two weeks kind of after the period stops.” And what we now know and there is a number of interesting papers and I had been involved with one. I had arrived in NIMH when I was deputy clinical director there of behavior endocrinology. That luteal phase, those last two weeks before the onset of the period, for about 20% of women, their blood alcohol intolerance goes down substantially. What we’ve now demonstrated is in the area of concussion. I’ll be able to file this because I take care of a number of female athletes. If they get concussed, take a little hit, during that two weeks before the onset of the period they have more significant symptoms and the post-concussive period is longer.

So, we now know that women who have had one or two or three sports concussions were very conservative getting them back when they are in the luteal phase. Why? Because we know they are at higher vulnerability. Now we are able to identify why that probably is. So, for those of you who are interested, it has probably to do with your effective compound called allopregnanolone (3α 5α tetrahydroprogesterone). It’s a naturally occurring metabolite. A progesterone, normal female hormone. That metabolite probably is playing into why we are seeing this. It helps us to understand some of the core pathophysiology with concussion.

So again, you can have loss of consciousness, fairly rare seizures as almost as never but problems with coordination. What do we see here as behavioral science: irritability, nervousness, emotional liability? Have you ever seen that in our patients when they are acutely intoxicated or coming off when they are in acute treatment? Patients a little bit more emotionally labile. It’s like their emotional nerves are a little raw. It doesn’t take much to set them off, uncoordination, poor concentration.

Now, the problem that we have in looking at substance abuse patients is how much is the result of their intoxication or withdrawal state versus how much might be related to having a mild concussion. They slipped, they fell. Whatever it might be. They took a jolt to the brain. It turns out you can’t tease those apart but we do know there’s an added effect. How we know that is from animal data. I think I threw in some of that data to share that with you.

To me, for every question, you’ve got to understand why is that. I used to ask myself why is it that people end up having an issue. Not everyone who drinks ends up having a problem with the substance abuse disorder. What’s different from those who have it? I had some interest early on in eating disorders. Why is it they can have like 78% of adolescent and young adult women were reported being concerned about their weight going on a diet and yet they only have 2-5%, depending on who you read, who are going to develop a clinically significant eating disorder? What’s different? Analogy is important because biology is in the context of psychosocial and I believe spiritual place in there absolutely as well.

I did some work a number of years ago. This is a cartoon because the images are unfortunately impossible to make sense of. But it turns out that the shine proteins which are scaffolding proteins within the neuron. Why I put that up there is now we can say “Yeah, there is something going on.” And it makes sense. If we think about it, if you disrupt kind of that scaffolding that’s holding something together – From an emotional perspective, if we disrupt the emotional supports that hold us together, our relationships go to hell. We are having problems at work, with our kids, whatever. When those things are shaking, that affects our ability to function to communicate. We can take it all the way back to the microlevel.
We’ve identified Jeremy Lins. I probably was just looking at this shanty, just these scaffolding proteins. So, sure enough at that tiniest level when you disrupt those, that then leads to this problem of the brain that believes it communicate with itself. That’s why we see these clinical phenotypes, the confusion, the irritability, the lability.

One of the things I’ve gotten very interested in recently is the wall. And some of you might follow through from the psychiatric and the medical literature is the role of infection, the inflammasome. I’m not talking about you get a cold or you get an infection but it turns out that the inflammasome was just a measure of the way the body fights infection. It turns out that’s a pretty darn good biomarker. And what we’re seeing in concussion is this issue with this inflammasome which is a neurotransmitter. It’s not just with infectious disease. Guys like Chuck Raison and Valerie Malitek have really looked at the role of this in mood disorders, in depression, and anxiety,y even in psychotic states.

One of the labs I worked with at USC in my area is we’re looking at specifically at that inflammasome that’s in the brain that functions as a neurotransmitter. We’ve identified a compound called Trim – 9 which modulates that inflammasome. It might be one of the first treatments for mild concussion. That and a compound called APC. We’re looking at that now.
If you understand the core ideology, maybe we can develop… If we understand that relationships are important to how someone is thinking, maybe we can deal with relationship issues. So, it’s no different at the macro clinical level than at the micro level. We need to understand how they work together. Why is it that supportive psychotherapy works? And it does work. Why doesn’t it work in everybody? Well, it’s the $64,000 question but we know from the work of Dr. Angres and Dr. Gold and many others who have done PHP is that if you stay engaged in treatment and in monitoring, the likelihood of maintaining sobriety is way up. If you just get through and get sober and then drop out and don’t have those, the likelihood of sobriety is pretty damn slim. We can understand that a bit from this micro level.

I’d like to save some time for some questions and comments. You’ve all taken your lunch hour here, maybe we can dialogue a bit. This is not that old data now but looking at the effects of alcohol on pre-TBI in rats. Now, unfortunately most of the data that we have looking at TBI and concussion has been done in rats and mice. So, when I first started looking at it, so what is the effect on mood and behavior and cognition? You’re not going to say “Well, no IRB in the world is going to say, “Oh we’ll, bring in some rats and we’ll just whack them over the head and then we’ll just follow them long term.” The problem is doing that prospectively is expensive. That’s what we’re doing now. We’re following groups prospectively but you can’t do it with rats. The problem with rats is if you want to study concussion and not TBI, it ain’t so easy.

Most of the literature they talk about rats where they open up the skull and literally concuss the brain in an open area or they’ll do something. That’s a TBI model. I wasn’t interested in TBI. I’m going to let our neurology and neurosurgeon colleagues take care of that. I’m interested in concussion because most of the concussive symptoms are what we as behavioral scientist see – mood, affect, cognition, motivation, organizational structure, executive functioning. Those are the things that are kind of in our wheelhouse.

So, it turns out we figure out others. We take four grams and you drop it 10cm on the rat or mice, you’ll stun them but you don’t fracture the skull. You don’t create what we would probably label as a TBI. Something that you’ll measure with the Glasgow coma scale. They get stunned so we can then measure. We’ve done this looking at if you do repetitive concussions where you’re not creating a TBI but you are stunning them, the equivalent of what we would call a concussion. We can start to understand some of what’s going on. That’s why I started to talk off with the problem that we have is this issue of we take TBI there and it isn’t the same in concussion. Answer is probably not. Although there is an added effect between the two. The presence of acute alcohol intoxication at the time of TBI.

If someone is drunk, or the mouse, and we can look at preference here. Prevents the resolution of no inflammation, the inflammasome. I got very lucky. I wrote about it. We didn’t know this data. And it’s always better to be lucky than good. I’ve been much lucky than I am good but it turns out that it actually supported a theory that we have a number of years ago. It prevents the resolution of no inflammation 24 hours post. So, here’s a proof of concept that tells us and our patient population if they in fact have intoxication, this was done with alcohol, it does have a biological effect on what’s going on in the brain. We know that the inflammasome now is probably one of the hottest things going in understanding the biology of mood disorders particularly depression. This is not new data. Chuck Raison has probably been doing this stuff at least a decade now.

Interestingly, what we see is modulation in some very particular parts of that inflammatory reaction. That’s very complicated. So for the physicians in the room, if you remember going back to understanding kind of the cascading of events with inflammation. You got chemokines and cytokines and lymphokines and a whole bunch of other things. It turns out the ones that are really important and would study all of these are various forms of these. There is actually a couple more IO9. This is the one that we’ve shown are associated with alcohol use. Interestingly, the Trim – 9 that we’ve identified turns out to have a direct effect exactly on this.

We think the closer we get to understanding one piece of this puzzle, it’s not the whole piece, we have to be very cautious not to come overly reductionist. Say “Oh, it’s just this. Let’s do this. It’s going to be fine.” Not at all. Successful treatment as we know, as you all know probably better than anybody in the addiction field, is integrated care. It’s physicians. It’s therapists. It’s everything we do. It’s involving ourselves in all the different check marks. It’s truly that biopsychosocial-spiritual approach.

Alcohol slows the writing reflex. Now, the writing reflex in rats is kind of the equivalent of coordination in humans. Again, I think we always have to be cautious to not make the direct correlation. These are proofs of concept. But if you talk to somebody, I can see it in football players all the time. They’ll come out and they’re just a little bit slowed.
The study we’re looking at now, we’re looking at high school football players. We take a video of every practice and every game. We have triangulated cameras so we can measure that. What we’ve demonstrated and continuing to follow four years prospectively is once they’ve taken a good hit, the likelihood of getting injured or concussed goes up because their reaction time slows them down. That’s not to slow a lot.

I’ll never forget a famous football player here in Chicago, Oliver Peyton, one of my favorite ballplayers of all. He was not a big guy. I mean he was muscular as hell but he was like 5’9”. But he rarely took a good hit. And if you look at tapes – and NFL Films used to be in Philadelphia so I used to get to watch that. Right when someone was coming at him, it was sweetness, he would just at that last split second would put just enough speed. He’d get hit but never took that big hit. And I think that’s why.

I had an interest in boxers, so I did a little bit boxing for a lot of years. Joe Frazier—some of you might remember Joe. Joe and Marvis were patients of mine. Joe passed away, so I have permission from them not filing any HIPAA. But if you look at good boxers, a good boxer – and I had to get out of it because I said, “How the hell can I work in a sport where I’m studying the event?” I said ethically it’s not right, so I haven’t done Olympic boxing for quite a number of games. I worked most of the Summer Games. But if you look at the tapes just at the time of impact, a really good boxer will get enough so it’s a grand . . . Rarely will they take that direct shot. And turns out that there isn’t a genetic role for how the brain responds. So, what they used to call tough boxers – Martin Marciano, others, you know they could get pummeled and they never went down. So, oh, I like that. That person’s really tough. I said, “Nah. It’s not toughness. These people are wired different.” But we used to call boxers who have what they call the glass jaw. They take one hit and boom they’d be out cold.

There’s some genetics because the brain – we get back to that scaffolding proof. The brain is wired differently just like blond hair, blue eyed. They don’t need as much sun exposure to get burnt as someone who’s dark skinned. And there’s a biology to that. So, this is just some data. The only thing that’s important to look at here, these are the ones with TBI. Here, smaller is better. If you have alcohol and TBI, it’s significantly different here than dextrose and other things. These again are all rat models. But each one of these we’ve been able to demonstrate that alcohol place a very significant clinical role.

I’ve been interested and we talked a little bit about the role of the younger mass. Now, why this is important is I believe that in the area of substance use disorders, those individuals who start abusing at an earlier age are wired differently. When they start to use, that different wiring gets exacerbated. So this plays into the genetic loading. If someone has a lower genetic threshold and they start using earlier, that downstream effect is magnified. This is where we used to have — I’m sure you’ve seen these. In my experience in dealing with it, parents would be distraught about “What I did to my kids. If I’d have been a better parent, they wouldn’t have this adverse outcome.” They blame themselves.

I said “Well, at least at one level you can blame yourself for passing your genes on. I don’t know if there’s a way to get around that. But, yes, that’s true.” Just like with ADHD. High genetic loading. Very high, about the same as eye color. So, parents are you know, “If I have been a better parent, my kid wouldn’t have ADHD.” We know that there’s a higher incidence of substance use with ADHD: 50-60% of substance abuse patients, depending on who you read, have that executive functioning and all bunch of the things, but the genes play a role. Not the only thing. It should never be an excuse but to understand. And this is exactly what we’re seeing.

The age of onset of use and abuse I believe is tied into the genetics, and then certainly the psychosocial. If you’re hanging out and all your buddies are drinking and using and you want to be a part of that group as a young adolescent, that’s a risk factor. As opposed to your peer group or you know the jocks or whoever who aren’t using so much. Not that the jocks don’t use. They use a lot. But it’s this combination of factors. As good clinicians, we have to be able to as best we can address all of them. Not just pick the one that makes the most sense to us. And we all can’t be expert in everything so this is why I believe successful addiction treatment requires physicians, caretakers, social workers, family members, to get involved. This is really a systems approach.

If we don’t do those and you have a wonderful program here with lots… You know you’ve got the full continuum covered. If we leave one of those pieces out, the likelihood of success is going to go down. We know that biologically at a micro as well as the macro level. This is getting it back into this reward pathway. What we see is animals with adolescent traumatic brain injury. Some of this with concussion had significantly greater preference for cocaine paired environment. This is the one study I could find. This was 2017 paper, a fairly recent one, looking more at a way from the alcohol story.

So, what we see, and again, proof of concept here is that concussion or TBI plays a role in that longitudinal course of drug and alcohol use. So that if we know and we identify early on, it should be part of our initial workup. Again, one other piece of data. How do we escalate? Because the estimate has you had a concussion was to say no.

I had a ballplayer. Just a quick vignette at USC. So, we filed the USC football players. We have a pretty good football team at USC. They put a lot of pride into their football, the Trojans. We were doing a prospective study. We used swimmers, because I’m a former swimmer, as our control group. Because these were elite athletes, they trained a lot. We figured there was a decent clinical paradigm.

We had one of our swimmers who came out with all of the work up who was actually looking worse than our freshman football players. Now, you don’t go to USC and play football unless you’ve been playing probably since you were five or six years old Pop Warner. He said “Well, I’m going to CF. I think I’ll go after the football team.” That ain’t happening. They only recruit the five-star recruits. They’re pretty accomplished before they even get there.

This one swimmer came up and, what the heck, he was throwing “What are you doing to me here?” So, I interviewed him. I said, “You checked on here that you’ve never had a concussion.” He said, “No. Never had.” I said “Tell me a little bit more. Where are you from?” “Well, I’m from Minnesota.” I said, “What do you do for fun in Minnesota?” “Doc, I’m a swimmer. I don’t swim for USC unless I was an All American.” I said, “That’s all you did was swim?” He said “No. No kid from Minnesota doesn’t . . . you know. On weekends when I wasn’t swimming, we’re playing ice hockey.” I said “Ah, ice hockey. On a team?” “No. I couldn’t really skate, but if I want to have friends I had to go out.” I said “You never played ice hockey and kind of like baby fell down or took a hit and you felt a little woozy? Maybe got a little sick to your stomach?” He said, “Every freaking weekend.” He had probably had more concussions than my NFL football players because he’s playing both.

So, what is the impact of that? Sure enough we’ve seen this additive effect over time. Based on genetic thresholds the effect can be greater or a little less. So again, multifactorial. This is just some data. You’ve got to do the control so we looked at – Well, maybe it’s just giving the animals a substance. So, if you look at sailing, the exact opposite.
So, cocaine from an animal model, clearly has an impact on a variety of types of symptoms that we would treat as clinicians. Now, this is what I find particularly interesting. This was in our paper from last year. It’s this window of intervention post TBI. I think we need to start looking at concussion. The question is what does it mean clinically? How does this data help us provide better care for our patients, for clients that we’re seeing? It turns out that again, I hate these broad words like that but they really demonstrate that post TBI, if someone is a substance abuser, you’ve got about one month when the use tends to drop down.

So, here’s what we see here. This is at one month. They’re down here. There’s more abstinence. At one month, they’re not using so much. You look at them at six months a year and then three years and five years. It’s still a little bit better than here but it drops down. Now the clinical implication of this is we have a window of opportunity and it’s in that first month. So that first month post-concussion / post TBI we really should be looking at how do we engage someone in treatment there. Not that you can’t later on but if we identify concussion we have a window where our opportunities are likely to expand if we can really intervene at all levels at that one moment. What would be fascinating to see is: Is there a difference in response to some of the medication-assisted treatments that we use? No one studied that yet. We need to look at that. We know that not only if your brain isn’t somehow affected by drugs or alcohol. Put them together. But the likelihood of getting concussed goes up. But the results of that concussion are expanded. The more you have, there is an additive effect.

If someone is drinking and they’re getting jostled around at the bar and they don’t even remember it, they’re blackouts. How the heck can we get a good history? I think we almost have to assume that this is a fairly reasonable likelihood. Now, what does that mean for treatment? I think that’s where we’re at right now. I think what we know is that here’s an important variable. How we come up with a treatment strategy that will somehow modulate that. That’s a really important clinical issue. And what’s it going to require is researchers doing the translation research working with programs like this where you have a big clientele. It’s not about just answering science questions, it’s about providing the highest level of care.

What can we do to expand the period of sobriety and hopefully expand it for the rest of their lives? Because that’s the end game here. How do we keep people from using? We know that if they’re not depressed, if there are social situations, a little bit better. If they have supports, we know that’s an important factor. I think we have to pick all these things together because again as substance use providers we know that there’s not one answer.

A size 10 shoe is a great shoe if you are a 10. Not so good if you are a 9 or 11. So we need to get, and I think this is where we’re kind of heading a little bit more, is, yes, there are kind of certain commonalities that are really important. But I think we’re going to be moving a bit more towards this personalized or precision medicine. Is the same treatment strategy going to work the same in every individual? I think the answer is probably not. Does it mean that the role of support in groups and stress reduction strategies and understanding the biology of resilience–? People have different resilience factors and we can actually measure that a bit biologically as well. What constellation of genes might actually make us a bit more resilient just like we saw with our boxers. But how do we understand this in the context of creating a treatment strategy that gets us to our end point of long term sobriety. I think the biology is just one way of maybe giving us one of the piece of the puzzle. You know concussion reduces alcohol tolerance. You know this was published a number of years ago, so ICD-10 list, reduced alcohol tolerance is one of the symptoms for post-concussive syndrome.

I think this were maybe a little bit off. But I think there’s clearly a relationship between an acutely intoxicated brain or one that has been exposed to intoxicants over a period of time and the relationship and the downstream outcome. Even some things like we talk about those scaffolding proteins, those scant proteins. I believe there’s probably some impact on those with chronic intoxication but it becomes kind of a chicken and the egg phenomena. Which came first? Well, as clinicians we don’t really care. What we’re concerned with is what do we see now? What can we do to intervene?

This literature is scarce but we got a change that. We as providers and as clinicians, we need to work together to understand more because I believe this role is an important one. It’s not like it’s the only thing we should be looking at, but I think to not look at it and to not appreciate what it might be doing in regard to neuro cognitive functioning, with psychosocial functioning, to not at least consider this as a factor we’re not doing right for our patients.

Heavy drinkers and illegal illicit drug users did not show increased risk for post-concussive syndrome. The problem is, though this was a bad study because — the reason I think it was bad is because people look at this, it’s an older study, and they go “Oh, you know.” The best predictors for this post-concussive syndrome are skull fracture, elevated serum S1RP. This is actually one of the biomarkers. Technically, this protein should stay in the brain. If it gets out to the system, it means something happened that disrupted that blood brain barrier. This is one of a handful of biomarkers, gene factors, a whole bunch of them that we use as a potential biomarker – dizziness and headache. The problem with this is people look at this data and say “Well, that’s the same with concussion.” No. We don’t know. We don’t know.

What we do know is that there are probably a series of predictors. Wouldn’t it be nice if we as clinicians could identify what patient population are going to do a whole lot better with predominantly maybe a psychotherapy, a non-medical? What group of patients are going to benefit the most from medication assisted treatment? Treat every patient beyond MEP. Maybe. Maybe not. We don’t know.

I think what we have to do is we need to advocate for our patients by saying we need to identify how to provide better personalized precision treatment. Not that every treatment strategy is going to be completely different because I think there are certain things that everyone can benefit from, but in a Venn diagram of overlap there are probably some issues that some patients are going to benefit more from this than from that.

I’m thrilled to see that now the world is starting to accept the fact that these are brain diseases and that maybe it makes sense in some patients to have medical interventions. But hopefully we never get to the point where we’ll say, “We’ll just come up with the right pill. Give me the right med and I’ll be fine.” Remember from the old Prozac, I guess it was a Zoloft commercial a number of years ago. You’d see on TV and see the little bouncing pill. A patient is going to say, “Doc, I think I’m about a quart low in my serotonin. So just put me on a pill and I’ll be fine.” This reductionist view that if you just do this. And to me it’s a way of denying the fact that this is very complicated.

I mean we talk about what three trillion connections in the brain, and the brain has backups to backups of the backups. Which is why I’m always so humbled because people say so I boarded in brain injury medicine. They say, “You know all about the brain.” I say, “No. I don’t.” What I know is that we’re scratching the surface of understanding but if we don’t keep digging we’re never going to be able to appreciate how we might be able to intervene in a way that’s going to get us to where we want to be with our patients. What if sort of cognitive impairment is . . . Here we get into interesting things. You get into things like executive functioning, decision making. It can be on a macro level, the ability to respond from some neuro psychological testing to something a bit more. What I’ve seen is a very interesting overlay between what we see in adult ADHD.

Guys like Tom Brown and others just came out with a book a couple of weeks ago looking at executive functioning in ADHD. I think this is an important role in our substance abusing patients. Those 50, 60 whatever percent we believe is out there that have it, this is a group that’s going to need a different or at least a modified form as opposed to those who don’t have that. I’m getting the question should we be using stimulants? What’s the risk of a stimulant with someone who has ADHD? I mean these are scheduled II drugs because they have abuse liability. Should we be putting them on Adderall or whatever methamphetamine? Or should we be going about . . . ? These are questions that we need to talk about. This is where we need to work together to help our physicians. We need to educate the primary care providers.

I think this is an area that really we can do what… you know we’ve seen this explosion of the opiate addiction, pain medications. Doctors in many ways are to blame for this. Why? Because it’s been bad education. We need to get out and educate the community. We need to educate doctors. I think we need to educate family physicians. I was so thrilled to hear Dr. Angres was telling me how closely you work with your internal medicine primary care group here. Because that’s really the linchpin.

Most folks are seeing their primary care doc hopefully, rather than ending up in the emergency room. So, it’s our role as experts in this field of addiction that we make sure that where the patients are showing up in the front line, whether it’s an emergency room or the primary care offices, that they understand what they should be asking about and we work together with them. That’s the way TBI would be less symptomatic and possibly not sufficient to discourage future substance use. So again, this is a little bit older paper but looking at substance use is known to be a risk factor for TBI and vice versa. It’s bidirectional.

So where do we go? I think we have to do prospective longitudinal trials. Again, at breakfast today Dr. Angres was sharing with me that you’ve got a really nice fairly large cohort prospectively following people. Because how do we understate? We can’t look retrospectively. We can’t look backwards. How many people saw the movie Concussion with Will Smith? It warms my heart that most of you saw it.

I got a call from Ridley Scott before the movie came out. I did a movie on concussion that was based on 35 years of research. Ridley Scott called and said, “We’re going to take a look at the script.” I looked at it and I said “You know there’s a couple real serious errors in this thing.” I made some comments on the script that he sent back. He said “Well, doc, you know we’re not really making a documentary. We’re trying to make money in Hollywood.” I said “Then, don’t make it out like it’s a documentary.” Because they don’t talk about Mike Webster who was the key figure in there. Mike Webster was a center for the old Pittsburgh Steelers. They didn’t talk about the fact that he had been in and out of foster care for 10 years. He’d been a substance abuser since he was 12. They made it sound like everything that happened to him was a result of his concussions.

Now, did concussion play a role? Without a doubt. But to say that it was only concussion, I thought was irresponsible. I had people coming out. So it was premiere in Hollywood. I’m sitting with Will Smith who is an old Philly guy. His kid played football, prep school football. And moms just say “Geez, man. I feel terrible. I let my kids play sports. They are playing soccer. They are playing football. This is terrible.” That shouldn’t be. What it should be is how we make them safer. But understand the good that can take place in being engaged with organized sports.

I’m very involved with the national high school coaches’ association. I’m training coaches how to make things safer. But let’s not throw out the baby with the bathwater. Because someone gets melanoma, should we say, “No, don’t go out in the sun anymore?” That has more significant health effects. But we should tell people if you’re going out in the sun and you’re fair skinned, put the SPF 30 on. Don’t go out in the middle of the day. If you go out, have an umbrella. Be safe. I remember when cars without seatbelts was an option. Now you get a ticket if you don’t wear one. I’m showing my age here a bit now.

So how do we make it safer as providers? These are the things that I think we need better public and professional education. I mean the word doctor, not MD. Those series are actually the Greek word to teach. It’s not the diagnosis. It’s not to treat. But it’s to teach. I think what we do as providers is we need to get involved with good professionals educating ourselves and the public.

My thesis work and my education degree was in public mental health literacy. It tends to stink in most parts of the world. People don’t — they understand that clean water is good. You should wash your hands. Nutrition you know. Sleep is important. But very few appreciate the role of mood and anxiety and other things that is the bread and butter of what we do. We need some better reliable biomarkers. And why that is so we can make better decisions on who should be going to this track versus that track. This will help us in a lot of ways. There’s reasonable amount of work going on in this area.
Public policy should be based on solid science not on what’s good for the politicians. We see this all the time. You know what makes for good political news isn’t necessarily what’s best for our patients. So, we need to focus on making sure that we are enlightening our politicians who ultimately might be affecting funding and insurance companies. It’s not, you know. What’s really best for the bottom line is probably to provide good quality long-term care. But there’s a savings by providing longitudinal care as opposed to “Well, it’s cheap. We’ll just treat them here.” No, because they’re going to keep rotating through.

I think we need to get involved with the political scene and educate politicians and public policy makers. I do a fair amount of work with ministers of health internationally to try to say this is why I need to spend a little money to develop at least some modicum of treatment for these folks with a brain disease that happens and manifests itself with an addiction. Again, I think we need to get medical students and PA students to nursing students, the social work students, we teach a course at our School of Social Work at Southern Cal that everyone is part of that treatment team, needs to be on the same page and understand what it is that we know and how we can and must work together to provide the best treatment.

For those who are interested, everything I shared has been referenced here. I’ll keep this here but… I know we’re almost out of time but some questions or comments or challenges. I mean usually when I go–. I presented at the APA a couple of weeks ago on advanced ADHD and we were just chatting. There is always somebody who feels the need to either give their own mini-lecture or to challenge you. I always enjoyed challenges because sometimes a good challenge gets you to think. You know what? You’re right. I’ve never really thought about that. I need to. We need to as a field. We all need to work together. We just have a few more minutes. I don’t want to hold you up from your busy days but questions or comments or challenges…

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Positive Sobriety: The Book
Daniel H. Angres, MD

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