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FY 2001 Congressional Budget Justification
National Institute on Alcohol Abuse and Alcoholism
Authorizing Legislation:
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Section 301 and Title IV, Sections 464H and 487d of the Public
Health Service Act, as amended. Reauthorizing legislation will be
submitted.
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Budget Authority:
FY 1999
Actual
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FY 2000
Estimate
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FY 2001
Estimate
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Increase or
Decrease
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FTE
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BA
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FTE
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BA
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FTE
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BA
|
FTE
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BA
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222
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$243,071,000
|
229
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$273,991,000
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237
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$288,578,000
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8
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$14,587,000
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This document provides justification for FY 2001 non-AIDS activities
of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Justification
of NIH-wide FY 2001 AIDS activities can be found in the NIH section entitled
"Office of AIDS Research (OAR)."
Introduction
The Burden of Alcohol Disorders
Second only to tobacco, alcohol is the most abused drug in the United
States. About 14 million adult Americans have an alcohol-use disorder,
such as alcohol dependence or abuse (alcoholism or hazardous drinking
that falls short of alcoholism, respectively)1. Children also
suffer from these disorders; for example, 23 percent of 14-to 18-year-old
urban and rural children interviewed in a state survey reported having
had at least one clinically diagnosable symptom of alcohol abuse or dependence
during their lifetime.2 Among college-age youth, alcohol abuse
is epidemic, as media headlines too frequently attest in reports of binge-drinking
fatalities.
Since last year's appropriations hearings, the direct and indirect costs
of alcohol disorders in the United States has been adjusted for such factors
as cost of living. Taking these factors into account, it is now estimated
that alcohol imposes a burden of $185 billion annually3. The
sequelae of alcohol disorders include damage to the liver, brain, and
other organs; cancer; fetal alcohol syndrome and the life-long deficits
it imposes; accidental injury to self and others; property damage; impaired
productivity; crime; and broken families.
NIAAA's Role
Alcoholism is caused by a variety of factors, both biological and psychosocial.
In the genetic arena, scientists now know that about half of the risk
for alcoholism can be attributed to multiple genes. These genes produce
key substances in biochemical pathways that contribute to drinking behaviors
and physiological responses to alcohol, such as organ damage or the lasting
damage that alcohol sometimes causes in the fetal nervous system. Among
the most important work of the NIAAA is not only elucidation of the many
steps in these pathways, but also identification of the genes involved
in them. The data produced by these types of studies feed into design
of treatments that target specific biological phenomena underlying alcohol-use
disorders.
Equally important is the study of psychosocial factors, since environment
plays a crucial role in moderating or exacerbating the influence of genes
that predispose an individual to alcohol-use disorders. The Institute
identifies these factors and designs interventions not only at the individual
level, but also at the community and policy level, to change environments
conducive to inappropriate drinking -- through outreach programs or policies
that regulate youths' access to alcohol, for example.
Brief Summary of Operations
To achieve its goals, the NIAAA:
conducts and supports basic-science studies that elucidate
the biological mechanisms by which alcohol exerts its effects;
explores the biological bases of alcohol-related behavior;
examines the contribution of environment to alcohol disorders;
develops and tests medications and behavioral interventions;
develops and tests behavioral interventions aimed at preventing
alcohol misuse and its consequences; and
disseminates scientific findings.
The Institute's extramural program provides grants and contracts that
enable scientists nationwide to conduct research on topics in need of
study; administers 15 major alcohol research centers; and supports training
of new alcohol researchers, including minority investigators. Scientists
of the intramural program conduct research on the campus of the National
Institutes of Health and at satellite sites. Together, these efforts comprise
more than 90 percent of the Nation's research on alcohol disorders. Findings
are disseminated via papers published in scientific journals; Alcohol
Health & Research, the Institute's peer-reviewed journal; Alcohol
Alerts, bulletins that rapidly notify health practitioners of significant
findings; press releases; the NIAAA Researcher-in-Residence Program; and
Alcohol and Health, the Institute's periodic reports to Congress.
Story of Discovery: Fetal Alcohol Syndrome (FAS)
The time that humans spend in the womb is one of the most vulnerable
periods in life, in which events that disrupt the fetus's development
can set the stage for a future of disability and hardship. Alcohol
is among the most potent disruptors of fetal development yet known
and is the leading cause of preventable birth defects in the United
States. In children exposed to alcohol in utero, developmental
disruptions may manifest as fetal alcohol syndrome, disabling deficits
that include damage to the nervous system, the command center that
includes the brain and regulates everything from movement to memory
and learning; retardation; impaired motor coordination; malformations
of the face and head; and damage to organs, including the heart.
Although the abnormal facial features of FAS may normalize with
age, other, more disabling deficits, such as mental retardation
and behavioral problems, persist throughout life.
Disparities in development of FAS are evident. The likelihood of
African-Americans giving birth to an FAS infant is six-fold that
of Caucasians. The likelihood rises to 33 times higher among some
tribes of Native Americans. While studies of social and cultural
issues that may affect these disparities are underway, the NIAAA
also places a strong emphasis on biological issues that underlie
FAS. Establishing a baseline of mechanisms that affect embryonic
development enables scientists to later identify deviations from
baseline in subgroups.
The NIAAA studies FAS in order to prevent, reverse, and ameliorate
it. Designing interventions to deter pregnant women from drinking
is among the research efforts underway at the NIAAA. Since completely
eradicating drinking among pregnant women is a desirable but unrealistic
goal, NIAAA studies that seek to reveal the biological mechanisms
underlying FAS are equally important. For children subjected to
maternal drinking in utero, identification of the biological
mechanisms underlying FAS may lead to better methods of diagnosing
it. More important, understanding these mechanisms may help scientists
learn how to stop the series of physiological interactions that
usually would go on to cause FAS once the initial event -- maternal
drinking -- has triggered them.
The Search for Biological Mechanisms that Underlie FASTrophic Factors
Trophic factors, substances that promote growth of cells and help
them differentiate into specialized body tissues, have long been
studied by various disciplines. FAS researchers are interested in
trophic factors because of their role in fetal development. One
trophic factor of interest to FAS researchers is vitamin A, since
enzymes known to play a key role in metabolizing alcohol also are
involved in metabolizing a precursor of vitamin A. FAS researchers
are considering the possibility that, when pregnant women drink,
the enzyme that normally would metabolize the vitamin A precursor
instead metabolizes alcohol. Researchers have found that alcohol
reduces levels of vitamin A in pregnant mice.
Some trophic factors affect growth and survival of nerve cells.
Alcohol researchers are interested in neurotrophic factors, since
the fetal nervous system is especially sensitive to the effects
of alcohol, and the development of the fetus's nervous system is
among the factors that decides how well that fetus functions after
birth. Researchers have done a series of studies on the effects
of adding neurotrophic factors to fetal cells exposed to alcohol.
In a recent study, researchers simulated the environment of an embryo
exposed to maternal drinking in rats' nerve cells. Two neurotrophic
factors, brain-derived neurotrophic factor and nerve-growth factor,
significantly prevented or reduced loss of nerve cells.
The Role of the Cell-Death Pathway
Cell death -- "apoptosis" -- is a normal part of life,
as cells die to make way for new ones. Paradoxically, this death
is accompanied by growth, and the cell-death pathway -- the series
of synchronized molecular interactions that result in normal
cell death -- reflects this in its inclusion of mechanisms that
promote cell growth and differentiation of cells into specialized
tissues. However, various events, such as exposure to toxins, can
divert apoptosis from its normal pathway, resulting in abnormal
pathways that may spur pathological molecular interactions.
Apoptosis is a very active area of interest in the research community,
from aging to cancer. Alcohol researchers are interested in apoptosis
because of its implications for growth and development in fetuses
exposed to alcohol via maternal drinking. The neural crest, a band
of precursor cells present only in the early embryo, develops into
nerve cells of the brain and spinal cord and into other organs.
Researchers have found that alcohol prematurely initiates apoptosis
in this crucial band of cells. Death of neural-crest cells is a
normal, necessary part of embryonic development, but scientists
have discovered that alcohol-induced apoptosis in the neural crest
follows an abnormal pathway likely to contribute to the development
of FAS.
Scientists discovered that two steps usually present in the normal
neural-crest apoptosis pathway are missing in the abnormal alcohol-induced
apoptosis pathway. In an animal model, researchers blocked both
the alcohol-induced and the normal neural-crest apoptosis pathways
by inhibiting a specific enzyme (one of the "caspase"
enzymes involved in cell death in mammals). This finding suggests
that, at least at one biological point, the two pathways have in
common a specific enzyme. In tracing the steps in the abnormal pathway,
scientists are looking for ways of blocking alcohol's effects.
Scientists also have found in vitro evidence that oxygen
free radicals, including those induced by alcohol -- a known generator
of this class of damaging molecules -- lead to excessive neural-crest
apoptosis. The scientists strengthened their finding by treating
alcohol-exposed neural-crest cells with free-radical scavengers,
which significantly improved the cells' viability. These antioxidants
appeared to reduce or mitigate the free radicals' harmful effects
on the neural crest, a finding that suggests potential for pharmacologic
interventions.
Common Causes
While these findings are immediately relevant to FAS research,
they also have implications for studies in other scientific areas
-- just as results of studies in other areas have informed the search
for mechanisms that underlie FAS. For example, by tracing the abnormal,
alcohol-induced apoptosis pathway, FAS researchers also glean information
about the normal pathway. Data on apoptosis pathways are important
to any research discipline with an interest in the growth and death
of cells.
Through continued investigations and information-sharing, FAS researchers
are moving closer to understanding the mechanisms that lead to a
prevalent, yet completely preventable, disease.
Story of Discovery: An Appetite for Alcohol
Alcohol is the most commonly abused of all of the abused substances
-- but is it also a food? Some scientists think so, and in an effort
to find the causes of alcohol-use disorders, they are examining
the biological factors that regulate appetite, to see if they apply
not only to eating and drinking but also to alcohol consumption.
Preliminary studies suggest that they do.
Appetitive behavior means far more than the simple concept of hunger.
Thinking of alcohol as a food means thinking of it as a source of
calories; that is, energy. How the body produces and uses energy
from food involves an exquisitely synchronized sequence of biochemical
pathways -- predictable series of chemical reactions triggered by
needs in the cellular environment. For example, molecular signals
notify the brain that the body needs more energy to perform its
activities and that an individual needs to eat. These molecular
signals consist of pieces of protein called "peptides"
that deliver chemical messages to cells.
Scientists from other disciplines have shown that certain neuropeptides,
the peptides of the nervous system, have a profound effect on eating
behavior. Alcohol researchers now have evidence that neuropeptides
also may be involved in appetite for alcohol.
Obesity Research Points to Peptides
A search of the scientific literature reveals that published findings
on neuropeptides and appetite have increased eight-fold over the
past 30 years, in large part because of obesity research on the
effects of neuropeptide levels on food consumption. For example,
researchers have shown that injections of neuropeptide Y (NPY),
the strongest of the appetite-stimulating neuropeptides, cause mice
to eat far past the point of obesity. When the injections stop,
the mice's eating normalizes, and they return to normal weight.
The study of peptides and appetitive behavior first gained significant
momentum in 1982, when researchers studied the effects, on eating,
of corticotropin-releasing factor (CRF), a peptide already known
to stimulate the secretion of stress hormones. A major impetus for
studies on the role of peptides in appetitive behavior came in 1994,
when obesity researchers identified the peptide leptin as a key
factor in the regulation of obesity. Identification of peptides
involved in appetite has progressed at a virtually exponential rate
since that time.
Because alcohol, too, is a source of calories, alcohol researchers
suspected that alcohol consumption may be regulated, in part, by
some of the biological pathways that regulate hunger and thirst.
Peptides are integral parts of these pathways, and researchers are
exploring the possibility that variations in them are among the
reasons people develop alcohol-use disorders.
What had to be in place for scientists to begin studying the relationship
between alcohol and the peptides involved in appetitive behavior
were animal models. Researchers from different fields have developed
strains of animals appropriate for their areas; for example, diabetes
investigators developed an obesity mouse model relevant to their
work. Alcohol researchers needed animals with a strong preference
for alcohol or a strong avoidance of it. About 20 years ago, scientists
bred rat strains with these characteristics, and since then have
developed many other animal models for alcohol-related research.
These models subsequently have played an integral part in peptide
and other studies.
The advent of transgenics, scientists' ability to act directly
on specific genes to eliminate or enhance their activity, thereby
reducing or increasing the amounts of proteins (peptides) the genes
produce, advanced the search considerably. Since the peptides involved
in appetitive behavior are fragments of proteins, scientists could
now alter the genes that produced peptides, giving a much clearer
picture of how specific genes and their proteins affected specific
behaviors, such as eating. Alcohol researchers, among others, have
used transgenic techniques to alter genes involved in producing
appetitive peptides, thereby creating animals that serve as research
tools.
Alcohol Research on NPY Raises New Questions
A recent study involving NPY yielded surprising results and raised
important questions for researchers who study appetitive behavior,
whether from the standpoint of obesity or alcohol disorders or other
conditions. For a long time, scientists have known that NPY is a
potent stimulator of appetite in laboratory animals when it is injected
into their brains. But when scientists instead used a genetic
approach to knock out the gene that produces NPY, meaning
that the animals could no longer produce NPY, they had an unexpected
result. Without NPY, the powerful food-appetite stimulator, it would
seem that appetite for alcohol would be eliminated, but exactly
the opposite happened. Now scientists are faced with a paradox:
Enhance NPY levels through injections, and appetite for food
goes up, but eliminate NPY through gene knockouts, and appetite
for alcohol goes up.
What the New Finding Means
Appetitive behavior has critical implications for a variety of
diseases and research disciplines. For example, obesity is involved
in many serious and costly diseases, such as diabetes and hypertension.
More than half of U.S. adults are overweight and a quarter are clinically
obese. The recent findings on NPY point the way to a number of questions
that alcohol researchers and other scientists need to address as
one of the next steps in elucidating NPY's role in appetite. Why
do injections of NPY increase food appetite, while eliminating NPY
genetically increases alcohol appetite? Does it mean that the NPY
gene is not the key to appetitive food-related behavior, but that
the key lies somewhere downstream in a pathway that the gene triggers?
Does it mean that the pathway that regulates appetite for food and
alcohol diverges at some point? NPY is known to attenuate anxiety.
Is the increase in alcohol consumption seen in NPY gene-knockout
mice their effort to compensate for the anxiety they feel in the
absence of this powerful neuropeptide? Can other researchers replicate
the NPY results in species other than the ones already studied?
By answering these kinds of questions, scientists will gain clues
that can help them trace pathways that end in disease. Ultimately,
the types of findings described here can help scientists design
medications that target key points in these pathways to pathology.
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Science Advances
New Medication, Nalmefene, Provides Another Option for
Alcoholism Treatment
One of the challenges researchers face in developing effective medications
to treat alcoholism is that the exact molecular sites at which alcohol
binds to cells remain unknown. Also under intensive study are the biological
pathways -- that is, the predictable series of molecular reactions --
that are triggered inside the cell once alcohol molecules have bound to
it. Ideally, medications are designed to target the binding sites or the
pathways that result in diseases, such as alcoholism.
While the search for optimal drugs for alcoholism treatment continues,
scientists have developed some medications that have shown better than
moderate success at preventing recovering alcoholics from relapsing. Key
among these medications has been naltrexone, a drug recently approved
by the Food and Drug Administration. Naltrexone is an opioid antagonist;
that is, it works by blocking the component of the nervous system involved
in processing substances that have opiate effects, such as alcohol.
Researchers recently completed a clinical trial of a new opioid antagonist
called "nalmefene." In previous studies in which naltrexone
and nalmefene were compared, nalmefene resulted in lower risk of liver
toxicity and entered the bloodstream more quickly. Nalmefene's effects
lasted longer than those of naltrexone, and data suggest that it may be
more potent than naltrexone.
In this clinical trial, nalmefene significantly reduced relapse to heavy
drinking among recovering alcoholics. Patients taking placebos were 2.4
times as likely to relapse as were patients taking nalmefene. None of
the 105 patients who took part in the clinical trial suffered major adverse
effects from nalmefene.
The study described here has provided the basis for industry (a Finnish
company) to plan further studies of nalmefene in heavy drinkers, with
the intent of obtaining FDA approval. If this medication receives approval
from the Food and Drug Administration (FDA), it will offer a new treatment
option for alcoholics who are unable to take naltrexone. For example,
nalmefene appears to be even less toxic to the liver than is naltrexone,
a significant issue for the many alcoholics who suffer from alcohol-induced
liver disease. For these patients and for those who are allergic to naltrexone
or for whom the drug is not effective, nalmefene may offer a valuable
alternative.
Scientists are making important discoveries regarding molecular sites
at which alcohol binds to cells and the pathways by which alcohol alters
cell function. These discoveries will contribute to design of more precisely
targeted drugs for alcoholism treatment. While the search continues, patients
now appear to have an improved medication option for the prevention of
relapse.
Adolescents May Be Vulnerable to Some Types of Alcohol-Induced
Memory Impairment
Intuitively, it might seem that people who can "hold their liquor"
are at low risk for alcohol-related problems. But the opposite is true:
these people are at higher risk, because their tolerance for alcohol allows
them to drink more. Even while they drink larger amounts of alcohol with
seeming equanimity, compared to other people, they are exposing themselves
in larger degree to the physiological changes that lead to trouble --
adaptations in the brain that require more and more alcohol in the future
in order to feel the same pleasurable effects, and changes in the "hard-wiring"
of the nervous system.
Some adolescents can tolerate large amounts of alcohol, previous studies
suggest. Researchers have found that, compared to adults, adolescents
do not feel as readily the uncomfortable sensations, such as sluggishness
and nausea, that alcohol causes. Their nervous systems are not as easily
dampened by alcohol. This means they can drink more, because it does not
make them feel badly as quickly.
Researchers are concerned by this capacity for drinking among some young
people. Adolescents have a disproportionately high rate of drinking, and
this phenomenon occurs at a biologically and behaviorally vulnerable time
of life. For example, adolescents, unlike adults, are still forming connections
between nerve cells that play a role in memory, and toxic substances may
damage the development of these connections. Does alcohol permanently
alter molecular or gene-related changes that normally take place in adolescence,
including changes in the nervous system? If so, what are these harmful
changes? Can they be therapeutically altered? These are among the questions
researchers are asking as part of an initiative to identify alcohol-induced
physiological and behavioral changes unique to adolescents.
Scientists can assess these types of changes by measuring different alcohol-induced
behaviors, then relating the behaviors to the anatomical structures and
biological mechanisms that underlie them. One behavior affected by alcohol
is spatial memory; that is, memory of location of objects in the environment
and how to get to them. Spatial memory is known to be processed by a brain
structure called the hippocampus.
For the first time, researchers have found that alcohol significantly
impaired spatial-memory acquisition in adolescent, but not adult, rats
in a water-maze test. In a separate experiment, alcohol did not impair
acquisition of nonspatial memory in either group performing a task in
the water maze.
The findings described here illustrate that the adolescent brain is in
a stage of continual change and differs from the adult brain, and suggest
that adolescents are especially susceptible to alcohol's imprint.
Violence Reduction Sustained After Alcoholics Receive
Behavioral Marital Therapy
Each year, one in every six couples in the United States engages in an
incident of physical assault. That heavy drinkers and alcoholics are more
prone to engage in physical abuse toward their spouses is intuitive. Researchers
not only have confirmed this conventional wisdom in scientific studies,
but also have documented the extent to which alcohol-related domestic
violence is a public-health problem. They found that more than 50 percent
of male alcoholics have abused a female partner in the year prior to alcoholism
treatment.
Researchers are in the beginning stages of examining domestic violence
among alcoholics. For example, scientists have found that alcoholism treatment
based on behavioral marital therapy (BMT) significantly reduces risk of
domestic violence. At first glance, this outcome might seem obvious. However,
among the questions researchers are trying to answer, having established
the immediate effectiveness of BMT in reducing spouse abuse, is whether
or not this effect is lasting. Researchers also are studying other factors.
For example, do spouse-abusing alcoholics who have stopped drinking continue
to abuse their wives? Or is alcohol per se the driving force for
domestic violence in this population?
In initial studies of a group of alcoholics undergoing BMT, researchers
established a baseline and conducted a one-year follow-up. They found
that, prior to BMT, these people were four to six times as likely to abuse
their spouses and to abuse them more frequently than were members of a
demographically similar comparison group of nonalcoholics. In the year
after treatment, alcoholics who began drinking again were significantly
more violent than the nonalcoholic comparison group. However, in the same
post-treatment year, the alcoholics who remained abstinent from drinking
were not more violent than their comparison-group counterparts. Researchers
also found that, during this year, the number of days that a person drank
correlated significantly with the frequency of his spouse abuse.
Researchers next conducted a two-year follow-up of the same group of
alcoholics, described above, who underwent BMT. They found that outcomes
were unchanged from those of the one-year follow-up; that is, in the second
year follow-up,
subjects engaged in significantly less domestic violence than
they did in the year prior to BMT and
abstinent alcoholics had domestic-violence levels similar to
those of the nonalcoholic comparison group post-treatment, but alcoholics
who began drinking again had elevated levels of domestic violence.
The follow-up study described here confirms and documents the powerful
role of alcohol in spouse abuse -- although all of the alcoholics in the
study underwent the same marital therapy, those who remained abstinent
afterward had significantly lower levels of domestic violence than did
those who resumed drinking. These findings suggest that treatments that
are successful in sustaining abstinence are key to reducing domestic violence
among alcoholics.
One In Four U.S. Children Witnesses Alcohol Abuse or Alcoholism
in the Family
The effects of alcoholism extend far beyond alcoholics themselves. For
example, children in families affected by alcohol often live in environments
that are stressful, chaotic, and frightening. Frequently, they are neglected
or abused and face economic hardship and social isolation. Children of
alcoholics are vulnerable to mental illness and medical problems, and
are more likely than others to become alcoholic at some point in life.
In 1992, the NIAAA conducted the largest national survey on alcohol use
ever performed in the United States or elsewhere. This research revealed
that almost 14 million adults meet medical criteria for a formal diagnosis
of alcohol abuse or alcoholism4. Given the magnitude of alcohol
disorders among adults and the harm these adults can impose on children,
NIAAA researchers sought to determine how many residents age 17 or younger
are exposed to alcoholism or alcohol abuse via a member of the family.
Using 1992 survey data, researchers recently estimated that almost 43
percent (more than 28 million) of children lived in households with one
or more adults who had been alcoholics or alcohol abusers at some point
in life. Approximately 15 percent of these children (about 10 million)
lived in households with an adult diagnosed in the past year.
Scientists considered other factors in their final estimate. For example,
they assumed that only half of the children living with an adult diagnosed
with an alcohol-use disorder prior to the past year might suffer adverse
consequences. Using these and other criteria, epidemiologists calculated
that one in four U.S. children witnesses alcohol abuse and alcoholism
in the family. This figure probably is conservative, since it does not
include homeless children.
Children at risk for consequences of exposure to familial alcoholism
constitute a major public health problem. Currently, social and health
services for these children are fragmented and often do not address the
far-reaching effects of familial alcohol exposure. The findings described
here illustrate the urgent need to establish a comprehensive strategy
for children at risk that will integrate existing services, broaden them,
and target each developmental stage of childhood.
Underage Drinking Successfully Reduced in Average Communities
Via Policy Changes
How to reduce drinking among youth is a complex issue and an urgent one.
Drinking among youth is a prevalent behavior that holds risk not only
for unintentional injury, but also, scientists now suspect, for damage
to still-developing nervous systems. The widespread occurrence of heavy
drinking among adolescents and younger children is of great concern, particularly
in view of evidence that initiation of drinking earlier rather than later
in youth is associated with increasing risk of becoming alcohol-dependent
at some point in life.
Communities Mobilizing for Change on Alcohol (CMCA) was a 6-year trial
designed to reduce drinking by young people. Rather than using the traditional
approach to preventing underage drinking -- that is, focusing on youth's
demand for alcohol -- CMCA intervened in youths' supply of alcohol.
Researchers randomly assigned 15 small-to-midsize Minnesota and Wisconsin
communities to either participate in an intervention or to not participate.
Seven of the communities thus organized to change local policies that
affected supply of alcohol to youth and made underage drinking less acceptable
in the local culture, while the remaining eight communities served as
control groups, for comparison.
Compared to the control communities, CMCA communities had (1) less drinking
by 18-to-20-year-olds, (2) reduced sale of alcohol to minors, (3) reduced
provision of alcohol to younger adolescents by older adolescents, and
(4) more identification-checking by alcohol merchants, who also were less
likely to sell to minors.
Average communities can be effectively mobilized to significantly reduce
youths' access to alcohol. Of particular importance is that the large,
controlled trial that produced these results was randomized and that the
communities involved had paid little attention to issues surrounding youth
drinking before they were approached by the researchers.
Thus, the positive outcomes achieved in the CMCA intervention do not
appear to be based on factors that existed in the communities prior to
the trial. These findings suggests that other average communities that
commit to the type of intervention described here could achieve similar
results.
New Initiatives in Alcohol Research
(Supported by FY 2001 Funding)
Exploiting Clinical Trials to Study the Biological Basis of RecoveryA
major challenge for alcohol researchers is to discover the biological
mechanisms that underlie recovery, in terms of both (1) recovery from
alcohol's damaging effects on the body, including the brain, and (2) behavior;
that is, abstinence and relapse. The NIAAA proposes to conduct clinical
trials of small, intensively studied cohorts to identify pathways that
either inhibit or accelerate recovery from physiological damage and abstinence/relapse.
These types of data are essential for design of treatments that target
mechanisms involved in recovery or failure to recover. Four research areas
that are highly promising to the field of recovery and would be conducive
to clinical trials would comprise key areas of the proposed initiative.
They include:
Pharmacogenetics -- Some patients are able to
abstain from drinking because they respond to alcoholism-treatment
drugs (naltrexone and acamprosate), while other patients fail to
respond to the same medications. Genes are likely to be involved
in the pathways that underlie this difference in response. Once
researchers confirm the presence of a genetic component, they will
undertake the difficult search for the genes involved.
Sleep -- During recovery, inability to regulate
sleep disturbances common in alcoholism promotes relapse. Evidence
suggests that this phenomenon may be related to alcohol-induced changes
in the brain's production of growth hormones. Scientists hypothesize
that regulating sleep disturbances and/or growth hormones may influence
recovery.
Cognitive recovery -- Cognition (memory and judgment,
for example) is impaired by long-term alcohol use. Scientists now
have the tools to test recovery of neurocognitive function in detail
and to attempt to accelerate neurocognitive recovery.
Imaging -- Newly developed imaging techniques
will allow researchers to identify structure and function of specific
areas of the brain during various phases of recovery. Scientists then
can relate changes in structure and function to sleep, cognitive recovery,
and other factors that predict an individual's ability to remain abstinent.
Integrative Neuroscience Initiative on Alcoholism (INIA)
Among the ways the brain responds to alcohol are neuroadaptive responses
-- tolerance, which leads to the need for more alcohol; physical dependence
on alcohol; and physical withdrawal from alcohol. The significant advances
that NIAAA is making in identifying networks of nerve cells, or "neural
circuits," involved in these neuroadaptive responses are crucial.
These circuits are biological pathways that hold potential for therapeutic
alteration with medications.
However, advances in the study of neuroadaptive responses emanate from
a variety of fields in the alcohol-research community and other disciplines.
The NIAAA plans to accelerate this highly informative area of research
by establishing an initiative to coordinate the efforts and findings of
these various fields and disciplines. The initiative will be entitled
"Integrative Neuroscience Initiative on Alcoholism" (INIA).
An example of INIA's potential follows. Researchers develop animal models
of various alcohol-related behaviors, such as mice that engage in excessive
alcohol intake. A behavioral scientist employing that particular model
may have little time or expertise for integrating his or her research
with highly relevant biological investigations. The INIA approach will
make possible simultaneous analysis of the underlying neurocircuitry propelling
the behavior in question, analysis of relevant cellular and molecular
activity, measures of gene expression, and, ultimately, molecular/genetic
manipulations. Together, these activities will provide systematic biological
explanations for the behavior under study. One example of an area that
will benefit under INIA is the study of the role a given neuroreceptor
plays in behavioral phenomena, such as alcohol preference and self-administration.
Another important aspect of INIA will be development of bioinformatics
databases containing alcohol-related neuroscience and behavioral data
that can be shared by researchers from various disciplines.
These efforts will accelerate discoveries in the area of neural networks
and their application to clinical issues surrounding alcoholism.
Development of Medications for Alcoholism Treatment
In the 1990s, scientists made a discovery that both complicated the field
of alcohol research greatly and, at the same time, dramatically increased
chances for designing effective medications to treat alcoholism. They
discovered that alcohol molecules interact with not just one type of neuroreceptor,
but with many. (Neuroreceptors are the protein "receivers" of
chemical messages
that travel between nerve cells.) Any of these interactions between alcohol
and multiple neuroreceptor systems are potential targets for therapeutic
interventions with medications.
Currently, at least nine compounds -- potential medications -- that hold
promise for alcoholism treatment await further testing at the NIAAA. A
barrier to testing them is the lack of a mechanism for moving promising
compounds from the laboratory to the clinical-trial stage. The NIAAA proposes
an initiative that would enable establishment of a program designed to
bring promising compounds for alcoholism treatment to clinical trial.
The goal of the initiative is to speed availability of new medications
to alcohol-dependent patients. In addition, the proposed clinical-testing
program would conduct trials of existing drugs that are used for other
purposes but have shown promise in treating alcoholism, and would test
critical issues regarding alcoholism-treatment practices.
Other Areas of Interest in Alcohol Research
Alcohol Abuse Among Adolescents
At the suggestion of the NIAAA, a recent episode of the popular television
series "ER" focused entirely on a teen with an alcohol problem,
attesting to the public's concern about underage drinking. This concern
reflects that of the NIAAA and other Federal entities, including the Office
of the Surgeon General. Alcohol is the drug most abused by adolescents,
making underage drinking a major focus at the Institute -- particularly
in view of recent findings that early initiation of drinking is associated
with a dramatically increased risk of becoming alcohol-dependent at some
point in life. Adolescents have a high rate of alcohol use, in general,
and an epidemic rate at the college level. Some of the association between
early initiation of drinking and alcoholism may be due to biological factors
unique to adolescents or to psychosocial factors, or both. Recently, the
NIAAA launched a major project designed to identify biological mechanisms
of adolescent alcohol abuse.
In addition to funding biology-based studies, the NIAAA funds studies
to identify psychosocial mechanisms of underage drinking. Raising the
minimum legal drinking age to 21 has been associated with important reductions
in alcohol consumption and fatalities from alcohol-related crashes. However,
the pervasiveness of drinking, binge drinking, and alcohol-induced problems
among underage youth requires comprehensive preventive interventions that
address individuals, families, schools, and communities as a whole. The
potential impact of alcohol-advertising on adolescent drinking is being
examined. Studies are testing the effectiveness of community-based interventions
in preventing sales of alcohol to minors, TV and radio messages intended
to reduce alcohol use among young adolescents, counseling aimed at reducing
alcohol problems among college students, and strategies to prevent American
youth from crossing the border into Mexico to binge-drink.
Completed research reveals that school curricula, combined with parental
involvement, can reduce adolescent drinking; that "zero tolerance" laws
for young drivers can reduce fatal crashes; that activating average communities
through task forces and policy changes can reduce drinking among older
adolescents; and that health care providers can be effective agents for
reducing alcohol abuse among youth.
The Surgeon General of the United States has recognized the public health
implications of underage drinking and has launched a prevention campaign
in which the NIAAA has taken a leadership role. The Institute also is
collaborating with the Robert Wood Johnson Foundation to enlist governors'
spouses in a National Leadership Initiative to Keep Children Alcohol-Free.
This project focuses on children 9 to 15 years old and is designed to
make illegal underage drinking a national priority. Several other Offices
of the NIH are participating in this effort. In addition, a recently established
subcommittee of the NIAAA Advisory Council, composed of prominent scientists
and college presidents, has been meeting regularly in an effort to identify
optimal strategies for reducing binge-drinking among college students.
Centers for Mouse Mutagenesis Screening
The NIAAA has joined other Institutes of the NIH in supporting Centers
for Mouse Mutagenesis Screening. The traditional way of determining what
systems are important in alcohol's effects has been to give drugs that
interfere with certain substances in the brain (for example, receptors
and enzymes) and to observe changes in alcohol-related behavior. However,
this approach entails two major problems: (1) scientists are limited by
having to target substances in the brain that already are known to be
affected by alcohol and (2) the drugs in use today are not completely
specific to an intended target, but also affect other, unintended targets,
confusing the results of experiments.
A newer, more effective approach involves mouse mutagenesis screening.
In this technique, scientists use low doses of chemicals to induce gene
mutations in mice. By doing so, scientists can cause dozens of types of
single-gene mutations in hundreds or thousands of mice simultaneously.
This large supply of mutated mice provides scientists with greatly expanded
opportunities to identify gene mutations that affect alcohol-related behavior.
Genes previously not known to affect alcohol-related behavior can be identified,
in addition to the substances in the brain that these genes produce. Ultimately,
researchers can use this type of information to design new therapies for
alcohol-use disorders.
Use of Essential Fatty Acids for Prevention and Treatment
of Brain and Liver Pathology Associated with Alcoholism
The NIAAA is pursuing promising results indicating that a dietary supplement
-- essential fatty acids or "EFAs" -- may be helpful in preventing
alcohol-induced organ and tissue pathology, such as liver disease. EFAs
are substances that the body cannot produce and that must be obtained
through food. They play such crucial roles as contributing to the integrity
of the membranes that surround all cells, protecting them from their environment.
The NIAAA Intramural Research Program has demonstrated that EFAs, particularly
docosahexaenoate, play
an important role in normal brain and liver function. These studies also
reveal that alcohol abuse has a negative impact on EFA levels and that
EFA supplementation may have a protective or therapeutic effect.
NIAAA Researcher-in-Residence Program
The NIAAA and the Center for Substance Abuse Treatment (CSAT) jointly
sponsor the Researcher-in-Residence Program. Transfer of scientific findings
to alcohol-treatment practices has been impeded by two major obstacles:
(1) treatment programs often adhere tenaciously to traditional methods
that have been in place for years -- methods that sometimes are not based
on current science advances, and (2) the difficulty of implementing science
advances in real-world settings, due to such factors as cost and other
logistics. The goal of the Researcher-in-Residence Program is to offer
treatment programs hands-on help in transferring science advances to clinical
practice. To accomplish this goal, NIAAA and CSAT join with State directors
of alcohol programs to place nationally recognized scientists in brief
residencies at participating clinical treatment sites. New York State
and North Carolina have completed Phase I of the Program, in which clinical
directors meet with the sponsors in a 1-day preparatory symposium. New
York State is preparing to enter Phase II, in which six volunteer researchers
will serve in residency in clinical programs. Pending results of these
exchanges, Phase III will formalize findings from these efforts in clinical
trials that will document successful treatment strategies for dissemination
to the treatment community.
Endnotes
1. BF Grant et al.: Prevalence of DSM-IV alcohol abuse and dependence
-- United States, 1992.
NIAAA's Epidemiologic Bulletin No. 35 18:243-248, 1994.
2. PM Lewisohn et al.: Alcohol consumption in high school adolescents:
Frequency of use and dimensional structure of associated problems.
Addiction 91:375-390, 1996.
3. H Harwood et al.: Update of The economic costs of alcohol and
drug abuse in the United States,1992. NIH Publication No.
98-4327 1-9, 1998. Updated October 1999.
4. BF Grant et al.: Prevalence of DSM-IV alcohol abuse and dependence
-- United States, 1992. NIAAA's Epidemiologic Bulletin No. 35
18:243-248, 1994.
Budget Policy
The Fiscal Year 2001 budget request for the NIAAA is $288,578,000, excluding
AIDS, an increase of $14,587,000,000 and 5.3 percent over the FY 2000
level. Included in this total is $5,000,000 for the following NIH Areas
of Special Emphasis: $2,000,000 for Biology of the Brain, $2,000,000 for
New Preventive Strategies Against Disease, $1,000,000 for the Development
of Therapeutics and the Genetics of Medicine.
A five year history of FTEs and Funding Levels for NIAAA are shown in
the graphs below:
|
|
One of NIH's highest
priorities is the funding of medical research through research project
grants (RPGs). Support for RPGs allows NIH to sustain the scientific momentum
of investigator-initiated research while providing new research opportunities.
To control the growth of continuing commitments and support planned new
and expanded initiatives, the Fiscal Year 2001 request provides average
cost increases of 2 percent over Fiscal Year 2000 for competing RPGs.
Noncompeting RPGs will receive increases of 2 percent on average for recurring
costs. This strategy will ensure that NIH can maintain a healthy number
of new awards, especially for first time researchers.
Promises for advancement
in medical research are dependent on a continuing supply of new investigators
with new ideas. In the Fiscal Year 2001 request, NIAAA will support 235
pre- and postdoctoral trainees in full-time training positions. Stipends
will increase by 2.2 percent over Fiscal Year 2000 levels.
The Fiscal Year 2001
request includes funding for 14 research centers, 92 other research grants,
including 6 new clinical career awards, and 34 R&D; contracts. The mechanism
distribution by dollars and percent change are displayed below:
National
Institutes of Health
National Institute
on Alcohol Abuse and Alcoholism
Budget Mechanism
Non-AIDS
|
FY
1999 |
FY
2000 |
FY
2001 |
MECHANISM |
Actual |
Estimate |
Estimate |
Research
Grants: |
No. |
Amount |
No. |
Amount |
No. |
Amount |
|
|
|
|
|
|
|
Research
Projects |
|
|
|
|
|
|
Noncompeting |
358
|
$90,295,000 |
401
|
$112,357,000 |
422
|
$129,938,000 |
Administrative supplements |
31
|
1,322,000
|
22
|
990,000
|
22
|
990,000
|
Competing: |
|
|
|
|
|
|
Renewal |
43
|
14,424,000
|
43
|
11,352,000
|
30
|
7,920,000
|
New |
127
|
31,288,000
|
117
|
35,601,000
|
83
|
26,130,000
|
Supplements |
0
|
100,000
|
2
|
200,000
|
2
|
200,000
|
Subtotal, competing |
170
|
45,812,000
|
162
|
47,153,000
|
115
|
34,250,000
|
Subtotal, RPGs |
528
|
137,429,000 |
563
|
160,500,000
|
537
|
165,178,000
|
SBIR/STTR |
20
|
4,293,000
|
22
|
5,372,000
|
24
|
6,000,000
|
Subtotal, RPGs |
548
|
141,722,000 |
585
|
165,872,000
|
561
|
171,178,000
|
|
|
|
|
|
|
|
Research
Centers |
|
|
|
|
|
|
Specialized/comprehensive |
14
|
22,450,000
|
14
|
22,210,000
|
14
|
23,098,000
|
Clinical research |
0
|
0
|
0
|
0
|
0
|
0
|
Biotechnology |
0
|
0
|
0
|
0
|
0
|
0
|
Comparative medicine |
0
|
0
|
0
|
0
|
0
|
0
|
Research Centers in Minority Institutions |
0
|
0
|
0
|
0
|
0
|
0
|
Subtotal, Centers |
14
|
22,450,000
|
14
|
22,210,000
|
14
|
23,098,000
|
|
|
|
|
|
|
|
Other
Research |
|
|
|
|
|
|
Research careers |
63
|
7,010,000
|
69
|
7,970,000
|
72
|
8,320,000
|
Cancer education |
0
|
0
|
0
|
0
|
0
|
0
|
Cooperative clinical research |
13
|
11,843,000
|
14
|
11,800,000
|
14
|
12,390,000
|
Biomedical research support |
0
|
0
|
0
|
0
|
0
|
0
|
Minority biomedical research support |
0
|
0
|
0
|
0
|
0
|
0
|
Other |
5
|
1,241,000
|
6
|
1,400,000
|
6
|
1,500,000
|
Subtotal, Other Research |
81
|
20,094,000
|
89
|
21,170,000
|
92
|
22,210,000
|
Total Research Grants |
643
|
184,266,000 |
688
|
209,252,000
|
667
|
216,486,000
|
|
|
|
|
|
|
|
Training |
FTTPs |
|
FTTPs |
|
FTTPs |
|
Individual awards |
34
|
876,000
|
50
|
1,440,000
|
54
|
1,586,000
|
Institutional awards |
170
|
5,733,000
|
165
|
6,095,000
|
181
|
6,812,000
|
Total, Training |
204
|
6,609,000
|
215
|
7,535,000
|
235
|
8,398,000
|
|
|
|
|
|
|
|
Research
& development contracts |
25
|
14,468,000
|
35
|
16,613,000
|
34
|
19,310,000
|
(SBIR/STTR) |
2
|
1,460,000
|
4
|
1,200,000
|
4
|
1,200,000
|
|
|
|
|
|
|
|
|
FTEs |
|
FTEs |
|
FTEs |
|
Intramural
research |
92
|
24,121,000
|
96
|
26,083,000
|
104
|
29,264,000
|
|
|
|
|
|
|
|
Research
management and support |
130
|
13,607,000
|
133
|
14,508,000
|
133
|
15,120,000
|
|
|
|
|
|
|
|
Cancer
prevention & control |
0
|
0
|
0
|
0
|
0
|
0
|
|
|
|
|
|
|
|
Construction |
|
0
|
|
0
|
|
0
|
|
|
|
|
|
|
|
Total, NIAAA |
222
|
243,071,000 |
229
|
273,991,000
|
237
|
288,578,000
|
|
|
|
|
|
|
|
(Clinical
Trials) |
|
28,592,000
|
|
31,500,000
|
|
34,000,000
|
Note:
Includes FTEs associated with HIV/AIDS research activities. Funds to support
these FTEs
are included
in the Office of AIDS Research.
National
Institutes of Health
National Institute
on Alcohol Abuse and Alcoholism
Budget Mechanism
AIDS
|
FY
1999 |
FY
2000 |
FY
2001 |
MECHANISM |
Actual |
Estimate |
Estimate |
Research
Grants: |
No. |
Amount |
No. |
Amount |
No. |
Amount |
|
|
|
|
|
|
|
Research
Projects |
|
|
|
|
|
|
Noncompeting |
29
|
$10,438,000 |
32
|
$12,350,000 |
39 |
$14,404,000 |
Administrative supplements |
5
|
225,000
|
0
|
0
|
0
|
0
|
Competing: |
|
|
|
|
|
|
Renewal |
4
|
1,450,000
|
3
|
933,000
|
3
|
915,000
|
New |
5
|
1,094,000
|
10
|
3,069,000
|
5
|
1,667,000
|
Supplements |
0
|
0
|
0
|
0
|
0 |
0
|
Subtotal, competing |
9
|
2,544,000
|
13
|
4,002,000
|
8
|
2,582,000
|
Subtotal, RPGs |
38
|
13,207,000
|
45
|
16,352,000
|
47
|
16,986,000
|
SBIR/STTR |
0
|
0
|
0
|
0
|
0 |
0
|
Subtotal, RPGs |
38
|
13,207,000
|
45
|
16,352,000
|
47
|
16,986,000
|
|
|
|
|
|
|
|
Research
Centers |
|
|
|
|
|
|
Specialized/comprehensive |
1
|
1,583,000
|
1
|
1,738,000
|
1 |
1,740,000
|
Clinical research |
0
|
0
|
0
|
0
|
0 |
0
|
Biotechnology |
0
|
0
|
0
|
0
|
0 |
0
|
Comparative medicine |
0
|
0
|
0
|
0
|
0
|
0
|
Research Centers in Minority Institutions |
0
|
0
|
0
|
0
|
0 |
0
|
Subtotal, Centers |
1
|
1,583,000
|
1
|
1,738,000
|
1
|
1,740,000
|
|
|
|
|
|
|
|
Other
Research |
|
|
|
|
|
|
Research careers |
4
|
355,000
|
2
|
284,000
|
4
|
440,000
|
Cancer education |
0
|
0
|
0
|
0
|
0
|
0
|
Cooperative clinical research |
0
|
0
|
0
|
0
|
0
|
0
|
Biomedical research support |
0
|
0
|
0
|
0
|
0
|
0
|
Minority biomedical research support |
0
|
0
|
0
|
0
|
0
|
0
|
Other |
0
|
0
|
0
|
0
|
0
|
0
|
Subtotal, Other Research |
4
|
355,000
|
2
|
284,000
|
4
|
440,000
|
Total Research Grants |
43
|
15,145,000
|
48
|
18,374,000
|
52
|
19,166,000
|
|
|
|
|
|
|
|
Training |
FTTPs |
|
FTTPs |
|
FTTPs |
|
Individual awards |
1
|
23,000
|
2
|
45,000
|
2
|
46,000
|
Institutional awards |
3
|
115,000
|
5
|
196,000
|
5
|
200,000
|
Total, Training |
4
|
138,000
|
7
|
241,000
|
7
|
246,000
|
|
|
|
|
|
|
|
Research
& development contracts |
1
|
422,000
|
4
|
292,000
|
2 |
301,000
|
(SBIR/STTR) |
0
|
0
|
0
|
0
|
0
|
0
|
|
|
|
|
|
|
|
|
FTEs |
|
FTEs |
|
FTEs |
|
Intramural
research |
0
|
150,000
|
0
|
0
|
0 |
0
|
|
|
|
|
|
|
|
Research
management and support |
0
|
332,000
|
0
|
336,000
|
0
|
370,000
|
|
|
|
|
|
|
|
Cancer
prevention & control |
0
|
0
|
0
|
0
|
0 |
0
|
|
|
|
|
|
|
|
Construction |
|
0
|
|
0
|
|
0
|
|
|
|
|
|
|
|
Total, NIAAA |
0
|
16,187,000
|
0
|
19,243,000
|
0
|
20,083,000
|
|
|
|
|
|
|
|
(Clinical
Trials) |
|
0
|
|
0
|
|
0
|
National
Institutes of Health
National Institute
on Alcohol Abuse and Alcoholism
Budget Mechanism
TOTAL
|
FY
1999 |
FY
2000 |
FY
2001 |
MECHANISM |
Actual |
Estimate |
Estimate |
Research
Grants: |
No. |
Amount |
No. |
Amount |
No. |
Amount |
|
|
|
|
|
|
|
Research
Projects |
|
|
|
|
|
|
Noncompeting |
387
|
$100,733,000 |
433
|
$124,707,000 |
461 |
$144,342,000 |
Administrative supplements |
36
|
1,547,000
|
22
|
990,000
|
22
|
990,000
|
Competing: |
|
|
|
|
|
|
Renewal |
47
|
15,874,000
|
46
|
12,285,000
|
33
|
8,835,000
|
New |
132
|
32,382,000
|
127
|
38,670,000
|
88
|
27,797,000
|
Supplements |
0
|
100,000
|
2
|
200,000
|
2 |
200,000
|
Subtotal, competing |
179
|
48,356,000
|
175
|
51,155,000
|
123
|
36,832,000
|
Subtotal, RPGs |
566
|
150,636,000 |
608
|
176,852,000
|
584
|
182,164,000
|
SBIR/STTR |
20
|
4,293,000
|
22
|
5,372,000
|
24 |
6,000,000
|
Subtotal, RPGs |
586
|
154,929,000 |
630
|
182,224,000
|
608
|
188,164,000
|
|
|
|
|
|
|
|
Research
Centers |
|
|
|
|
|
|
Specialized/comprehensive |
15
|
24,033,000
|
15
|
23,948,000
|
15 |
24,838,000
|
Clinical research |
0
|
0
|
0
|
0
|
0 |
0
|
Biotechnology |
0
|
0
|
0
|
0
|
0 |
0
|
Comparative medicine |
0
|
0
|
0
|
0
|
0
|
0
|
Research Centers in Minority Institutions |
0
|
0
|
0
|
0
|
0 |
0
|
Subtotal, Centers |
15
|
24,033,000
|
15
|
23,948,000
|
15
|
24,838,000
|
|
|
|
|
|
|
|
Other
Research |
|
|
|
|
|
|
Research careers |
67
|
7,365,000
|
71
|
8,254,000
|
76
|
8,760,000
|
Cancer education |
0
|
0
|
0
|
0
|
0
|
0
|
Cooperative clinical research |
13
|
11,843,000
|
14
|
11,800,000
|
14
|
12,390,000
|
Biomedical research support |
0
|
0
|
0
|
0
|
0
|
0
|
Minority biomedical research support |
0
|
0
|
0
|
0
|
0
|
0
|
Other |
5
|
1,241,000
|
6
|
1,400,000
|
6
|
1,500,000
|
Subtotal, Other Research |
85
|
20,449,000
|
91
|
21,454,000
|
96
|
22,650,000
|
Total Research Grants |
686
|
199,411,000 |
736
|
227,626,000
|
719
|
235,652,000
|
|
|
|
|
|
|
|
Training |
FTTPs |
|
FTTPs |
|
FTTPs |
|
Individual awards |
35
|
899,000
|
52
|
1,485,000
|
56
|
1,632,000
|
Institutional awards |
173
|
5,848,000
|
170
|
6,291,000
|
186
|
7,012,000
|
Total, Training |
208
|
6,747,000
|
222
|
7,776,000
|
242
|
8,644,000
|
|
|
|
|
|
|
|
Research
& development contracts |
26
|
14,890,000
|
39
|
16,905,000
|
36 |
19,611,000
|
(SBIR/STTR) |
2
|
1,460,000
|
4
|
1,200,000
|
4
|
1,200,000
|
|
|
|
|
|
|
|
|
FTEs |
|
FTEs |
|
FTEs |
|
Intramural
research |
92
|
24,271,000
|
96
|
26,083,000
|
104 |
29,264,000
|
|
|
|
|
|
|
|
Research
management and support |
130
|
13,939,000
|
133
|
14,844,000
|
133
|
15,490,000
|
|
|
|
|
|
|
|
Cancer
prevention & control |
0
|
0
|
0
|
0
|
0 |
0
|
|
|
|
|
|
|
|
Construction |
0
|
0
|
0
|
0
|
0 |
0
|
|
|
|
|
|
|
|
Total, NIAAA |
222
|
259,258,000 |
229
|
293,234,000
|
237
|
308,661,000
|
|
|
|
|
|
|
|
(Clinical
Trials) |
|
28,592,000
|
|
31,500,000
|
|
34,000,000
|
|