Family history of alcoholism does not influence adrenocortical hyporesponsiveness in abstinent alcohol-dependent men.
ABSTRACT Early abstinence in alcohol-dependent subjects is marked by adrenocortical hyporesponsivity. However, it is uncertain whether the blunted response is primarily attributable to a genetic vulnerability or to the chronic abuse of alcohol. In the present study, the authors investigated the influence of a family history (FH) of alcoholism upon suppressed glucocorticoid reactivity.
Twenty-two abstinent alcohol-dependent and 14 control men were studied. The cortisol response was assessed in 11 patients following oCRH infusion (.4 ug/kg) and in a separate group of 11 patients following cosyntropin infusion (.01 ug/kg) preceded by high-dose intravenous dexamethasone (8 mg). FH, as determined by self-report, was assessed using two different methods: history of parental alcoholism and number of alcohol-dependent first- and second-degree relatives.
Neither a parental history or familial loading of alcoholism had a significant effect upon glucocorticoid responsivity in abstinent alcohol-dependent men.
Adrenocorticol responsiveness in recently abstinent alcohol-dependent men does not appear to reflect a preexisting biologic vulnerability to alcoholism.
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ABSTRACT: Patients and families often are aware of research on genetic factors influencing eating disorders. Accurate interpretations of research on environmental and genetic risk factors can be empowering to patients and families; however, misinterpretations could prove detrimental. Clinicians who are not versed in genetic research may believe they are ill prepared to discuss the nuances of genetic research with patients and families. In this article the authors discuss what is known about genetic and environmental risk factors with an emphasis on gene-environment interplay to improve clinicians' comfort level in discussing these complex issues with their patients.Child and adolescent psychiatric clinics of North America 02/2009; 18(1):67-82. · 2.88 Impact Factor
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ABSTRACT: The primary objectives of this study were to: (a) examine the neuroendocrine effects of naltrexone vs. placebo by comparing serum cortisol levels; and (b) test the biobehavioral correlates of naltrexone-induced changes in cortisol. Non-treatment seeking heavy drinkers (n=37) completed two intravenous alcohol administrations, one after naltrexone (50 mg) and one after placebo. Cortisol levels were measured at baseline and after alcohol intake (BrAC=0.06 g/dl) on both sessions, as were subjective responses to alcohol. Analyses revealed that naltrexone significantly raised overall cortisol levels compared to placebo. Cortisol levels decreased during alcohol administration and a stronger decrease was observed in the naltrexone condition. Cortisol levels were, in turn, inversely related to some of alcohol's the reinforcing effects (i.e., alcohol 'high,' vigor) and positively associated with some of its unpleasant effects (i.e., sedation and subjective intoxication). These results suggest that naltrexone alters cortisol levels in heavy drinkers and that its effects on subjective responses to alcohol may be related, in part, to naltrexone's ability to activate the HPA-axis.Pharmacology Biochemistry and Behavior 10/2008; 91(4):489-94. · 2.82 Impact Factor