Internet and Psychiatry

D. Deas; H. Upadhyaya; S. Thomas. Psychiatry, Medical University of S.Carolina, Charleston, SC, USA.

Co-occurring psychiatric disorders in adolescents with substance abuse is common. While many studies have explored the prevalence of psychiatric disorders in adolescent substance using samples, few have explored the relationship between comorbid psychiatric disorders and drinking behaviors in adolescents.

L. Sher^{1, 2}; M. S. Milak^{1, 2}; R. V. Parsey^{1, 2}; T. B. Cooper^{1, 3}; J. J. Carballo ^{1, 2}; M. A. Oquendo^{1, 2}; J. J. Mann^{1, 2}
1. Department of Psychiatry, Columbia University, New York, NY, USA.
2. Department of Neuroscience, New York State Psychiatric Institute, New York, NY, USA.
3. Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA.

Major depression (MDD) and alcohol dependence (alcoholism) are often comorbid. Depressed subjects with alcoholism have more chronic morbidity and mortality than individuals with either diagnosis alone. The serotonergic system is involved in the pathophysiology of both depression and alcoholism. Studies have used fenfluramine challenge to elucidate regional serotonergic function in addition to measures of resting regional glucose metabolic rate responses (rCMRglu). Fenfluramine causes a release of serotonin, consequent changes in rCMRglu can be measured by 18FDG and positron emission tomography (PET). This is the first study contrasting these changes in responses to a serotonergic challenge in major depressive disorder with and without comorbid alcoholism.

J. I. Nurnberger^{1, 4}; R. Wiegand¹; L. Bierut²; K. Bucholz²; T. Foroud^{4, 1}; H. Edenberg^{3, 4}; E. T. Meyer¹; J. Kramer⁵; D. Dick²; W. Reich²; S. Kuperman⁵; V. Hesselbrock⁷; A. Goate²; B. Porjesz⁶; H. Begleiter⁶
1. Psychiatry, Indiana University School of Medicine, Indianapolis, IN, USA.
2. Psychiatry, Washington University School of Medicine, St. Louis, MO, USA.
3. Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
4. Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
5. Psychiatry, University of Iowa School of Medicine, Iowa City, IA, USA.
6. Psychiatry, State University of New York Health Sciences Center, Brooklyn, NY, USA.
7. Psychiatry, University of Connecticut School of Medicine, Farmington, CT, USA.

1022 subjects from 448 families in the Collaborative Study of the Genetics of Alcoholism (COGA) were assessed at two time points separated by an interval of 4-5 years. The age of subjects at Time 2 was 17.4 + 3.4 years. At Time 2, 230 subjects were diagnosed with DSM IV alcohol dependence or abuse by personal interview and/or interview of a parent about the subject.

T. E. Thiele^{1, 4}; M. Navarro⁴; I. Cubero⁵; D. J. Knapp^{2, 4}; G. R. Breese^{3, 4}
1. Psychology, University of North Carolina, Chapel Hill, NC, USA.
2. Psychiatry, University of North Carolina, Chapel Hill, NC, USA.
3. Pharmacology, University of North Carolina, Chapel Hill, NC, USA.
4. Bowles Center for Alcohol Studies, University of North Carolina, Chapel Hill, NC, USA.
5. Neurociencia Y Ciencias de la Salud, University of Almeria, Almeria, Spain.

Background: Ethanol is a caloric compound, and ethanol drinking and feeding involve both appetitive and consummatory behaviors. It is therefore possible that overlapping central pathways are involved with uncontrolled eating and excessive ethanol consumption. Neuropeptide Y (NPY) and the melanocortin (MC) peptides produce orexigenic and anorectic effects, respectively. Recent investigations have implicated NPY and MC neuropeptides in the regulation of ethanol consumption. The purpose of the present research was to determine if compounds targeting central NPY or MC receptors (MCR) would produce similar effects on behaviors associated with the ingestion of ethanol or food.

J. M. Littleton. Kentucky Tobacco Research & Development Center, University of Kentucky, Lexington, KY, USA.

Effective medications for drug and alcohol dependence are greatly needed, but progress has been slow. One problem is that, although several molecular targets can be identified, many of these present specific difficulties. For example it is quite clear that nicotinic receptors for acetylcholine (nAChRs) are targets for smoking cessation medications, and the involvement of nAChRs in "reinforcing" pathways means that they are important for other types of dependence also. The difficulty here is the complexity of the subtypes of nAChRs, and their many roles in physiological function. Drugs that targeted different nAChR subtypes specifically might be valuable for different types of dependence, including alcoholism, and might have fewer of the side effects and abuse potential that reduce the value of agents like nicotine. Similarly, there is little doubt that the glutamatergic transmitter system in brain also plays an important role in reinforcement, and that glutamate receptors are therefore important molecular targets. In addition, the role of glutamate/NMDA receptors (NMDARs) in conditioning is well known, suggesting that this receptor is a target for medications aimed at reducing relapse caused by conditioned stimuli ('cues') previously associated with drug-taking (for example acamprosate in alcohol dependence). Once again, abuse potential and side effects related to the physiological role of this receptor (e.g. in learning and memory) make the NMDAR a difficult molecular therapeutic target. In this case the problem is less one of sub-type selectivity and more of targeting mechanisms that prevent NMDAR "overactivation" but which preserve normal function.

Haynes JC, Farrell M, Singleton N, Meltzer H, Araya R, Lewis G, Wiles NJ. Br J Psychiatry. 2005 Dec;187:544-51.

BACKGROUND: Longitudinal studies have been inconclusive in identifying alcohol as a risk factor for anxiety and depression.

AIMS: To examine whether excessive alcohol consumption is a risk factor for anxiety and depression in the general population, and whether anxiety and depression are risk factors for excessive alcohol consumption.