Articles, Blog

“What Science Can Teach Us About Prevention/Diagnosis/Treatment of AUD”

August 24, 2019


[applause] GEORGE KOOB:
Thank you, John Carr. It’s a pleasure to be here. I actually was in
Salt Lake City in April and we did Capitol
Reef, Bryce Canyon, and Zion. And it was delightful.
Highly recommended. If you’re like me, you never go to any
place where you live. But visit Utah.
(Laughter) On a more sobering
note I have recently heard Angus Deaton give us
a talk on this issue and there is a phenomenon
that we’ve been recognizing both at the NIAAA, at the National
Institute on Drug Abuse, and the National
Institute of Mental Health, which is that there is
a decrease in mortality in many countries in the world, but there is an
actual increase in mortality in a subgroup of Americans, particularly those age 45
to 54, many of them are white, Anglo-Saxon in background. And you can see
that on the yellow line. And what contributes to
this mortality are three major, four major things,
but three of them are relevant to alcohol and
substance use disorders. One is poisonings, which would
be overdose, one is suicide, which has to do with
what I’ll tell you about the dark side of addiction, and the third
is chronic liver disease. And we know now that
alcohol is responsible for about half of liver
disease in this country. And we’re seeing shifts
in the age of individuals with onset of liver disease, and I’ll speak to
some of the things that we attribute that to, one of which is
on the next bullet, an increase in the
intensity of binge drinking, emergency department visits, and hospitalizations
over the last 10 years. And so a conservative
estimate is that there are at least 15 million people
with an alcohol use disorder in the United States. And that’s, like I said, a relatively
conservative estimate, and the cost is of
course in billions of dollars. And so I often say
in public lectures, and when I go to
down to Capitol Hill, that alcohol is the
elephant in the room. We do have an opioid crisis, there is absolutely
no doubt about that, but there is pretty
good evidence that alcohol is lurking
somewhere in the shadows and probably accounts
for, or contributes to, at least 15 to 20
percent of opioid overdoses. And then finally I think I’ll
speak to this in some detail, but less than 10
percent of people with an alcohol use disorder
get any treatment whatsoever and less than 4 percent
actually get a pharmacotherapy. So the charge of the NIAAA
is basically to fund research on the mechanisms
of alcohol action, the diagnosis, prevention, and
treatment of alcohol misuse, and enhance the public impact
of NIAAA-supported research. And what I hope to
do in my talk today is outline with you where
we’re working in these areas, what we’ve done, and what we’re currently
considering as high priorities and moving into. We are the largest funder of
alcohol research in the world. So this is my talk,
you’re going to get a lesson in the
neurocircuitry of addiction because it’s one
of my first loves. But I’m going to
use it as a framework to describe many of the things that we are
doing in the Institute based on science to
further our mission of improving
diagnosis, prevention, and treatment of
alcohol use disorders. And I will also
talk about the liver. So I’m going to move, you’re going to get a
little bit of a neuroanatomy, neurocircuitry
lesson for a brief moment, and then we’re going
to move to prevention, diagnosis, treatment, and
some of the emerging challenges that we face at NIAAA. So let’s focus on
the neurocircuitry of addiction for a minute. If you’ve heard me give
this talk before, it’s okay. Every time I give
this talk at ASAM, the American Society
of Addiction Medicine, somebody comes up
afterward and says, well, Dr. Koob, I’ve heard
you talk at least six times and now I think I’m getting it. (Laughter) So what is addiction? So everyone here would define it
probably in some different way. But most of us would agree, a
chronically relapsing disorder characterized by compulsion
to seek and take drugs or stimulants,
loss of control, and intake. But I have a Koob add-on, and that’s the emergence of
a negative emotional state, dysphoria, anxiety, irritability when access to the
drug is prevented, and I define this as
the dark side of addiction. I’m going to emphasize this because it feeds back to
that first slide I showed on the despair and
I think it’s an area that we’ve
neglected in the field. So over the years,
myself and many others, much of the
conceptualization on this slide comes from my collaborative
work with Nora Volkow, the director of NIDA. I think she and I always have
a review article being written. In any event, over
the years I think we have largely from my perspective
from social psychology, not from rat work, but
from social psychology, from Nora’s perspective it’s
been through imaging studies, some of which some of you
have contributed to mightily, we’ve identified
three stages for addiction. And these are arbitrary. They weren’t handed
down from Mount Olympus to Moses on stone tablets. You know I said that, I heard
a little titter out there. I said that at an ASAM meeting
and two priests wrote me and said I needed to
take religious studies. (Laughter) It’s an oxymoron. Okay? Mount Olympus had
nothing to do with Moses. I think it was Mount Arafat
if I have my knowledge memory. Anyway, the three stages:
binge, intoxication; withdrawal, negative affect; preoccupation,
anticipation or craving. These mediate three
domains of addiction. Incentive,
salience; reward, deficit. Stress surfeit, and
executive function. And we can now argue, I think from an
extraordinary amount of work, that there are
three major circuits that mediate these
three major domains or functional
domains that go wrong in the
pathophysiology of addiction. So let’s drill down very
quickly in my quick overview. The basal ganglia represent
many of the neuroadaptations that take place in
the reward system. Here’s my favorite
Eric Nestler diagram that I’ve probably
showed more than Eric, describing the fact
that opioid peptides and dopamine converge
on the nucleus accumbens to make you feel good, but they also
converge there to mediate the rewarding
effects of drugs and abuse. And this is one of the circuits
inside the basal ganglia that change as you engage
in the addictive process. We know that the changes now, many of them are
neurotransmitters and molecular changes, but
they’re also circuitry changes. And so as the drug-seeking
becomes more habitual we know now that the ventral
part of the basal ganglia gets taken over by the dorsal
part of the basal ganglia and their corticostriatal,
palatal, and thalamic loops that get engaged. I hope you’re impressed
that I remembered that. But that’s the
binge intoxication stage and there’s
enormous, like I said, enormous amount
of basic research feeding into this ongoing. But another part of
the addiction cycle that I personally have worked
on now for about 30 years is what I call, as I
said, the dark side, the “withdrawal/negative
affect stage.” And this is
characterized by withdrawal. But I focus more on the motivational
parts of withdrawal, like dysphoria,
anxiety, irritability, malaise. And we know now that there are two major
changes that occur. One is you lose that reward
system I just told you about, the dopamine
system is compromised, but we also know that
you gain a stress system, a whole series
of stress systems, and they’re
illustrated on this slide. And I could literally
spend an hour telling you all the work that we’ve done
and many other laboratories showing that the
neurotransmitters on the left up
there are actually activated and sensitized
during withdrawal. And some of these persist long
into protracted abstinence. And probably you don’t
know this, many of you, but there are buffers
to these stress systems. These are
neurotransmitter systems that actually try to
return you to homeostasis. But they can be
compromised as well, such as neuropeptide Y, which is a very powerful
anxiolytic in animal studies. And then there’s an enormous
amount of work ongoing. This is a very hot area. Steve may talk about this a
little bit more in some detail, Steve Grant, when he follows me. But we know now
that there are circuits in the frontal cortex that
control this reptile brain that I’ve been talking about. They control the basal ganglia and they control the
extent of the amygdala, which is what I showed you on
the immediately previous slide. And probably one of
the major transmitters involved is glutamate, modulated in both
ends of the circuit with GABAergic systems. And like I said, there’s a lot of emphasis
on trying to dissect out how the prefrontal cortex,
both dorsal and ventral, controls these urges,
cravings, desire for the drug, long after you’ve gone
through acute withdrawal. And I’m not going to
show a lot of data today, but this is one of my favorite
slides from Rajita Sinha, and it basically shows you that the smaller the volume
in that prefrontal cortex in individuals who
are alcohol dependent or have a moderate to
severe alcohol use disorder, the smaller that volume
the more quickly they relapse. So they lose their
ability to resist relapse because they have an
underactive prefrontal cortex. And you’re welcome to look
up this paper and examine it, but it really is compelling. So that’s my whole lesson. It’s a background.
It’s a framework. It’s the framework
that guides my thinking not only for my laboratory, which is by the way in the National
Institute on Drug Abuse. I still have five
postdoctoral fellows working. But it also guides our
conceptual thinking at NIAAA on everything that’s focused
on the central nervous system. And you know the
argument is that there are multiple
ways to get there. There are multiple
ways to enter the cycle, but ultimately there is another
source of reinforcements, which we call
negative reinforcement where you end up
taking the drug, to be honest to fix the
problem that the drug caused. And the problem that the
drug caused is in your brain. It’s in the
circuits of your brain. Okay, so let’s
now drill down into what is NIAAA
doing in these domains and how can this
information I just imparted to you inform us on
where we go, where we’ve been, and where we should be going? So one piece
that’s quite critical is that we now know that
the front end of the brain that I just talked about – the preoccupation,
anticipation, craving stage, the frontal cortex – does not fully
develop until the age of 25. Any of you that
have raised a teenager know what I’m talking about. And so during this
developmental period you’re losing cells
in the frontal cortex, there is a culling of neurons from the ones that are
going to be functional. But you’re growing connections, that’s the frontal white matter
at the bottom graph there, you’re growing
connections to the brain stem and those reptile brain elements
that I was talking about. And that means that this is a particularly vulnerable
period for young people to be assaulted
with drugs of abuse. And so I would make
an argument with you, without showing data, that we have a
neurobiological reason for the
21-year-old drinking age. And there is absolutely no
one that’s going to get me to recommend lowering our
drinking age in this country. First of all there’s been a
steady decline in drunk driving since Reagan and it was
Reagan who signed the law about the 21-year-old
drinking age. Alright? So one of the things we
really need to focus on and not just with alcohol,
but all drugs of abuse, is how do we
understand what happens to the developing brain and what is the
impact of alcohol exposure and can we then
provide young people with more and more
information to illustrate that it’s not a good
idea to be binge drinking before the age of 21. And so we developed,
it was before my time, about five years ago,
sorry, we studied 800 … yeah, 500 years ago.
(Laughter) NIAAA hasn’t been
around that long. I meant to say we
studied 800 youth between the ages of 12 and 21 in a cross-sectional
longitudinal prospective design. So in other words
they recruited people anywhere from 12
to 21 in the cohort and then they’ve
been imaging their brain and doing
neuropsychological tests and comparing it with
their intake of alcohol and we call this the
National Consortium on Alcohol and Neurodevelopment
in Adolescence. And in fact the
data are now coming in because it has been five years and there’s a lot
of data to suggest that indeed the brain regions in the frontocortical
part of the brain have steeper reductions
in gray matter volume in those individuals
who inputted in this study with heavy drinking as
heavy drinking adolescents. Now remember in this study we took them all
the way through to 21, so there are some
people who are 18, some people who are 19,
some people who are 12. But in any of those groups
if they were heavy drinking when they entered the study there have been now charted
steeper declines in cortical, particularly
frontocortical, gray matter. And this paper just came out in the American
Journal of Psychiatry. And it was my first joint
NIDA-NIAAA council meeting where Nora got very excited
seeing what we were doing with NCANDA and
announced that we should, we discussed this and
we announced together that we should do
something purely prospective with a large, much larger N. And so that
launched the now-famous Adolescent Brain
Cognitive Development study, which is well underway. More than 9,500 children
between the ages of 9 to 10 have been imaged and
neuropsychologically tested and are being followed. And, in fact, half the
data have just been uploaded to the NIH data archive. And those of you interested can access that data
and start doing studies. There was actually a
slide that Gaya Dowling showed of how many of
these 9 to 10-year-olds actually had a sip of alcohol. It was infinitesimally low,
but there’s data. So what have we been
doing knowing this information? Well, one of the things we put a lot of
energy into in the Institute is screening and
brief intervention. The acronym for it is SBIRT. We know that it works in adults. But we now have
about six studies underway evaluating the Alcohol Screening and Brief
Interventions for Youth guide. And we hope, and these evaluations are
being done in primary care, emergency
departments with children with chronic
medical illness, schools, juvenile justice systems. And the school-based
universal SBI grounded in the NIAAA screening guide, as well as
community-based interventions, both reduced alcohol
use among American Indians and other use in
rural areas in one study that’s already been published. So I think this is an area that we’re
continuing to work on. We’re trying to change
policy with this information. But if you simply, if
your primary care doc simply asks you two questions: How much do you drink? And, how much do your
friends drink? You lie. But on the way home you
start thinking about it. And it really
does have an impact. And more and more data
suggests that it does. So prevention of
underage drinking requires a whole
bunch of things, not just brief intervention. But we have
environmental interventions. I’ve already referred to
the 21-year-old drinking age. Individual-level interventions. School-based interventions. And family-based interventions. And all of these impact. But there’s some success here. This is actually some good news, which is there’s
been a steady decline in alcohol use in the
past 30 days in teenagers over the last 10 years. And we do a lot of
work in this domain. I’m going to highlight
one thing on this slide, and that is that we launched – when I first arrived in
NIAAA – we launched CollegeAIM. This is a resource for helping
colleges address harmful and underage student drinking. It’s a menu
administrators can access to see what prevention programs
at the community level, what at the
individual level work, how much they cost, and what’s
the data to support them. And any of you as parents
can go to the university or college and ask them: Have you been
addressing anything that was outlined in
this menu CollegeAIM? So that’s a challenge to you. So the argument is
that there is a good case for screening and
brief intervention, and in 2012 the U.S.
Preventive Services Task Force recommended alcohol screening and brief intervention
for adults in primary care. It’s recognized now as one of the highest ranking
preventive services among 28 effective services. And it has a similar
score as cervical cancer and colorectal cancer. We have a lot of
publications on this. You can also check
it out on our website. I just want to
mention in this regard that we do have a pretty
strong policy portfolio. And one of the things
we’ve done since Deborah Hasin, who’s going to be
talking later today, is that we’ve
extended, first of all, we’ve had a recent
program announcement on policy effects of
alcohol and marijuana and other substance-related
behaviors and outcomes. And we maintain an Alcohol
Policy Information System, known as APIS, which is a large
searchable database of alcohol-related
federal and state policies. And we renewed this
for five years this year, but we also added
marijuana policies to this information system. So you can chart now
changes in marijuana laws along with
changes in alcohol laws. So it’s out there
and this is a big, also a big part
of our portfolio. Now what about diagnosis? What are we
doing with diagnosis? Well, one of the first
things that occurred to me when I got to NIAAA, it’s a bit of a
story how we got there, but it really had to
with our HIV consortium, which works on a lot of
prevention, is I asked them: What do they need? And they said we need something that measures blood alcohol
levels online in real time. And so I challenged our staff to do a reward
challenge to the world, which we would
give an award to anyone who could come up with a device where you could
measure blood alcohol levels in real time over time. Now there is such a device. It’s called the SCRAM device.
It’s on the market. It’s a big clunker, you may have
seen Lindsay Lohan wearing it on the cover of People magazine. (Laughter) And I wanted something sexier that you could wear
on the runway in Paris, not the airplane
runway, the other one. In any event,
BACtrack won the award, they’ve come up with a device
that looks like an Apple iPhone and so theoretically the
information we currently have is it may be on the market, or at least close to
being on the market, this year. And a number of investigators
are already tracking this. But I just want you to
think about the implications for any clinical research and then I’ll
let you think about the implications
for your teenager. On a more sobering
and very sobering note, we just published
a paper from NIAAA that was funded by NIAAA, the research was
funded by NIAAA, on fetal alcohol
spectrum disorder identifying that the incidence
in the United States is approximately 1 to 5 percent. That’s up there with
autism. 1 to 5 percent. And this was done by
a team of individuals, medical doctors and
clinical psychologists, who do neuropsychological tests but also the
dysmorphology exams in situ with the individuals. And it was basically
6,000 first-grade children in eight sites
in four locations, one of which was
actually San Diego, you know, where I
lived for 40 years. So, you know, I think we have a problem
that is avoidable, preventable, and not a whole
lot of recognition that this is out there. We have an enormous program in fetal alcohol
spectrum disorder at NIAAA. One of the
things that we’re doing is trying to develop
ways of diagnosis that will be quicker
and simpler and earlier that will allow
early interventions. And one of the
things we know is that now three-dimensional
imaging can capture those facial features
that are part of the diagnosis for fetal alcohol syndrome and fetal alcohol
spectrum disorder. And they tell me now that if you take a picture
this way, and at this angle, and straight on,
like cross-sectional, that they can actually develop a three-dimensional image
just from three photographs. In any event, this is underway as well as a lot of basic
research trying to identify what are the
genetic vulnerabilities and what are the
developmental pieces that we can
possibly address, or stop, or reverse once someone
has been exposed to alcohol. You might ask, well, how does all this brain
stuff impact on diagnosis? Well, one of the other areas that I’m
personally involved with, led by Laura
Kwako and David Goldman in our intramural program, Nora Volkow and I are
part of this program, but we’ve addressed, we’ve decided to use a research
domain criterion approach but limit it to
alcohol use disorders and the domains
that I’ve talked about – binge, intoxication, withdrawal, negative affect,
preoccupation, anticipation – to develop, our
plan is to develop an addictions
neuroclinical assessment. And so we’re going to be
measuring different tasks that reflect
changes in these domains. So, for example,
for incentive salience perhaps a queue reactivity
task for executive function. Perhaps delayed discounting for withdrawal
negative affect stage, perhaps facial
emotional matching tasks. And by no means are
these the only tasks that we’re going to apply. And so we’re not
only analyzing data that’s already been generated
in the clinical center over the last 10 years but we’re going to be
doing a prospective study that’s just about underway. What about treatment? I told you that less than
10 percent of individuals with an alcohol use
disorder get any treatment. And even fewer get
a medical treatment. In fact, many
people don’t even know that there are three
medications approved by the FDA for the treatment of
alcohol use disorder. So I formed a medications
development division at NIAAA. I broke them off
from our treatment and recovery research group, and over the last four
years they’ve developed a plan and a program that I
think is heuristically useful, one of which is we’ll
take molecular targets. We’ll run them
through animal models. We’ll run them also
through human laboratory tests before we go to clinical trials. And then the clinical trials
in human laboratory models can inform also the animal model so we get cross
feedback and validation. And I’ll be honest with you, I’m not funding with
my own in-house money any clinical trials if
they haven’t been through a human laboratory model
first with positive results. You can do a
clinical trial on an R01 any which way you want, as
long as you get a good score. You know, I
challenged my division of neurobiology and neuroscience and behavior to
come up with targets, this was about a year ago, based on the three
stages of the addiction cycle. And you get this
enormous herd of targets, molecular targets. But you know we
haven’t been testing them. We haven’t been
moving them translationally I should say into human domain. But there are two that
have been, showed some success. One is a
vasopressin 1B antagonist and a glucocorticoid
receptor antagonist. And I illustrate those because
you know I like the dark side. But the
glucocorticoid antagonist is a recent human
laboratory study, double-blind placebo-controlled, done by Barbara Mason at
the Scripps Research Institute, showing that just
one week of treatment with a glucocorticoid antagonist actually blocked
drinking afterward in these nontreatment-seeking
individuals with alcohol use disorder. And she also had a
lowering of liver enzymes and a lowering of
craving. Promising. Other human laboratory studies and clinical
trials are underway. And then there was a positive
multisite clinical trial with a
vasopressin 1B antagonist. One of the
challenges we have, though, is that we can’t get
industry very interested in picking up some of these
targets and moving them forward which costs millions
and millions of dollars. So that’s a
challenge for the future. But I might add that
industry is not working on any psychiatric
medications for the moment. Another area that we work on, and this doesn’t have to do with
the brain I outlined to you, but you know liver
disease, I told you, is probably to a
large extent caused now by alcohol in the United States. We also have an enormous
amount of basic research in liver disease identifying that the different
stages of liver impairment from steatosis
and hepatotoxicity from inflammation,
fibrogenesis and carcinogenesis, all these targets we know some
of the mechanisms involved. And this is my infamous
“Liver in the Brain” slide to illustrate to you
that a lot of the targets that affect the liver
also affect the brain and probably drive
some of the stress system that I was talking about
in the extended amygdala. So what are we doing about it? Well, we’ve had a consortium on alcohol-associated
liver diseases. We’re establishing a clinical
and translational network to streamline the design,
initiation, and conduct of clinical trials
for alcoholic hepatitis, reduce
administrative redundancy, and optimize the use of
scientific innovations. This is well underway. We had a meeting with the FDA
and the American Association for the Study of Liver Diseases, a two-day workshop in March, to develop recommendations
for standardized definitions, variable sets,
screening and assessment tools, and research and drug
development procedures. I don’t know
whether you can envision how difficult it is
to do a clinical trial on a disease where death
is the end point. Alright. But people die of liver
disease, alcoholic hepatitis. But it’s a real challenge and what we’re trying to do
is bring our groups together and get them to standardize
many of the elements so that we can focus down and drill down into
actually doing clinical trials. A final plug here, you know, and I get grief
from basic researchers when I tell them
they should do this, because they say we
don’t do clinical studies. Well, you don’t
do clinical studies, but you probably
have a buddy someplace that has a small business. So I’m going to challenge
all of you basic researchers as well as clinical researchers. We can’t test any of
these targets in humans unless we get an IND, an investigational new
drug approved by the FDA. So we’ve modified
based on what NIDA did, where they modified
their SBIR program, and you know we have
basically made it easier for you to
actually get the money to streamline getting an IND, which requires a
lot of toxicology and a whole bunch
of other elements. Now keep it in mind. If you have any questions
call Meg Ryan at NIAAA. So I want to quickly, because I’m going
to run out of time, I want to quickly go over some of the things
we’re planning on doing and some of which are underway
at NIAAA this current year. So I already mentioned
this, but here’s the data. We have a
problem with what I call extreme binge drinking. You know what a binge is. It’s where you reach
.08 blood alcohol level, grams percent in
a two-hour period. It’s usually four drinks
for a female on average, five drinks for a male. But we call
extreme binge drinking two to three times that amount. And young people, in
particular 20 to 30-year-olds, but even into the more
elderly population are, there’s a steady increase
in emergency department visits and overdoses with alcohol. And we think it’s attributable to a large extent to
this extreme binge drinking. There are cultural reasons. There are
biological reasons for this. Those people that can drink
everybody else under the table have an inherent low
sensitivity to alcohol that probably contributes. But we extol the virtues of drinking
everybody under the table. This is a study
from Ralph Hingson showing that if you double the
amount of alcohol in a binge you have a 70 times
further increased risk of an emergency room visit. If you triple it,
it’s 93 times greater. These are, if I may
say so, sobering thoughts. Alcohol and women’s
health is a big issue at NIH. It’s a big issue for NIAAA. I’m pretty sure it’s
a big issue for NIDA. The gaps between women and men are narrowing for the
prevalence, frequency and intensity of drinking, early onset drinking,
having an alcohol use disorder, drunk driving, and
self-reported consequences. Women are more likely, and here’s the killer
part of this, pun intended, women are more likely
to experience blackouts, liver
inflammation, brain atrophy, cognitive deficits,
certain cancers, and to experience negative
affect during withdrawal and stress or
anxiety-related relapse. And we know very
little about why. Now there’s some
good steps taken, but if you actually go back and look at 230
structural neuroimaging studies on substance use
over the last 23 years, only about a quarter of
them evaluated sex differences. The data may be in there,
but they don’t analyze it. You now know that all NIH grants from molecular
studies to cells in dishes to rodents to
primates require that female subjects be included. And so the data will be coming. And then I mentioned
the elderly population, individuals over 65, there’s
again a narrowing of the gap between males and females, but there’s a steady increase
in drinking in this population. And elderly have
a very, you know, a lot of vulnerabilities, not the least of which is
falling and breaking your hip, but also interactions
with many of the medications that they’re taking. So this is an area we
hope to put some energy into. Co-occurring disorders. We’ve already put a good
bit of energy into an RFA on animal models associated
with alcohol use disorder and
post-traumatic stress disorder. We’re cooperating
and collaborating with the Department of Defense,
with NIMH, on this issue. But we really do need
more work in this domain if we’re going to
address the issue of the deaths of despair, because they are
most likely linked. And I would argue most likely
linked through the dark side. We need to grow the
addiction medicine workforce. Many providers do
not perform screenings. In a study of 54
primary care clinics we found that 88 percent had no
policies or requirements to ask patients
about alcohol use. No evidence-based methods
for screening or referrals. We need to improve
physician training and substance use prevention
treatment at all levels from undergraduate, graduate, medical education
through residency, fellowship and beyond. And we need to
integrate prevention, early intervention and treatment
into routine medical care. And I might add it’s
not just physicians. We need to train
clinical psychologists, we need to train nurses,
we need to train pharmacists, we need to train
physician assistants. We’ve got a big
challenge ahead of us. ABAM and ASAM have
done a marvelous job of initiating specialization
and addiction medicine, psychiatry medicine is now a subspecialty
of preventive medicine. And that’s all wonderful. But we need a
bottoms-up approach from the very early
stages of education. And that brings me to the
Alcohol Treatment Navigator that we launched in October. This is actually on the website.
I challenge you to check it out. It’s a one-of-a-kind resource
that outlines the features of evidence-based
alcohol use disorder treatment, describes the
varied routes to recovery, which are not just
Alcoholics Anonymous and not just a
28-day detoxification, but everything in-between from
cognitive behavioral therapy to motivational interviewing,
to family therapy. It provides a strategy for locating qualified
treatment specialists. There are two locators
linked up to this website. The SAMHSA locator and
the Psychology Today locator. And we are planning to develop a similar treatment
navigator for physicians and other health professionals, a more streamlined version for what your
doctor should know. We need to continue to
increase the participation of under-represented
minorities in clinical trials as the diversity of the
U.S. population increases so should the participation
of under-represented groups at NIAAA-sponsored
clinical research. We’ve done many things
including translating pamphlets into different languages. We even did Mandarin Chinese
for a group in New York. And that was in honor of T.K.
Li, one of my predecessors. So this is my last slide. I think I’ve blitzkrieged a
bit through what we’re doing. There are other
things we’re doing that I really don’t have time
to get into the details on, but I mean I think
I’ve illustrated to you we have a big program on
identifying the mechanisms of alcohol action,
pathology, and recovery. I would argue our science
is as good as anybody’s. We’ve been
applying that to diagnosis, prevention, and treatment. And we’ve been,
since my tenure at least, trying to get this out to
the public in a useable fashion so that you who
are in the trenches can actually use this
information and help people. Thank you very much. (Applause)

3 Comments

  • Reply Timothy Bucky August 10, 2018 at 6:49 pm

    The anti-smoking drug varenicline (marketed under the name Chantix) significantly reduced alcohol consumption and craving among people with alcoholism.
    Gabapentin, a medication used to treat pain conditions and epilepsy, was shown to increase abstinence and reduce heavy drinking. Those taking the medication also reported fewer alcohol cravings and improved mood and sleep.
    The anti-epileptic medication topiramate was shown to help people curb problem drinking, particularly among those with a certain genetic makeup that appears to be linked to the treatment’s effectiveness.

  • Reply Franko Mamani August 10, 2018 at 7:54 pm

    LOL

  • Reply ctwatcher August 13, 2018 at 5:17 pm

    We're trying to drink ourselves to death now so all the special little groups of mentally ill people can be followed to see how they treat each other as inquiring tax thieves want to know! Bringing good life for a few tax thieves. Tear it down. No institute for health in this nation now.

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