Alcohol serial killer
Alcohol in de EU: de 'serial killer' wordt
ontmaskerd.
De cijfers in het rapport L'alcool en
Europe, une approche en sante publique' van Dr. Peter Anderson (L'Institute of Alcohol in
Londen) zijn afschrikwekkend.
Europa is wereldkampioen als we het hebben
over de consumptie van alcohol. Zo'n 23 miljoen personen zijn alcoholafhankelijk. Meer dan
1 op de 6 jongeren waren meer dan 3x dronken de afgelopen maand. Deze overconsumptie
vertegenwoordigt 7,4 % van vroegtijdig overlijden. De 3e doodsoorzaak in de EU. Een
rapport roept op om efficiënte maatregelen te nemen
..De Europese Commissie tracht
een gemeenschappelijk strategie te vinden om de consumptie van alcohol op het continent te
beperken en de faktuur voor de maatschappij te verminderen.
Waarom ? De kosten van deze
catastrofe zijn 125 miljard euro per jaar, 650 euro per gezin.
Alcohol en tabak: de 2 grote 'serial
killers'.
De ontmaskering van alcohol als serieuze
doder is vrij recent. Men interesseerde zich niet echt voor de consequenties van gebruik
van alcohol en autorijden. Nu begint men zich bewust te worden van de schaden die dit
veroorzaakt. Alles heeft tijd nodig, net zoveel tijd als nodig was om te begrijpen dat
tabak ook een serieuze doder was. De studie van Doll die de relatie tussen longkanker en
tabak aantoonde is van 50 jaar geleden. Dus zo'n 40 jaar hebben we moeten wachten tot er
anti-tabakmaatregelen werden genomen.
Laten we hopen dat deze periode minder lang
is om anti-alcohol maatregelen te nemen. De twijfel is er; het heeft al meer dan 10 jaar
geduurd voordat zwangere vrouwen gewaarschuwd werden dat gebruik van alcohol tijdens de
zwangerschap slecht is voor hun toekomstig kind. Meer dynamisme wordt verwacht van
bedrijven: directeuren van personeelszaken zijn steeds meer op zoek naar oplossingen,
omdat het overbodig alcoholgebruik een sociaal en een produktief risico inhoudt voor het
bedrijf.
Om een idee te krijgen van de weg die nog
bewandeld moet worden het volgende: in Amerika ligt de consumptie van alcohol per inwoner
meer dan 2x lager en het percentage van dood door kanker is ook veel lager. In Europa
drinken mannen net zoveel als vrouwen, 1 glas per dag
en 1 glas per dag is de
ideale dosis om van alcohol te genieten zonder nadelige consequenties eraan over te
houden. Dus
.de hoeveelheid per persoon zal herzien dienen te worden en we kunnen
toekomstige berichten verwachten vanuit de hoek van de Volksgezondheid die deze boodschap
gaan brengen.
Bron: www.e-sante.fr
14/08/2006
Dr Philippe Presles
Conférence de presse "Alcool, enjeux
et politiques en Europe ?
Quelles réponses efficaces face au risque alcool ?",
21 juin 2006 - Paris.
Vertaalde samenvatting door Ditta van Herk
Eerste bewijs voor relatie tussen
alcohol en kanker
Wat niemand tot nu toe was gelukt is de Dr.
Jian-Wei Gu van de University of Mississippi Medical Center bij toeval gelukt, een bewijs
vinden van de relatie tussen alcohol en tumorgroei. Deze onderzoeker was eigenlijk bezig
met onderzoek naar de groei van bloedvaten ivm hart- en vaatziekten. Bij toeval ontdekte
hij een relatie tussen tumorgroei en lage dosis alcohol. Eerdere onderzoekers hadden deze
relatie niet gevonden omdat men de proefdieren te hoge dosis alcohol (20%) had gegeven.
Dr. Jian-Wei Gu gebruikte echter 1% wat overeen komt met 1-2 drankjes.
http://info.umc.edu/news/?n=mcnews&id=3127
Download het volledige EU rapport
over alcohol
Het Europese rapport over de kosten en
risico's van alcohol kun je
nu downloaden:
http://ec.europa.eu/health-eu/doc/alcoholineu_sum_nl_en.pdf
Een stukje uit het rapport:
Los van het feit dat alcohol een
verslavende stof is, is alcohol ook de oorzaak van 60 verschillende soorten ziektes en
aandoeningen, zoals verwondingen, geestelijke stoornissen, gedragsafwijkingen, maag-
darmaandoeningen, verschillende vormen van kanker, cardiovasculaire ziektes,
immunologische afwijkingen, longziektes, bot- en spierziektes, afwijkingen in de
voortplanting en prenatale schade zoals een groter risico op vroeggeboorte en laag
geboortegewicht. Voor de meeste aandoeningen geldt dat het risico toeneemt naarmate men
meer alcohol drinkt. Voor sommige aandoeningen, zoals cardiomyopathie, ernstige acute
ademhalingsproblemen en spierbeschadigingen lijkt de schade alleen veroorzaakt te worden
door een langdurig hoog niveau van alcohol consumptie. Maar zelfs bij een hoog
consumptieniveau verhoogt alcohol
het risico en de ernst van deze aandoeningen op een dosis-gerelateerde manier. De
frequentie en de omvang van periodiek zwaar drinken spelen een grote rol bij de toename
van het risico op aandoeningen en bepaalde cardiovasculaire ziektes (hartinfarct en
beroerte).
Tobacco and alcohol use independently
increase risk of head and neck cancer
cigarette smoking is more strongly associated with head and neck cancers than drinking
alcohol, according to a study in the May 16 issue of the Journal of the National Cancer
Institute. The study found that smoking is responsible for a quarter of head and neck
cancers among individuals who do not drink alcohol.
http://jnci.oxfordjournals.org/cgi/content/abstract/99/10/777
Alcohol use during pregnancy leads to
greater risk of extreme preterm delivery
Preterm delivery, and particularly "extreme prematurity" -- defined as less than
32 weeks of gestation -- are major contributors to perinatal sickness and death worldwide.
A new study has found that maternal alcohol use during pregnancy can contribute to a
substantial increase in risk for extreme preterm delivery.
http://www.eurekalert.org/pub_releases/2007-05/ace-aud051707.php
Moderate drinking lowers women's risk of
heart attack
Women who regularly enjoy an alcoholic drink or two have a significantly lower risk of
having a non-fatal heart attack than women who are life-time abstainers, epidemiologists
at the University at Buffalo have shown.
http://www.eurekalert.org/pub_releases/2007-05/uab-mdl052307.php
Acetaldehyde 30x more toxic than alcohol
In the 1980s Dr. Victor R. Preedy of King's College in London reported that acetaldehyde,
a powerful poison that damages muscle tissue even more than it does the liver or brain, is
approximately 30 times more toxic than alcohol itself.
http://www.cheerzhangover.com/acetaldehyde.htm
Drinking heavily in college may lead to
heart disease later in life
College-age students who drink heavily may increase their risk for future heart disease,
researchers reported at the American Heart Association's 8th annual Conference on
Arteriosclerosis, Thrombosis and Vascular Biology.
http://www.americanheart.org/presenter.jhtml?identifier=3047060
Choline shows promise in reducing
behavioral effects associated with prenatal alcohol exposure
Giving choline to infants who were exposed in the womb to alcohol may mitigate some of the
resulting problems. Prenatal alcohol exposure affects physical and central nervous system
development, putting children at risk for fetal alcohol spectrum disorders that at their
worst include full-blown fetal alcohol syndrome. These disorders can mean a lifetime of
potentially serious problems with learning, attention, motor skills and social behavior.
The findings appear in the February issue of Behavioral Neuroscience, which is published
by the American Psychological Association (APA).
At San Diego State University, research led by Jennifer Thomas, PhD, is using an animal
model to assess the potential therapeutic value of choline. Because scientists have been
unable to determine a safe threshold for alcohol consumption during human pregnancy,
abstention is the only sure means of prevention. However, warnings about the dangers of
drinking during pregnancy either dont reach or arent heeded by all pregnant
women. As a result, researchers are seeking effective remedies to give after birth, when
health professionals may be better able to intervene.
Choline plays a number of roles in brain development. It is also a precursor to
acetylcholine, a neurotransmitter involved in learning and cognition, among other
functions. Choline is available in many foods, such as eggs and liver, and sold over the
counter in well-tolerated forms such as lecithin, choline bitartrate or chloride, and
phosphatidylcholine. Due to cholines beneficial effects on nervous-system
development, women are advised to consume 450 mg a day while pregnant and 550 mg a day
while breast feeding (the tolerable upper limit has been set at 3.5 g per day). For
infants, 125-150 mg/day is considered adequate during the first year, rising as the child
grows older. Choline is added to some prenatal vitamins and baby formulas, and is now
added to some childrens multivitamins and cereals.
http://www.eurekalert.org/pub_releases/2007-02/apa-csp022607.php
Genetic link to heavy substance abuse in
teenagers
A team led by School of Medicine researchers has made important new discoveries about
teenagers use of addictive substances.
The team found that family and community experiences play an important role in whether
teenagers experiment with alcohol, cigarettes and marijuana, but genetic influences become
more important for progression to heavy substance use.
Researchers questioned more than 1,200 pairs of identical and non-identical twins aged
11-19 in Wales and Manchester about their use of these substances.
The study, published in Addiction, the journal of the Society for the Study of Addiction,
found 86 per cent of youngsters had drunk alcohol at some point in their lives. Of these,
one third reported binge drinking, drunkenness, or getting into situations they later
regretted because of alcohol. Cigarettes had been tried by 58 per cent, with 24 per cent
reporting heavy use. Just 22 per cent reported trying marijuana and of these, 62 per cent
had used it fewer than six times in their life.
There was a strong link between starting to smoke tobacco or marijuana and going on to
heavy use. There was a weaker link for alcohol, suggesting that many teenagers may
experiment with drink without developing a problem.
http://www.cardiff.ac.uk/newsevents/23596.html
Stress and alcohol cues appear to target
the brain differently to produce craving
Both stress and "alcohol cues" (reminders of drinking) can produce craving and
possibly relapse in alcoholics trying to avoid drinking. New findings indicate that stress
and alcohol cues work on the brain differently to produce craving. Results suggest that
independently addressing the effects of stress and alcohol cues on craving may improve an
alcoholic's chances of remaining sober.
http://www.eurekalert.org/pub_releases/2007-02/ace-saa021507.php
Binge-drinking teenagers are damaging
their brains
Teenagers who drink heavily are risking permanent damage to their brain functions,
scientists warned last night. Alcohol has been shown to cause significant ongoing memory
loss in youngsters which could extend into adulthood.
http://www.dailymail.co.uk/pages/live/articles/health/dietfitness.html?in_article_
id=444154&in_page_id=1774&in_a_source=&ito=1490
Scientist Finds First Evidence Of
Alcohol-Cancer Link
Dr. Jian-Wei Gu came to Mississippi to study the cardiovascular system with a special
interest in the process of blood vessel growth. So how does a cardiovascular physiologist
attract national headlines about his research in cancer? According to Gu, assistant
professor of physiology and biophysics at the University of Mississippi Medical Center, it
was completely by accident.
Reports of Gus research have appeared in USA Today, Science News, the New Scientist
and on CBS News. It was big news because Gu has done what many scientists before him have
failed to do: describe the mechanism by which alcohol consumption causes tumor growth.
Scientists have known for a hundred years that there was a strong association
between alcohol consumption and several types of cancer, Gu said. He cites a study
from Paris in 1910 that showed that 80 percent of patients with cancer of the esophagus or
gastric track were alcoholics.
More recently, epidemiological studies show a strong correlation between alcohol
consumption and cancer of the mouth, pharynx, larynx, esophagus, liver, and large bowel.
Alcohol consumption seems to be a risk factor even for breast cancer. But experiments in
the lab have failed - until now - to show the effects in animals that observers knew to be
true in humans.
The problem, it turns out, was that investigators were using too much alcohol.
Most all the previous studies used alcohol concentrations of 20 percent, far more
than the equivalent human consumption, Gu said. The animals wasted away but they
didnt show abnormal tumor growth, he said.
Gu used alcohol concentrations of one percent, about the equivalent of one or two drinks a
day in humans, or moderate alcohol consumption. Using what he terms physiologically
relevant levels of alcohol, he stimulated tumor growth in both chick embryos and in
mice.
Gu came to Mississippi in 1995 to work on angiogenesis, or blood vessel growth, and what
stimulates or controls it. Seven years ago, working in the lab, he and his colleagues
noticed that the growth factor that stimulates vessel growth (vascular endothelial growth
factor or VEGF) increased unexpectedly in certain cell cultures.
They determined that it was the alcohol they used as a solvent, in very low
concentrations, that caused the increase in the growth factor.
That serendipitous finding by Gu in 2000 led to the study in chick embryos and, most
recently, to a study showing that melanoma cancers in mice grew significantly faster and
larger in the mice who consumed the equivalent of one or two alcoholic drinks a day than
the mice that received no alcohol.
The mice used in the most recent study were given drinking water that had an alcohol
concentration of one percent for 12 hours. The next 12 hours, they received water with no
alcohol. Another group of mice received no alcohol in their water.
After a week, Gu and his colleagues inoculated all the animals with mouse melanoma cells.
Three weeks later, the tumors were removed to be analyzed. All the mice had tumors, but
the mice given alcohol had tumors that had progressed much more rapidly than the mice that
had no alcohol. The larger tumors also had more blood vessel growth.
Dr. Thomas Adair, professor of physiology and biophysics and Gus mentor when he came
to Mississippi, said that Gus findings have been confirmed by other scientists.
When he presented his findings at a FASEB (Federated Societies for Experimental
Biology) meeting, someone from a group in San Diego came up to me afterward and told me
they had found the same thing in their lab and didnt know what to make of it. They
went back and did a study on rats and found the same thing.
Angiogenesis is an area of keen interest for its application to cancer therapy. Right now,
Adair estimates there may be as many as 40 drugs that act by controlling angiogenesis in
clinical trials.
But angiogenesis isnt necessarily pathological, according to Adair. Stimulating
angiogenesis would be helpful in repairing heart tissue damaged by a heart attack or in
wound healing.
Gus research is funded by the National Alcohol Abuse and Alcoholism Institute of the
National Institutes of Health (NIH), the National Heart, Lung and Blood Institute of NIH
and the American Cancer Society.
http://info.umc.edu/news/?n=mcnews&id=3127
Females more prone to brain damage from
alcohol abuse
Alcoholism has traditionally been considered a male disease because there are many more
alcoholic males than females. But a study by researchers at Oregon Health & Science
University and the Portland Veterans Affairs Medical Center suggests that women are more
prone to brain damage from alcohol abuse than men. The study found that female mice are
more susceptible to neurotoxic effects of alcohol withdrawal, including significantly
increased brain cell death, than male mice.
http://www.ohsu.edu/ohsuedu/newspub/071807alcohol.cfm
Prenatal alcohol exposure alters brain
activity in the frontal-striatal areas
Heavy prenatal alcohol exposure does not always lead to fetal alcohol syndrome (FAS);
sometimes it can lead to cognitive and behavioral deficits in the absence of craniofacial
features needed to make an FAS diagnosis. A new study has found that children and
adolescents prenatally exposed to alcohol have altered responses in frontal-striatal
areas, brain regions that may inhibit behavior.
http://www.eurekalert.org/pub_releases/2007-07/ace-pae071607.php
Children with attention deficit
hyperactivity disorder at risk for alcohol problems
Prior research has shown that children with ADHD can develop alcohol problems later in
life. Two studies confirm this association, indicating that drinking problems begin around
age 15. Parental alcoholism and family stress appear to add to the risk of children with
ADHD developing alcohol problems themselves.
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1530-0277.2007.00340.x
Sequence variation in the alpha
synuclein gene contributes to alcohol craving
The protein alpha synuclein (SNCA) plays an important role in the regulation of dopamine
function. Craving is a common symptom in alcoholics. New findings show that sequence
variation in the gene that encodes SNCA contributes to whether or not an individual craves
or does not crave alcohol.
http://www.eurekalert.org/pub_releases/2007-03/ace-svi031907.php
Drinking heavy amounts of alcohol
shrinks your brain
Drinking heavy amounts of alcohol over a long period of time may decrease brain volume,
according to research that will be presented at the American Academy of Neurology's 59th
Annual Meeting in Boston
http://www.eurekalert.org/pub_releases/2007-05/aaon-dha041007.php
Increased alcohol intake associated with
decreased risk of developing rheumatoid arthritis
New data presented today at EULAR 2007 suggest that alcohol may protect against rheumatoid
arthritis, with three units a week exhibiting protective effects and ten units a week
being more protective still. An alcohol consumption of three units per week or more also
reduced the risk by smoking or by a genetic predisposition to RA.
http://www.eular.org/congresspressreleases/OPO129_-_press_release_Kallberg_-_ethanol_-_FINAL.pdf
Research offers hope for alcoholics
Australian scientists have found a system in the brain that stops the craving for alcohol
and prevents relapse after one recovers from the addiction.
http://www.hfi.unimelb.edu.au/content/news/hm_news01_curn.html
New Evidence On Why Alcohol
Consumption Is A Risk Factor For Cancer
Now researchers in Japan have discovered direct molecular evidence supporting that link
between acetaldehyde and alcohol-related cancers. In a report published in the current
(October) issue of the monthly ACS journal Chemical Research in Toxicology, Tomonari
Matsuda and colleagues studied DNA from the blood of 44 patients being treated for
alcoholism.
http://pubs.acs.org/cgi-bin/abstract.cgi/crtoec/
2006/19/i10/abs/tx060113h.html
Long-term effects of alcohol
abuse during adolescence
There is mounting evidence that repeated
exposure to alcohol during adolescence leads to long-lasting deficits in cognitive
abilities, including learning and memory, in humans. Much of this work has been pioneered
by Drs. Susan Tapert and Sandra Brown, alcohol researchers at the University of California
, San Diego (UCSD). Drs. Tapert and Brown have conducted a series of studies examining the
impact of alcohol abuse on neuropsychological functioning in adolescents and young adults.
In one such study (Brown et al., 2000), adolescents in an in-patient substance abuse
treatment program, at least three weeks sober, were compared to controls from the
community on a battery of neuropsychological tests. Ages ranged from 15-16. Frequent
drinkers (100 or more total drinking sessions), particularly those that had experienced
alcohol withdrawal, performed more poorly than controls on several tests, including tests
of learning, memory, and visuospatial functioning.
http://www.duke.edu/~amwhite/Adolescence/adolescent6.html
Alcohol + zwangerschap = sloper van
je baby
Volgens de Australische profesor Elizabeth
Elliott kan alchohol bij een jonge vrouw die zwanger is leiden tot het Foetaal alcohol
syndroom waarbij de baby schade aan hersenen, hart en nieren kan oplopen. Verder kan het
op school leiden tot leer- en gedragsproblemen en voor afwijkingen in het gezicht zorgen.
Een avondje flink doorzakken met veel
alcohol in de laatste fase van de zwangerschap is al genoeg: de baby kan het Foetaal
Alcohol Syndrome (FAS) ontwikkelen.
Laat je baby dus niet de dupe worden van
alcohol....
http://www.medfac.usyd.edu.au/news/features/2006/061110a.php
Meer informatie over dit syndroom
http://www.fasstichting.nl/
http://www.erfelijkheid.nl/zena/foeta.php
http://www.czmedicinfo.nl/%7Bf1232b3a-09d0-4f41-a1
http://www.e-gezondheid.be/nl/ZwangerschapAlcohol-10567-541-art.htm
http://www.mobiel-pleegzorg.nl/archief/2003/mo03505.htm
http://news.bbc.co.uk/1/hi/health/3651050.stm
Een filmpje over deze aandoening
http://www.modemmedia-awards.com/fas.html
Eén avond drinken is voldoende om hersenbeschadiging te veroorzaken
Deze studie onderzocht een van de meerdere mechanismen die door
alcohol beschadigt in hersenen die nog in ontwikkeling zijn. De schrijvers vonden vooral
dat door het blokkeren van de NMDA receptoren and over-activeren van de GABA receptoren,
ethanol een kettingreactie veroorzaakt van het afsterven van cellen (apoptosis) in de
ontwikkelende hersenen van de rat. De kwetsbare periode was tijdens de synaptogenesis, dit
is de periode dat de hersencellen verbindingen vormen. Deze periode vindt bij mensen
plaats tussen de 6 maanden in de zwangerschap tot verscheidene jaren na de geboorte.
Kortdurende blootstellingen aan ethanol in deze periode dood miljoenen hersencellen. Er
werd gevonden dat de veroorzaker van het afsterven van cellen gerelateerd was aan de
hoeveelheid alcohol in het bloed. Zo zal een percentage van 200 mg/dl gehandhaafd over 4
uur het afsterven van neuronen veroorzaken, en langere blootstelling op dit niveau zal
leiden tot nog ernstigere beschadigingen.
Ethanol-induced apoptotic neurodegeneration and fetal
alcohol syndrome. (Engels).
Ikonomidou et al. Science 287, p 1056-1060 (2000).
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=
pubmed&dopt=Abstract&list_uids=10669420
Effect alcohol op de hersenen -
wetenschappelijke studies
Acheson S, Stein R., Swartzwelder HS (1998)
Impairment of semantic and figural memory by acute alcohol: Age-dependent effects. Alc
Clin Exp Res 22:1437-1442.
Aguayo L, Peoples R, Yeh H, Yevenes G (2002) GABAA
receptors as molecular sites of alcohol action: Direct or indirect actions? Current Topics
in Medicinal Chemistry 2:869-885.
Becker HC, Hale RL (1993) Repeated episodes of
alcohol withdrawal potentiate the severity of subsequent withdrawal seizures: An animal
model of alcohol withdrawal "kindling". Alc Clin Exp Res 17:94-98.
Behringer K, Gault L, Siegel R (1996) Differential
regulation of GABAA receptor subunit mRNAs in rat cerebellar granule neurons: Importance
of environmental cues. J Neurochem 66:1347-1353.
Best PJ, White AM. (1998) Hippocampal cellular
activity: a brief history of space. Proc Natl Acad Sci 95:2717-2719.
Bliss TVP, Collinridge GL (1993) A synaptic model of
memory: Long-term potentiation in the hippocampus. Nature 361:31-39.
Blitzer RD, Gil O, Landau EM (1990) Long-term
potentiation in rat hippocampus is inhibited by low concentrations of ethanol. Brain Res
537:203-208.
Bond NW (1979) Impairment of shuttlebox avoidance
learning following repeated alcohol withdrawal episodes in rats. Pharmacol Biochem Behav
11:589-591.
Bray RM (1996) Department of defense survey of
health related behaviors among military personnel. The Research Triangle Institute,
February.
Brown AS , Tapert SF, Granholm E, Delis DC (2000)
Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcohol Clin
Exp Res 24:164-171.
Brown M, Anton R, Malcolm R, Ballenger J (1988)
Alcohol detoxification and withdrawal seizures: Clinical support for a kindling
hypothesis. Biol Psychiat 23:507-514.
Casey B (1999) Images in neuroscience. Brain
development, XII: maturation in brain activation. Am J Psychiatry 156:504.
Cherubini E, Gaiarsa J, Ben-Ari Y (1991) GABA: An
excitatory transmitter in early postnatal life. Trends Neurosci 14:515-519.
Chin JH, Goldstein DB (1977) Effects of low
concentrations of ethanol on the fluidity of spin-labeled erythrocyte and brain membranes.
Molec Pharmacol 13:435-441.
Chugani H (1998) Biological Basis of Emotions: Brain
Systems and Brain Development. Pediatrics 102:1225-1229
Crews F, Chandler L (1993) Excitotoxicity and the
neuropathology of alcohol. In: Alcohol Induced Brain Damage (W.A. Hunt and S.J. Nixon,
Eds.). NIH Publication No. 93-3549: 355-371.
Crews, FT.; Braun, CJ.; Hoplight, B; Switzer, RC
III; Knapp DJ. (2000) Binge Ethanol Consumption Causes Differential Brain Damage in Young
Adolescent Rats Compared With Adult Rats. Alcoholism: Clinical & Experimental
Research. 24(11):1712-1723.
Criswell HE, Simson PE, Duncan GE, McCown TJ,
Herbert JS, Morrow AL, Breese GR (1993) Molecular basis for regionally specific action of
ethanol on gamma-aminobutyric acidA receptors: Generalization to other ligand-gated ion
channels. J Pharmacol Exp Ther 267:522-537.
De Bellis MD, Clark DB, Beers SR, Soloff PH, Boring
AM, Hall J, Kersh A, Keshavan MS (2000) Hippocampal volume in adolescent-onset alcohol use
disorders. Am J Psychiatry 157:737-744.
Dolin SJ, Little HJ (1989) Are changes in neuronal
calcium channels involved in ethanol tolerance?. J Pharmacol Exp Ther 250:985-91.
Fleming R (1935) A psychiatric concept of acute
alcoholic intoxification. Am J Psychiatry 92:89-108.
Giedd J, Blumenthal J, Jeffries N, Castllanos F, Liu
H, Zijdenbos A, Paus T, Evans A, Rapoport, J (1999) Brain development during childhood and
adolescence: a longitudinal MRI study. Nature Neurosci 2:861-863.
Grant K, Valverius P, Hudspith M, Tabakoff B (1990)
Alcohol withdrawal seizures and the NMDA receptor complex. Eur J Pharmacol 176:289-296.
Hoffman P, Tabakoff B (1994) The role of the NMDA
receptor in alcohol withdrawal. EXS 71: 61-70.
Huttenlocher P (1979) Synaptic density in human
frontal cortex - developmental changes and effects of aging. Brain Res 163:195-205.
Iorio K, Reinlib L, Tabakoff B, Hoffman P (1991)
NMDA-induced [Ca2+]i enhanced by chronic alcohol treatment in cultured cerebellar granule
cells. Alc Clin Exp Res 15:333.
Iorio K, Reinlib L, Tabakoff B, Hoffman P (1992)
Chronic exposure of cerebellar granule cells to alcohol results in increased NMDA receptor
function. Mol Pharmacol 41:1142-1148.
Johnston LD, O'Malley PM, Bachman JG (2003)
Monitoring the Future national survey results on drug use, 1975-2002. Volume I: Secondary
school students (NIH Publication No. 03-5375). Bethesda , MD : National Institute on Drug
Abuse, 520 pp.
Kapur J, MacDonald R (1996) Pharmacological
properties of GABAA receptors from acutely dissociated rat dentate granule cells. Mol
Pharmacol 50:458-466.
Kapur J, MacDonald R (1999) Postnatal development of
hippocampal dentate granule cell GABAA receptor pharmacological properties. J Pharmacol
Exp Ther 55:444-452.
Li Q, Wilson WA, Swartzwelder HS (2002) Differential
effect of alcohol on NMDA receptor-mediated EPSCs in pyramidal cells in the posterior
cingulate cortex of adolescent and adult rats. J Neurophysiol 87: 705-711.
Lidow M, Goldman-Rakic P, Rakic P (1991)
Synchronized overproduction of neurotransmitter receptors in diverse regions of the
primate cerebral cortex. Proc Nat Acad Sci 88:10218-10221.
Liljequist S, Engel J (1982) Effects of GABAergic
agonists and antagonists on various alcohol-induced behavioral changes. Psychopharmacol
78:71-75.
Lister RG, Gorenstein C, Fisher-Flowers D,
Weingartner HJ, Eckardt MJ (1991) Dissociation of the acute effects of alcohol on implicit
and explicit memory processes. Neuropsychologia 29:1205-1212.
Little HJ (1999) The contribution of
electrophysiology to knowledge of the acute and chronic effects of ethanol. Pharmacol Ther
84:333-353.
Little PJ, Kuhn CM, Wilson WA, Swartzwelder HS
(1996) Differential effects of alcohol in adolescent and adult rats. Alc Clin Exp Res
20:1346-1351.
Luna B, Thulborn K, Munoz D, Merriam E, Garver K,
Minshew N, Keshavan M, Genovese C, Eddy W, Sweeney J (2001) Maturation of widely
distributed brain function subserves cognitive development. Neuroimage 13:786-793.
Markwiese BJ, Acheson SK, Levin ED, Wilson WA,
Swartzwelder HS (1998) Differential effects of ethanol on memory in adolescent and adult
rats. Alc Clin Exp Res 22:416-421.
Martin SJ, Morris RGM (2002) New life in an old
idea: The synaptic plasticity and memory hypothesis revisited. Hippocampus 12:609-636.
Mereu G,Gess G (1985) Low doses of alcohol inhibit
the firing of neurons in the substantia nigra, pars reticulara: a GABAergic effect? Brain
Res 360:325-330.
Moy S, Duncan G, Knapp D, Breese G (1998)
Sensitivity to alcohol across development in rats: comparison to [3H]zolpidem binding. Alc
Clin Exp Res 22:1485-1492.
Mueller R-A, Rothermel RD , Behen ME, Muzik O,
Mangner TJ, Chugani HT (1998) Developmental changes of cortical and cerebellar motor
control: A clinical positron emission tomography study with children and adults. J Child
Neurol 13:550-556.
Peoples RW, Li C, Weight FF (1996) Lipid vs protein
theories of alcohol action in the nervous system. Annu Rev Pharmacol Toxicol 36:185-201.
Peoples RW, Stewart RR (2000) Alcohols inhibit
N-methyl-D-aspartate receptors via a site exposed to the extracellular environment.
Neuropharmacology 10:1681-1691.
Pyapali G, Turner D, Wilson W, Swartzwelder HS
(1999) Age and dose-dependent effects of alcohol on the induction of hippocampal long-term
potentiation. Alcohol 19: 107-111.
Rubia K, Overmeyer S, Taylor E, Brammer M, Williams
SC, Simmons A, Andrew C, Bullmore, ET (2000) Functional frontalisation with age: mapping
neurodevelopmental trajectories with fMRI. Neurosci Biobehav Rev 24:13-19.
Ryback RS (1970) Alcohol amnesia: observations in
seven drinking inpatient alcoholics. Q J Stud Alcohol 31:616-632.
Ryback RS (1971) The continuum and specificity of
the effects of alcohol on memory. Quart J Stud Alc 32:995-1016.
Schummers J, Browning MD (2001) Evidence for a role
for GABA(A) and NMDA receptors in ethanol inhibition of long-term potentiation. Brain
Research 94:9-14.
Seeman P (1999) Images in neuroscience. Brain
development, X: pruning during development. Am J Psychiatry 156:168.
Silveri M, Spear L (1998) Decreased sensitivity to
hypnotic effects of alcohol early in ontogeny. Alc Clin Exp Res 22:670-676.
Smith RF (2003) Animal models of periadolescent
substance abuse. Neurotox Teratol 25:291-301.
Snell L, Tabakoff B, Hoffman P (1993) Radioligand
binding to the NMDA receptor/ionophore complex: Alterations by alcohol in-vitro and by
chronic in-vivo alcohol ingestion. Brain Res 602:91-98.
Spear L (2000) The adolescent brain and age-related
behavioral manifestations. Neurosci Biobehav Rev 24:417-463.
Spear LP (2002) The adolescent brain and the college
drinker: biological basis of propensity to use and misuse alcohol. J Stud Alcohol
Suppl(14):71-81
Swartzwelder HS, Wilson WA, Tayyeb MI (1995a).
Differential sensitivity of NMDA receptor-mediated synaptic potentials to alcohol in
immature vs. mature hippocampus. Alc Clin. Exp Res 19:320-323.
Swartzwelder H S, Wilson WA, Tayyeb MI (1995b).
Age-dependent inhibition of long-term potentiation by alcohol in immature vs. mature
hippocampus. Alc Clin. Exp Res 19:1480-1485.
Swartzwelder HS, Richardson R, Markwiese B, Wilson
W, Little P (1998) Developmental differences in the acquisition of tolerance to alcohol.
Alcohol 15:311-314.
Tapert SF. Brown SA. (1999) Neuropsychological
correlates of adolescent substance abuse: four-year outcomes. Journal of the International
Neuropsychological Society. 5(6):481-93.
Tapert, SF, Brown, SA. (2000) Substance dependence,
family history of alcohol dependence and neuropsychological functioning in adolescence
.Addiction 95 (7), 1043-1053.
Tapert SF. Brown GG. Kindermann SS. Cheung EH. Frank
LR. Brown SA. (2001) fMRI measurement of brain dysfunction in alcohol-dependent young
women. Alcoholism: Clinical & Experimental Research. 25(2):236-45.
Tapert SF. Granholm E. Leedy NG. Brown SA. (2002).
Substance use and withdrawal: neuropsychological functioning over 8 years in youth.
Journal of the International Neuropsychological Society. 8(7):873-83.
Tapert SF. Brown GG. Baratta MV. Brown SA. (2004)
fMRI BOLD response to alcohol stimuli in alcohol dependent young women. Addictive
Behaviors. 29(1):33-50.
Teicher MH, Andersen SL, Hostetter JC (1995)
Evidence for dopamine receptor pruning between adolescence and adulthood in striatum but
not nucleus accumbens. Dev Brain Res 89:167-172.
Weissenborn R, Duka T (2003) Acute alcohol effects
on cognitive function in social drinkers: Their relationship to drinking habits.
Psychopharmacol 165:306-312.
White A, Bae J, Truesdale M, Ahmad S, Wilson W,
Swartzwelder HS (2002c) Chronic intermittent alcohol exposure during adolescence prevents
normal developmental changes in sensitivity to alcohol-induced motor impairments. Alc Clin
Exp Res 26:960-968.
White AM, Best PJ (2000) Effects of ethanol on
hippocampal place-cell and interneuron activity. Brain Res 876:154-165.
White, A.M., Ghia, A.J., Levin, E.D. and
Swartzwelder , H.S. Binge pattern alcohol exposure: differential impact on subsequent
responsiveness to alcohol. Alcoholism: Clin. Exp. Res. 24: 1251-1256, 2000.
White AM, Jamieson-Drake D, Swartzwelder HS (2002a)
Prevalence and correlates of alcohol-induced blackouts among college students: Results of
an e-mail survey. J Am College Health 51:117-131.
White AM, Matthews DB, Best PJ (2000) Ethanol,
memory and hippocampal function: a review of recent findings. Hippocampus 10:88-93.
White A, Truesdale M, Bae J, Ahmad S, Wilson W, Best
P, Swartzwelder HS (2002b) Differential effects of alcohol on motor coordination in
adolescent and adult rats. Pharmacol Biochem Behav 73:673-677.
Xia Y, Haddad G (1992) Ontogeny and distribution of
GABAA receptors in rat brainstem and rostral brain regions. Neurosci 49:973-989.
Zhang L, Spigelman I, Carlen P (1991) Development of
GABA mediated, chloride dependent inhibition in CA1 pyramidal neurons of immature rat
hippocampal slices. J Physiol 444: 25-49.
Zola-Morgan S, Squire LR, Amaral DG (1986). Human
amnesia and the medial temporal lobe region: enduring memory impairment following a
bilateral lesion limited to field CA1 of the hippocampus. J Neurosci 16:2950-2967.