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When you look at Elaine as a record-braking athlete, her super muscles don’t tell the whole story. Her accomplishments on the track field become meaningless as soon as you learn of the serious health consequences of her regular use of anabolic-androgenic steroids (AAS). She now suffers from high blood pressure, which makes her nose bleed during strenuous exercise. She has stopped menstruating. Lately, and to her total dismay, she has even started growing facial hair.
Source: www.nursingspectrum.com
Photo source: www.magnet.fsu.edu
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Steroid abuse disrupts the normal production of hormones in the body, causing both reversible and irreversible changes. These changes include infertility and testicle shrinkage in men as well as masculinization in women.
| Drugs that can cause hormonal problems: |
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| Selected Research Findings on Hormonal Effects of Drugs of Abuse |
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Stress and HPA Axis Activity Interact to Create Risk For Drug Abuse
Uma Rao and colleagues at UT-Southwestern Medical Center examined whether hypothalamic-pituitary-adrenal (HPA) activity and stressful life experiences are related to the development of substance use disorder in depressed and nondepressed adolescents, and whether substance use disorder predicts a worsening course of depression. They measured urinary free cortisol for 3 nights in adolescents with no prior history of substance use disorder and collected information on recent stressful life experiences. They followed these adolescents for up to 5 years to assess the onset of substance use disorder, course of depression, and stressful experiences. They found that elevated cortisol was associated with onset of substance use disorder and that stressful life experiences moderated this relationship. Cortisol and stress accounted for the effects of a history or risk of depression on the development of substance use disorder. Substance use disorder was associated with higher frequency of subsequent depressive episodes. They concluded that higher cortisol prior to the onset of substance use disorder may indicate vulnerability to substance use disorder and that stressful experiences increase the risk for substance use disorder in such vulnerable youth. The high prevalence of substance use disorders in depressed individuals may be explained, in part, by high levels of stress and increased HPA activity. Rao U, Hammen CL, Poland RE. Mechanisms underlying the comorbidity between depressive and addictive disorders in adolescents: Interactions between stress and HPA activity. Am J Psychiatry. 2009 Mar;166(3):361-369.
Prenatal Cocaine Exposure and Infant Cortisol Reactivity and Regulation
In these two studies by Dr. Rina Eiden, the role of prenatal cocaine exposure on infant hypothalamic-pituitary-adrenal axis activity, infant reactivity and regulation were examined at 7 months of infant age. Participants were 168 caregiver-infant dyads (87 cocaine exposed, 81 not cocaine exposed; 47% boys). In the first study, maternal behavior, caregiving instability, and infant growth and behavior were assessed and children's saliva was sampled before, during, and after standardized procedures designed to elicit emotional arousal. Results revealed cocaine-exposed infants had greater cortisol reactivity compared to non-cocaine-exposed infants. Infant gender and caregiving instability moderated this association. The findings support a dual hazard vulnerability model and have implications for evolutionary-developmental theories of individual differences in biological sensitivity to context. In the second study, it was hypothesized that cocaine exposed infants would display higher arousal or reactivity and lower regulation during a procedure designed to arouse anger/frustration. Results indicated that cocaine exposed infants were more reactive to increases in the level of stress from trial 1 to trial 2 but, unlike the control group infants, exhibited no change in the number of regulatory strategies as stress increased, Infant birth weight moderated the association between cocaine exposure and infant regulation; among cocaine exposed infants, those with lower birth weight displayed higher reactivity compared to those with higher birth weight. Contrary to expectations, there were no indirect effects between cocaine exposure and infant reactivity/ regulation via environmental risk, parenting, or birth weight. Results are supportive of a terato-logical model of prenatal cocaine exposure for infant reactivity/regulation in infancy. Eiden RD, Veira Y, Granger DA. Prenatal cocaine exposure and infant cortisol reactivity. Child Dev. 2009 Mar-Apr;80(2):528-543 and Eiden RD, McAuliffe S, Kachadourian L, Coles C, Colder C, Schuetze P. Effects of prenatal cocaine exposure on infant reactivity and regulation. Neurotoxicol Teratol. 2009 Jan-Feb;31(1):60-68.
| Relevant NIDA Meetings |
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Drs. Cora Lee Wetherington and Sherry McKee (Yale University School of Medicine) co-organized and co-chaired the symposium, "Role of Sex and Stress in Smoking Maintenance and Relapse," at the annual meeting of the American Psychological Association, August 6-9, 2009 in Toronto, Canada. The panel included: Mariella De Biasi, Ph.D. (Baylor College); Sherry A. McKee, Ph.D. (Yale); Sudie Back, Ph.D. (Medical University of South Carolina); Mustafa al'Absi, Ph.D. (University of Minnesota Medical School). Rajita Sinha, Ph.D. (Yale) will be discussing the presentations.
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