EVENT-RELATED POTENTIAL RESPONSES TO ALCOHOL-RELATED STIMULI IN AFRICAN–AMERICAN YOUNG ADULTS: RELATION TO FAMILY HISTORY OF ALCOHOLISM AND DRUG USAGE

Cindy L. Ehlers*, Evelyn Phillips, Antonio Sweeny and Craig J. Slawecki

Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA, USA

Received 11 September 2002; in revised form 30 January 2003; accepted 6 March 2003


    ABSTRACT
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
Aims: To use event-related potentials (ERPs) to investigate the response to alcohol-related stimuli in African–American young adults. Methods: ERPs to an object recognition task, that included pictures of objects, food and alcohol-related and non-alcohol-related drinks as stimuli, were obtained in 81 African–American young adult men and women (18–25 years old) without a personal history of alcohol dependence. Information on: psychiatric diagnoses, personal drinking and drug use history, and familial history of alcoholism was also obtained. Results: Family history was found to be associated with lowered P3 components and higher N1 components in response to the non-alcohol-related drinks. Additionally, an exploratory analyses revealed that lower amplitude N1 components were generated in response to alcohol-related stimuli in regular marijuana users compared with non-regular users. No associations of N1 or P3 amplitudes with conduct disorder symptoms or current drinking status were found in this population. Conclusions: These studies demonstrated that family history is significantly and selectively associated with lower P3 amplitudes in this group of young adult men and women of African–American heritage. Additionally, current usage of marijuana and alcohol do not modify P3 amplitudes. However, regular marijuana use may diminish N1 response to alcohol-related stimuli, whereas, family history of alcoholism may augment N1 responses. Taken together these studies further suggest that ERPs can provide specific information on alcoholism risk as well as use of other misused drugs.


    INTRODUCTION
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
In a large national survey it was documented that Black adults, as compared with White and Hispanic adults, have the highest volume of alcohol intake and frequency of heavy drinking (Dawson, 1998Go). However, in several studies, African–American young adults were found to be more likely to abstain from alcohol, not engage in heavy drinking, and have lower rates of alcohol use disorders, when compared with EuroAmericans and some other ethnic groups (Herd, 1988Go, 1990Go; Johnston et al., 1991Go; Group for the Advancement of Psychiatry, 1996Go). Risk and protective factors, particularly in the biological realm, that may explain differences in drinking patterns in the African–American community are yet to be completely identified. However, within the psychosocial realm, family factors, peer involvement (Barnes and Farrell, 1992Go) and academic performance (Rodney et al., 1997Go) appear to be more important than poverty or psychosocial status in predicting drug and alcohol involvement.

One measure that has received considerable attention as a possible marker for alcoholism risk is the P3 component of the event-related potential (ERP). ERPs are time-locked electric fields generated by synchronous neural activity within specific brain areas engaged in neurosensory and cognitive processing. In human subjects, a series of waves of differing polarity and amplitude designated ‘components’ of ERPs are generally obtained from the averaged EEG when a subject is asked to attend to and/or discriminate a target stimulus from a series of background stimuli (see Roth, 1973Go; Squires et al., 1975Go; Polich and Bloom, 1987Go). The P3 component is positive in polarity, occurs at approximately 300 ms, and has been suggested to reflect stimulus evaluation and memory function (see Donchin et al., 1986Go; Donchin and Coles, 1988Go). Many studies have demonstrated that the amplitude of the P3 is reduced in individuals who have a family history of alcoholism but who have not yet developed the disorder (see Elmasian et al., 1982Go; Begleiter et al., 1984Go; O’Connor et al., 1986Go, 1987Go; Hill et al., 1987Go, 1988Go, 1990Go, 1995Go, 1999aGo, bGo; Whipple et al., 1988Go; Porjesz and Begleiter, 1990Go, 1998Go; Berman et al., 1993aGo,bGo; Hill and Steinhauer, 1993Go; Steinhauer and Hill, 1993Go; Ramachandran et al., 1996Go; Ramsey and Finn, 1997Go; Van der Stelt et al., 1998aGo,bGo; Begleiter and Porjesz, 1999Go; Ratsma et al., 2001Go). Other studies are less convincing or do not support this hypothesis (see Baribeau et al., 1987Go; Polich and Bloom, 1987Go, 1988Go; Hill et al., 1988Go; Bauer, 1994aGo,bGo, 1997Go; Rodriguez-Holguin et al., 1998aGo,bGo, 1999Go; Bauer and Hesselbrock, 1999aGo,bGo). However, a meta-analysis of the literature up to 1993 concluded that the P3 ‘may be useful as an index for predicting alcoholism vulnerability’ (Polich et al., 1994Go).

It has been suggested that differences in ERP findings between studies may relate to heterogeneity in samples based on such factors as co-morbidity (Bauer et al., 1999Go; Hill et al., 1999aGo,bGo; Hill and Shen, 2002Go), alcoholism phenotypes in the parents, and the presence of other drug use disorders. Bauer, Hesselbrock, and colleagues have made a cogent case for the hypothesis that P3 reduction in individuals with a family history of alcoholism is primarily related to conduct disorder and its subtypes. In adults diagnosed with antisocial personality disorder (ASPD) (Bauer, 1994aGo,bGo, 1997Go; O’Connor et al., 1994Go; Costa et al., 2000Go) or in youths with elevated numbers of conduct disorder behaviours or externalizing disorders (Bauer and Hesselbrock, 1999aGo,bGo, 2001Go; Iacono et al., 2002Go), decrements in P3 amplitude were observed. P3 decrements have also been correlated with level of subsequent substance use (Berman et al., 1993aGo,bGo; Iacono et al., 2002Go).

Another difference between studies is related to the tasks used to generate ERPs. Tasks utilized to generate ERPs in studies of high- and low-risk individuals have varied. The meta-analysis conducted by Polich et al. (1994)Go indicated that results were stronger when ERPs are generated by ‘difficult’ visual tasks. Generally the tasks used in high/low-risk studies employ ‘neutral’ stimuli such as: lines or words or feature orientation to generate ERPs. However, in one recent study (Ehlers et al., 2001aGo) high- and low-risk subjects of Native American Heritage were required to discriminate between photographs of faces with different affective expressions. This task was found to be particularly sensitive to a family history of alcoholism, when compared with a visual line orientation task, even though the latter task was a more difficult discrimination than the facial recognition task.

Two recent studies have introduced the use of paradigms that elicit ERPs with alcohol-related stimuli. In both studies, the stimuli were words presented on a computer screen that were either alcohol-related (bottle, tin, brandy, booze) or ‘neutral’ (coffee, water, apple, chips). Using these stimuli, it was found that alcoholics had higher P3 amplitude responses to the alcohol-related, vs non alcohol-related, stimuli, whereas controls did not (Herrmann et al., 2000Go), and that heavy social drinkers had higher P300s to the alcohol-related stimuli when compared with light social drinkers (Herrmann et al., 2001Go). The increase in P3 amplitude in those studies may be the result of heightened responsiveness to alcohol-related stimuli, due to enhanced expectations of the effects of alcohol, or may reflect a general hyperexcitability associated with acute or protracted abstinence from heavy drinking (Begleiter and Porjesz, 1999Go). No information was given as to whether the subjects participating in these studies differed with respect to familial risk for alcoholism. Thus, it is not known whether the differences seen were a result of chronic exposure to alcohol or inherent differences in stimulus processing. In addition, most publications describing P3 effects in alcoholics, or those at risk for alcoholism, do not indicate the ethnicity of the sample or use ethnicity as a co-factor in analyses.

The present report is part of a larger study exploring risk factors for alcoholism among African–American young adults (see Ehlers et al., 2001bGo; Ehlers and Phillips, 2003). The present study was designed to explore the relationships between visual P3 and N1 amplitudes generated to alcohol- and non-alcohol-related beverage stimuli and potential vulnerability factors associated with risk for alcohol dependence in African– American young adults. While most studies have focused on the relationship between P3 and family history of alcoholism, recent studies have reported augmented N1 amplitudes in alcoholics that correlated with memory function (Ahveninen et al., 2000Go). A comparison of N1 and P3 amplitudes allows for determination of the specificity of an effect on late positive components vs earlier potentials. Thus, the specific aims of this study were (1) to evaluate whether visual P3 and N1 amplitudes to alcohol- and non-alcohol-related stimuli were associated with family history of alcoholism in African– American young adults; (2) in an exploratory analysis, to test whether symptoms of conduct disorder and/or personal drinking and drug use history were also associated with changes in the amplitude of the P3 or N1 components.


    MATERIALS AND METHODS
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
Participants
Participants were recruited by fliers placed on local college and university campuses, and by word of mouth within the African–American community. The fliers stated the participation requirements as being: African–American and between 18 and 25 years of age. One hundred and thirty individuals inquired, by phone, about participation in the study. Ninety-eight participants eventually elected to participate. After complete description of the study to the subjects, written informed consent was obtained using a protocol approved by The Internal Review Board of The Scripps Research Institute. Information on demography, personal medical and psychiatric history, and family history of alcohol and other substance dependence was obtained using two family history questionnaires (Schuckit, 1985Go) and the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA). The SSAGA is a poly-diagnostic psychiatric interview that has undergone both reliability and validity testing (Bucholz et al., 1994Go; Hesselbrock et al., 1999Go). Interviewers were all trained by personnel from the collaborative study on the genetics of alcoholism (COGA). All best final diagnoses were made by a board-certified psychiatrist. Participants were excluded from further inclusion if they were taking any prescribed medication or had any major medical condition (i.e. organ system disease, neurological disorder, head injury, endocrine disorder, etc.)

A participant was classified as family history-positive (FHP) if s/he had a biological parent (mother or father) who met DSM-III-R criteria for alcohol dependence (American Psychiatric Association, 1987Go). Family history-negative (FHN) participants lacked a history of alcohol dependence in all their first-degree relatives. Participants were further classified with respect to their drinking status, marijuana use and conduct disorder symptoms. Regular drinkers were defined as individuals who drank at least one drink a month over the preceding 6 months. They were compared with individuals who were not regular drinkers by this definition from the SSAGA. Marijuana users were defined by criteria specified in the SSAGA, namely, having used marijuana over 21 times in a single year. Their data were compared with participants who did not meet criteria for marijuana use. Additionally, the numbers of symptoms reported by the subjects for conduct disorder were tallied and those subjects with three or more symptoms were compared with those with two or less, as previously described by Bauer and Hesselbrock (1999a)Go.

ERP collection and analyses
Seven channels of ERP data (Fz, Cz, Pz, F3, F4, F7, F8) referenced to linked ear lobes with a forehead ground, international 10–20 system) were obtained using gold-plated electrodes with impedance held below 5 K{Omega}. An electrode placed left lateral infraorbitally and referenced to the left earlobe was used to monitor both horizontal and vertical eye movement. ERP recording signals were amplified at a sensitivity of 7 µV/mm (time constant 0.3 s, 35 Hz low pass) using a Nihon Kohden EEG machine and were transferred on-line to a Macintosh computer for digitization. Visual stimuli were presented on a video screen and consisted of three classes of pictures of objects. The first class was pictures of ‘non-food or drink objects’ (camera, chair, phone, scissors, tennis shoe), the second was ‘foods’ (corn, banana, apple, canned green beans, white bread) and the third was ‘drinks’. The participant was instructed to press one button for food and another button for drink objects. Individual ERP trials were averaged separately for the categories of objects (non-food objects, food objects, drinks). However, the drink category was further separated into non-alcoholic drinks (milk carton, Perrier water bottle, Arrowhead water bottle, tall water glass, short water glass) and alcoholic drinks (Jack Daniels bottle, beer in mug, Budweiser can, King Cobra can, wine in glass) for averaging. Fifty trials of each class of stimuli (non-food objects, food objects, non-alcoholic drinks, alcoholic drinks) were presented randomly for a total number of 200 trials. Thus each class had equivalent probability. The stimuli were presented for 1000 ms, the inter-stimulus interval was 1000 ms, with a 100 ms pre-trial baseline, the total trial length was 2000 ms.

The ERP trials were digitized at a rate of 256 Hz. Individual trials containing excessive eye movement artifact as well as trials where the EEG exceeded ±250 µV (<5% of the trials) were eliminated before averaging. The N1 was defined as the occurrence of a negative peak 75–150 ms after stimulus presentation. The P3 was defined as the occurrence of a peak after the N1–P2–N2 complex within 250–600 ms after stimulus presentation. The amplitude was determined as baseline to that peak (µV). The baseline was determined by averaging the 100 ms of pre-stimulus activity obtained for each trial. The routine is user-driven and each peak detection must be verified by the user. All peaks were initially identified by one investigator (E.P.), and verified by a second investigator (C.L.E.) both of whom were blind to participant characteristics.

The first aim was to describe the relationship between N1 and P3 amplitude and a participant’s parental history of alcohol dependence. To investigate this aim, N1 and P3 amplitudes generated by the alcohol/non-alcohol-related stimuli from three leads across the head (Fz, Cz, Pz), were used as dependent variables for comparison to previous studies and as suggested by Polich and Bloom (1999)Go. Using ANOVA, FH and gender were treated as between subjects variables. Post-hocs (Tukeys HSD) were used to test significant differences where interactions were found. The second aim was to explore the relationship between N1 and P3 amplitudes and factors that have previously been suggested to possibly influence component amplitudes: conduct disorder symptoms, current drinking status, and marijuana use status. For these analyses, N1 and P3 amplitudes to the target stimuli for the three leads were compared for the two groups of participants in each category (current drinkers vs non-current drinkers; three or more conduct symptoms obtained from information in the SSAGA to have occurred before the age of 15 vs two or less conduct symptoms; marijuana usage vs no regular marijuana usage). Statistical significance was set at the 0.05 probability level.


    RESULTS
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
The young adults who participated in the study had a mean age (±SD) of 19.6 years (±2.0), with roughly equal numbers of men (40%) and women (60%). Demographic data, including age, gender, number of years of education, current drinking and drug use history, and number of conduct disorder symptoms in relation to parental history of alcoholism are presented in Table 1Go. FHP participants had a mean of 1.2 first-degree alcoholic relatives. In this group of 81 young adults, 32 reported never drinking regularly (regular drinking = one or more drinks a month over a 6 month period). In those individuals who were currently drinking regularly, the average quantity per occasion was three drinks and the average frequency was 3 times/month. There were no significant differences between the groups (FHP vs FHN) on any of these variables, except age, where FHP participants were found to be 1 year older than FHNs (F = 7.9; df = 1, 96; P < 0.005).


View this table:
[in this window]
[in a new window]
 
Table 1. Demographic characteristics of study subjects
 
Figure 1Go displays ERP responses to the four stimuli categories (objects, food, alcohol-related drinks, non-alcohol-related drinks) over the three electrode sites (Fz, Cz, Pz) evaluated in the entire sample (n = 81). P3 amplitudes appeared to be larger to objects as compared with food or drinks in the Fz lead.



View larger version (19K):
[in this window]
[in a new window]
 
Fig. 1. Grand averages of event-related potentials (ERPs) elicited by an object recognition task in young adult African–American men and women.

Averages for n = 81 are presented for frontal (Fz), central (Cz), and parietal (Pz) leads. N1 and P2, and P3 components are visible in response to objects (solid lines), food (large dashed lines), alcoholic drinks (small dashed lines) and non-alcoholic drinks (dotted lines).

 
To address the first major research question, P3 and N1 amplitudes were compared between FHPs and FHNs for the alcohol- and non-alcohol-related beverage stimuli. Those participants with at least one alcoholic parent were found to have smaller P3 amplitudes, which were significant in the central lead (Cz), in response to the non-alcohol-related beverage stimuli (main effect of FH: F = 4.3; df = 1, 80; P < 0.04) as seen in Fig. 2Go. Gender and family history were also found to be associated with P3 amplitudes generated by the non-alcohol-related beverage stimuli in the frontal lead (Fz) [main effect of Gender: F = 4.3 df = 1, 80; P < 0.04, Gender x Family History interaction (F = 5.4; df = 1, 80; P < 0.02)]. Post-hoc analyses revealed that the differences were contributed by a lowered P3 amplitude in the FHP young men (Tukey’s HSD: P < 0.04) [FHP males: 0.6 ± 1.5; FHN males: 4.9 ± 1.2; FHP females: 5.8 ± 1.1; FHN females: 4.5 ± 0.7 (mean ± SE µV)]. N1 amplitudes were also influenced by a family history of alcoholism. Those participants who were FHP had larger N1 amplitudes when compared with FHNs in posterior leads (main effect of FH: F = 5.6; df = 1, 80; P < 0.02) [FHP = 3.3 ± 0.6; FHN = 1.5 ± 0.5 (mean ± SE µV)] to the non-alcohol-related stimuli. No gender differences were found in those analyses.



View larger version (36K):
[in this window]
[in a new window]
 
Fig. 2. Grand averages of event-related potentials (ERPs) elicited by alcoholic and non-alcoholic drinks for an object recognition task in young adult African–American men and women. Averages for n = 81 are presented for frontal (Fz), central (Cz), and parietal (Pz) leads. Data are presented for young adults who were family history-positive (FHP, solid line, n = 18) and those who were family history-negative (FHN, dashed line, n = 63) for parental alcohol dependence.

 
Our second hypothesis was to test for associations, in an exploratory analysis, between N1 and P3 amplitudes and current drinking and marijuana use history, and conduct disorder symptoms. No significant associations were found between those participants who were current drinkers and those not currently drinking, or between those participants with three or more conduct disorder symptoms and those with two or less for any variables. However, a significant association was found between marijuana users and those who did not meet criteria for regular marijuana use in N1 amplitudes. Thus, as seen in Fig. 3Go, those individuals identified as regular marijuana users had significantly lower N1 amplitudes in the frontal (main effect of marijuana usage: Fz: F = 5.7; df = 1, 80; P < 0.02) and central (main effect of marijuana usage: Cz: F = 5.6; df = 1, 80; P < 0.02) leads, but not in the posterior lead (Pz: F = 2.8; df = 1, 80; P < 0.09). No gender effects were significant in these analyses.



View larger version (20K):
[in this window]
[in a new window]
 
Fig. 3. Amplitudes of the N1 component of the event-related potential (ERP) to an object recognition task as a function of regular marijuana use.

Amplitudes were compared between participants who were regular marijuana smokers (black bar), and those who were not regular users (open bar). Regular marijuana use was significantly associated with lower N1 amplitudes in the frontal (Fz) and central (Cz) leads.

 

    DISCUSSION
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
Findings on the importance of genetics in the aetiology of alcohol dependence have stimulated a number of investigators to search for familial-based factors that might mediate increased risk for the disorder (Schuckit, 1985Go; Devor and Cloninger, 1989Go; Goldman, 1993Go). A positive family history of alcoholism is one of the most consistent and powerful predictors of a person’s risk for the development of the disorder. First-degree relatives of alcoholics are up to 7 times more likely than the general population to develop problems associated with alcohol at some time during their life (Cotton, 1979Go; Schuckit and Smith, 1996Go; Merikangas et al., 1998Go). This study assessed the amplitude of the N1 and P3 components of the ERP using alcohol- and non-alcohol-related stimuli. The study was designed to explore N1 and P3 amplitudes in African–American young adults in relation to parental history of alcoholism.

P3 amplitude is perhaps the most studied electrophysiological ‘marker’ of potential vulnerability to alcohol dependence. A meta-analysis in which P3 amplitude from 30 separate studies were analysed found that smaller P3 amplitudes were obtained from males with family histories of alcoholism compared with controls (Polich et al., 1994Go). However, a moderator analysis accomplished in the above study also indicated the ERP paradigms that used difficult visual tasks in younger participants, particularly in males, yielded the most reliable effects. Ethnicity was not evaluated in the meta-analysis. The present study confirms the findings of the meta-analysis and extends the studies to an African–American young adult population. In the present study, FHPs, particularly males, were found to have lower P3 amplitudes when compared with FHNs using a visual task. Approximately twice as many studies have used visual tasks to generate late positive components, as compared with auditory tasks, which may partly explain some discrepancies in the literature.

In the present study, both alcohol- and non-alcohol-related stimuli were employed to elicit ERPs. Both sets of stimuli elicited a late positive component occurring between 400 and 600 ms after presentation of the stimuli. The few ERP studies that have used alcohol-related stimuli have reported that the differences in the amplitudes of the late positive components elicited by alcohol-related stimuli, as compared with non-alcohol-related stimuli, are larger in male alcoholics and heavy social drinkers as compared with non-alcoholics and light social drinkers, respectively (Herrmann et al., 2000Go, 2001Go). The effect of family history was not assessed in these studies. A significant relationship between parental history of alcoholism and the amplitude of the P3 late positive component elicited to the non-alcohol-related stimuli, but not to the alcohol-related stimuli, was found in the present study. One interpretation of these results is that presentation of alcohol-related stimuli may mitigate the effect of family history on P3 component amplitudes. This might occur through a mechanism whereby an enhancement in the ‘attention/salience’ of the alcohol-related stimuli is produced and overcomes the intrinsic deficit in P3 amplitudes often seen in FHPs.

Marijuana use, but not alcohol use or conduct disorder symptoms, was also found to modify ERP component amplitudes in the present study. Reduced N1 amplitudes were found in regular marijuana users, as compared with non-regular users. Previous studies have also found that the ‘frontal processing negativity to irrelevant stimuli’ was impaired in long-term marijuana users using an auditory paradigm (Solowij et al., 1995Go). However, other studies have stressed that auditory and visual P300s are not impaired in medically and psychiatrically normal chronic marijuana users (Patrick et al., 1995Go), which was also the case in the present study. In contrast to the findings of decreased N1 amplitudes in regular marijuana users, FHPs were found to have increases in N1 amplitudes. Increased N1 amplitudes have been reported previously in alcoholics (Ahveninen et al., 2000Go). Taken together, these studies suggest that risk for alcoholism and marijuana misuse may have different neurophysiological substrates.

The lack of a significant association between drinking history and ERPs is also consistent with other studies of younger alcoholic and non-alcoholic subjects, where P300 amplitudes were not found to be affected either by sobriety length or drinking history (Keenan et al., 1997Go). Finally, the present study did not find a relationship between ERP amplitudes and conduct disorder symptoms. One possible explanation is that the current population was recruited from the community and not treatment or detention facilities; thus, the severity of the conduct disorder was more likely to be milder, as compared with previous studies (Bauer and Hesselbrock, 1999aGo). Alternatively, it is possible that the particular ERP task employed in the present study may not be sensitive to brain processes affected by conduct disorder. However, it can be tentatively concluded that parental history of alcoholism significantly affects P3 amplitude in these young adult African–American study participants, and this variable appears more selectively to modify P3 amplitudes than conduct disorder symptoms, or current alcohol or drug usage.

It is important to consider some of this study’s limitations. First, a modest, non-randomly selected sample was assessed. Thus, the findings may not generalize to all African–Americans. Secondly, the study was limited to young adults between the ages of 18 and 25 years. This allowed an investigation of the association between parental alcohol dependence and ERP components. However, since the participants in the study had not passed through the age of risk, associations with misuse and dependence were limited. Further studies employing a longitudinal design will be required to test the relationship of component amplitudes and eventual alcohol-related morbidity and mortality. Despite these limitations, this report represents an important first step in an ongoing investigation to determine risk and protective factors associated with the development of substance use disorders in this ethnic group.


    ACKNOWLEDGEMENTS
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
The authors would like to thank Phil Lau, Melanie Walpole, Vince Wong, Lilach Harris, Susan Lopez, Michelle Betancourt and David A. Gilder for assistance in data collection and analyses. This work has been supported in part by the National Institute of Alcoholism and Alcohol Abuse Grants: AA04620, AA00223, AA10201, the Office of Minority Health/Health Disparities and a General Clinical Research Center Grant AA00833.


    FOOTNOTES
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
* Author to whom correspondence should be addressed at: TSRI, CVN-14, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. Back


    REFERENCES
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGEMENTS
 REFERENCES
 
Ahveninen, J., Jaakelainen, I. P., Pekkonen, E., Hallberg, A., Hietanen, M., Naatanen, R. and Sillanaukee, P. (2000) Global field power of auditory N1 correlates with impaired verbal-memory performance in human alcoholics. Neuroscience Letters 285, 131–134.[CrossRef][ISI][Medline]

American Psychiatric Association (1987) Diagnostic and Statistical Manual of Mental Disorders, 3rd edn, revised. American Psychiatric Association, Washington, DC.

Baribeau, J. C., Ethier, M. and Braun, C. (1987) Neurophysiological assessment of selective attention in males at risk for alcoholism. In Current Trends in Event Related Potential Research, EEG Supplement #40, Johnson, R., Rohrbaugh, J. and Parasuraman, R. eds, pp. 651–656. Elsevier, Amsterdam.

Barnes, G. M. and Farrell, M. P. (1992) Parental support and control as predictors of adolescent drinking, delinquency, and related problem behaviors. Journal of Marriage and the Family 54, 763–776.[ISI]

Bauer, L. O. (1994a) Electroencephalographic and autonomic predictors of relapse in alcohol dependent patients. Alcoholism: Clinical and Experimental Research 18, 755–760.

Bauer, L. O. (1994b) Frontal P300 decrements in antisocial personality disorder. Alcoholism: Clinical and Experimental Research 18, 1300–1305.

Bauer, L. O. (1997) Frontal P300 decrements, childhood conduct disorder, family history, and the prediction of relapse among abstinent cocaine abusers. Drug and Alcohol Dependence 44, 1–10.[CrossRef][ISI][Medline]

Bauer, L. O. and Hesselbrock, V. M. (1999a) P300 decrements in teenagers with conduct problems: implications for substance abuse risk and brain development. Biological Psychiatry 46, 264–272.

Bauer, L. O. and Hesselbrock, V. M. (1999b) Subtypes of family history and conduct disorder: effects of P300 during the Stroop test. Neuropsychopharmacology 21, 51–62.[CrossRef][ISI][Medline]

Bauer, L. O. and Hesselbrock, V. M. (2001) CDS/BEM localization of P300 sources in adolescents ‘at-risk’: evidence of frontal cortex dysfunction in conduct disorder. Biological Psychiatry 50, 600–608.[CrossRef][ISI][Medline]

Bauer, L. O., Costa, L. and Hesselbrock, V. M. (1999) Effects of alcoholism, anxiety and depression in women: a pilot study. Journal of Studies on Alcohol 62, 571–579.

Begleiter, H. and Porjesz, B. (1999) What is inherited in the predisposition toward alcoholism? A proposed model. Alcoholism: Clinical and Experimental Research 23, 1125–1135.[ISI][Medline]

Begleiter, H., Porjesz, B., Bihari, B. and Kissin, B. (1984) Event-related brain potentials in boys at risk for alcoholism. Science 225, 1493–1496.[ISI][Medline]

Berman, S. M., Martinez, R. A. and Noble, E. P. (1993a) Familial alcoholism and ERPs: differences in probability sensitivity? Alcohol and Alcoholism 28, 695–707.[Abstract]

Berman, S. M., Whipple, S. C., Fitch, R. J. and Noble, E. P. (1993b) P3 in young boys as a predictor of adolescent substance abuse. Alcohol 10, 69–76.[CrossRef][ISI][Medline]

Bucholz, K. K., Cadoret, R., Cloninger, C. R., Dinwiddie, S. H., Hesselbrock, V., Nurnberger, J. I., Jr, Reich, T., Schmidt, I. and Schuckit, M. A. (1994) A new semi-structured psychiatric interview for use in genetic linkage studies: a report on the reliability of the SSAGA. Journal of Studies on Alcohol 55, 149–158.[ISI][Medline]

Costa, L., Bauer, L., Kuperman, S., Porjesz, B., O’Connor, S., Hesselbrock, V., Rohrbaugh, J. and Begleiter, H. (2000) Frontal P300 decrements, alcohol dependence, and antisocial personality disorder. Biological Psychiatry 47, 1064–1071.[CrossRef][ISI][Medline]

Cotton, N. S. (1979) The familial incidence of alcoholism: a review. Journal of Studies on Alcohol 40, 89–116.[ISI][Medline]

Dawson, D. A. (1998) Beyond black, white and Hispanic: race, ethnic origin and drinking patterns in the United States. Journal of Substance Abuse 10, 321–339.[CrossRef][ISI][Medline]

Devor, E. J. and Cloninger, C. R. (1989) Genetics of alcoholism. Annual Review of Genetics 23, 19–36.[CrossRef][ISI][Medline]

Donchin, E. and Coles, M. G. H. (1988) Is the P300 component a manifestation of context updating? Behavioral Brain Science 11, 357–374.[ISI]

Donchin, E., Karis, D., Bashore, T. K., Coles, M. G. H. and Gratton, G. (1986) Cognitive psychophysiology and human information processing. In Psychophysiology Systems, Processes, and Applications, Coles, M. G. H., Donchin, E. and Porges, S. W. eds, pp. 244–267. The Guilford Press, New York.

Ehlers, C. L., Wall, T. L., Garcia-Andrade, C. and Phillips, E. (2001a) Visual P3 findings in Mission Indian youth: relationship to family history of alcohol dependence and behavioral problems. Psychiatry Research 105, 67–78.[CrossRef][ISI][Medline]

Ehlers, C. L., Gilder, D. A., Harris, L. and Carr, L. (2001b) Association of the ADH2*3 allele with a negative family history of alcoholism in African American young adults. Alcoholism: Clinical and Experimental Research 25, 1773–1777.[ISI][Medline]

Elmasian, R., Neville, H., Woods, D., Schuckit, M. and Bloom, F. E. (1982) Event-related brain potentials are different in individuals at high and low risk for developing alcoholism. Proceedings of the National Academy of Science of the USA 79, 7900–7903.

Goldman, D. (1993) Recent developments in alcoholism: genetic transmission. Recent Developments in Alcoholism 11, 231–248.[Medline]

Group for the Advancement of Psychiatry (1996) Committee on Cultural Psychiatry, Dallas, TX. In Alcoholism in the United States: Racial and Ethnic Considerations. American Psychiatric Press, Inc., Washington, DC.

Herd, D. (1988) Drinking by black and white women: results from a national survey. Social Problems 35, 493–505.[ISI]

Herd, D. (1990) Subgroup differences in drinking patterns among black and white men. Journal of Studies on Alcohol 51, 221–232.[ISI][Medline]

Herrmann, M. J., Weijers, H. G., Wiessbeck, G. A., Bomomg, J. and Fallgatter, A. J. (2000) Event-related potentials and cue-reactivity in alcoholism. Alcoholism: Clinical and Experimental Research 24, 1724–1729.[CrossRef][ISI][Medline]

Herrmann, M. J., Weijers, H. G., Wiessbeck, G. A., Bomomg, J. and Fallgatter, A. J. (2001) Alcohol cue-reactivity in heavy and light social drinkers as revealed by event-related potentials. Alcohol and Alcoholism 36, 588–593.[Abstract/Free Full Text]

Hesselbrock, M., Eastpm, C., Bucholz, K. K., Schuckit, M. A. and Hesselbrock, V. M. (1999) A validity study of the SSAGA — a comparison with the SCAN. Addiction 94, 1261–1370.

Hill, S. Y. and Shen, S. (2002) Neurodevelopmental patterns of visual P3b in association with familial risk for alcohol dependence and childhood diagnosis. Biological Psychiatry 51, 621–631.[CrossRef][ISI][Medline]

Hill, S. Y. and Steinhauer, S. (1993) Assessment of prepubertal and post-pubertal boys and girls at risk for developing alcoholism with P3 from a visual discrimination task. Journal of Studies on Alcohol 54, 350–358.[ISI][Medline]

Hill, S. Y., Steinhauer, S. R. and Zubin, J. (1987) Biological markers for alcoholism: a vulnerability model conceptualization. In Alcohol and Addictive Behaviors. Nebraska Symposium on Motivation, 1986, Rivers, P. C. ed., pp. 207–256. University of Nebraska Press, Lincoln, NE and London.

Hill, S. Y., Steinhauer, S., Zubin, J. and Baughman, T. (1988) Event-related potentials as markers for alcoholism risk in high density families. Alcoholism: Clinical and Experimental Research 12, 545–554.[ISI][Medline]

Hill, S. Y., Steinhauer, S., Park, J. and Zubin, J. (1990) Event-related potentials characteristics in children of alcoholics from high density families. Alcoholism: Clinical and Experimental Research 14, 6–17.[ISI][Medline]

Hill, S. Y., Muka, D., Steinhauer, S. and Locke, J. (1995) P300 amplitude decrements in children from families of alcoholic female probands. Biological Psychiatry 38, 622–632.[CrossRef][ISI][Medline]

Hill, S. Y., Locke, J. and Steinhauer, S. (1999a) Absence of visual and auditory P300 reduction in nondepressed male and female alcoholics. Biological Psychiatry 46, 982–989.[CrossRef][ISI][Medline]

Hill, S. Y., Shen, S., Locke, J., Steinhauer, S. R., Konicky, C., Lowers, L. and Connolly, J. (1999b) Developmental delay in P300 production in children at high risk for developing alcohol-related disorders. Biological Psychiatry 46, 970–998.[CrossRef][ISI][Medline]

Iacono, W. G., Carlson, S. R., Malone, S. M. and McGue, M. (2002) P3 event-related potential amplitude and the risk for disinhibitory disorders in adolescent boys. Archives of General Psychiatry 59, 750–757.[Abstract/Free Full Text]

Johnston, L. D., O’Malley, P. M. and Bachman, J. G. (1991) Drug use among American high school seniors, college students, and young adults. In High School Seniors 1975–90, Vol. I, publication no. DHHS-ADM-91-1813. National Institute on Drug Abuse, Rockville, MD.

Keenan, J. P., Freeman, P. R. and Harrell, R. (1997) The effects of family history, sobriety length, and drinking history in younger alcoholics on P300 auditory-evoked potentials. Alcohol and Alcoholism 32, 233–239.[Abstract]

Merikangas, K. R., Stolar, M., Stevens, D. E., Goulet, J., Preisig, M. A., Fenton, B., Zhang, H., O’Malley, S. S. and Rounsaville, B. J. (1998) Familial transmission of substance use disorders. Archives of General Psychiatry 55, 973–979.[Abstract/Free Full Text]

O’Connor, S., Hesselbrock, V. and Tasman, T. (1986) Correlates of increased risk for alcoholism in young men. Progess in Neuropsychopharmacology and Biological Psychiatry 10, 211–218.[CrossRef]

O’Connor, S., Hesselbrock, V., Tasman, T. and DePalma, N. (1987) P3 amplitude in two distinct tasks are decreased in young men with a history of paternal alcoholism. Alcohol 4, 323–330.[CrossRef][ISI][Medline]

O’Connor, S., Tasman, A., Bauer, L. O. and Hesselbrock, V. M. (1994) Reduced P3 amplitudes of ERPs are associated with both a family history of alcoholism and antisocial personality disorder. Progress in Neuropsychopharmacology and Biological Psychiatry 18, 1307–1321.[CrossRef][ISI][Medline]

Patrick, G., Straumanis, J. J., Struve, F. A., Nixon, F., Fitz-Gerald, M. J., Manno, J. E. and Soucair, M. (1995) Auditory and visual P300 event-related potentials are not altered in medically and psychiatrically normal chronic marihuana users. Life Sciences 56, 2135–2140.[CrossRef][ISI][Medline]

Polich, J. and Bloom, F. E. (1987) P3 from normals and adult children of alcoholics. Alcohol 4, 301–305.[CrossRef][ISI][Medline]

Polich, J. and Bloom, F. E. (1988) Event-related brain potentials in individuals at high and low risk for developing alcoholism: Failure to replicate. Alcoholism: Clinical and Experimental Research 12, 368–373.[ISI][Medline]

Polich, J. and Bloom, F. E. (1999) P300, alcoholism heritability, and stimulus modality. Alcohol 17, 149–156.[CrossRef][ISI][Medline]

Polich, J., Pollock, V. E. and Bloom, F. E. (1994) Meta-analysis of P3 amplitude from males at risk for alcoholism. Psychological Bulletin 115, 55–73.[CrossRef][ISI][Medline]

Porjesz, B. and Begleiter, H. (1990) Event-related potentials in individuals at risk for alcoholism. Alcohol 7, 465–469.[CrossRef][ISI][Medline]

Porjesz, B. and Begleiter, H. (1998) Genetic basis of event-related potentials and their relationship to alcoholism and alcohol use. Journal of Clinical Neurophysiology 15, 4–57.

Ramachandran, G., Porjesz, B., Begleiter, H. and Litke, A. (1996) A simple auditory oddball task in young adult males at high risk for alcoholism. Alcoholism: Clinical and Experimental Research 20, 9–15.[ISI][Medline]

Ramsey, S. E. and Finn, P. R. (1997) P300 from men with a family history of alcoholism under different incentive conditions. Journal of Studies on Alcohol 58, 606–616.[ISI][Medline]

Ratsma, J. E., van der Stelt, O., Schoffelmeer, A. N., Westerveld, A. A. and Gunning, W. B. (2001) P3 event-related potential, dopamine D2 receptor A1 allele, and sensation-seeking in adult children of alcoholics. Alcoholism: Clinical and Experimental Research 25, 960–967.[CrossRef][ISI][Medline]

Rodney, H. E., Mupier, R. and O’Neal, S. (1997) African-American Youth in public housing showing low alcohol and drug use. Journal of Child and Adolescent Substance Abuse 6, 55–73.

Rodriguez-Holguin, S. C., Corral, M. and Cadaveira, F. (1998a) Event-related potentials elicited by infrequent non-target stimuli in young children of alcoholics: family history and gender differences. Alcohol and Alcoholism 33, 281–290.[Abstract]

Rodriguez-Holguin, S. C., Corral, M. and Cadaveira, F. (1998b) Visual and auditory event-related potentials in young children of alcoholics from high- and low-density families. Alcoholism: Clinical and Experimental Research 22, 87–96.[ISI][Medline]

Rodriguez-Holguin, S. C., Corral, M. and Cadaveira, F. (1999) Event-related potentials elicited by a visual continuous performance task in children of alcoholics. Alcohol 19, 23–30.[CrossRef][ISI][Medline]

Roth, W. T. (1973) Auditory evoked responses to unpredictable stimuli. Brain Research 622, 105–112.

Schuckit, M. A. (1985) Genetics and the risk for alcoholism. Journal of the American Medical Association 254, 2614–2617.[Abstract]

Schuckit, M. A. and Smith, T. L. (1996) An 8-year follow-up of 450 sons of alcoholics and controls. Archives of General Psychiatry 53, 202–210.[Abstract]

Solowij, N., Michie, P. T. and Fox, A. M. (1995) Differential impairments of selective attention due to frequency and duration of cannabis use. Biological Psychiatry 37, 731–739.[CrossRef][ISI][Medline]

Squires, N. K., Squires, K. C. and Hillyard, S. A. (1975) Two varieties of long-latency positive waves evoked by unpredictable auditory stimuli in man. Electroencephalographic and Clinical Neurophysiology 38, 387–401.[CrossRef][ISI][Medline]

Steinhauer, S. R. and Hill, S. Y. (1993) Auditory event-related potentials in alcoholics and their first-degree relatives. Journal of Studies on Alcohol 54, 408–421.[ISI][Medline]

Van der Stelt, O., Geesken, R., Gunning, W. B., Snel, J. and Kok, A. (1998a) P3 scalp topography to target and novel visual stimuli in children of alcoholics. Alcohol 15, 119–136.[CrossRef][ISI][Medline]

Van der Stelt, O., Geesken, R., Gunning, W. B., Snel, J. and Kok, A. (1998b) Event-related potentials during visual selective attention in children of alcoholics. Alcoholism: Clinical and Experimental Research 22, 1877–1889.[ISI][Medline]

Whipple, S., Parker, E. and Nobel, E. (1988) An atypical neurocognitive profile in alcoholic fathers and their sons. Journal of Studies on Alcohol 49, 240–244.[ISI][Medline]





This Article
Abstract
FREE Full Text (PDF)
Alert me when this article is cited
Alert me if a correction is posted
Services
Email this article to a friend
Similar articles in this journal
Similar articles in ISI Web of Science
Similar articles in PubMed
Alert me to new issues of the journal
Add to My Personal Archive
Download to citation manager
Search for citing articles in:
ISI Web of Science (2)
Request Permissions
Google Scholar
Articles by Ehlers, C. L.
Articles by Slawecki, C. J.
PubMed
PubMed Citation
Articles by Ehlers, C. L.
Articles by Slawecki, C. J.