Ingemar Thiblin

Cause and Manner of Death Among Users of Anabolic Androgenic Steroids

Medicolegally investigated deaths among 34 male users of anabolic androgenic steroids (AAS) are described. Nine persons were victims of homicide, 11 had committed suicide, 12 deaths were judged as accidental and 2 as indeterminate. In two cases of accidental poisoning, the levels of pharmaceuticals and illicit drugs were considered too low to be the sole cause of death and AAS was considered part of the lethal polypharmacia. Chronic cardiac changes were observed in 12 cases. In two cases of accidental poisonous deaths, these changes were regarded as contributory cause of death. Homicides, suicides, and poisonings determined accidental or indeterminate in manner were related to impulsive, disinhibited behavior characterized by violent rages, mood swings, and/or uncontrolled drug intake. The observations in the present study indicate an increased risk of violent death from impulsive, aggressive behavior, or depressive symptoms associated with use of AAS. There are also data to support earlier reports of possible lethal cardiovascular complications from use of AAS. Furthermore, a contributing role of AAS in lethal polypharmacia is suggested. Finally, the observations indicate that use of AAS may be the gateway of approach to abuse of other psychotropic drugs.

Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids

The effects of treating groups of rats with four different anabolic androgenic steroids (AAS) (testosterone, nandrolone, methandrostenolone, and oxymetholone) on 5‐hydroxytryptamine (5‐HT) and dopamine (DA) neurones in different brain regions were examined. The AAS was injected six times with 1 weeks interval and the rats were sacrificed 2 days after the final injection. 5‐HT and its metabolite 5‐hydroxyindoleacetic acid (5‐HIAA), DA and its metabolites 3,4‐dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. The effect on DA and 5‐HT synthesis rate was analysed as the accumulation of 3,4‐dihydroxyphenyl‐alanine (DOPA) and 5‐hydroxytryptophan (5‐HTP), respectively, after inhibition of the amino acid decarboxylase with NSD‐1015 (3‐hydroxy‐benzylhydrazine dihydrochloride). Additionally, the monoamine oxidase (MAO) activity was analysed in the hypothalamus. The DOPAC+HVA/DA ratio was increased in the striatum in all treatment groups. However, the synthesis rate of DA was significantly increased only in the methandrostenolone treated group. The 5‐HIAA/5‐HT ratio was increased in all treatment groups in the hippocampus, in the frontal cortex in the methandrostenolone‐treated animals and in the hypothalamus in the testosterone‐ and oxymetholone‐treated rats, while the 5‐HT synthesis rate was not affected by the AAS‐treatments. The MAO‐A activity was increased in the oxymetholone‐treated rats while the other treatment groups were unaffected. The MAO‐B activity was not changed. The results indicate that relatively high doses of AAS increase dopaminergic and 5‐hydroxytryptaminergic metabolism in male rat brain, probably due to enhanced turnover in these monaminergic systems.

High‐dose anabolic androgenic steroids modulate concentrations of nerve growth factor and expression of its low affinity receptor (p75‐NGFr) in male rat brain

The effects of treatment with a high dose of nandrolone or testosterone on nerve growth factor (NGF) levels and NGF low‐affinity receptor (p75‐NGFr) distribution in the brain were analyzed. Nandrolone, subcutaneously injected in rats for several weeks, caused an increase of NGF levels in the hippocampus and septum and a decrease in the hypothalamus. The number of p75‐NGFr‐immunoreactive neurons and the p75‐NGFr expression levels were reduced in the septum and vertical and horizontal Brocas bands. Testosterone injections caused an increase of NGF levels in the hippocampus, septum, and occipital cortex and induced an upregulation of p75‐NGFr in the forebrain NGF target regions. This testosterone effect suggests that nandrolone and testosterone affect brain NGF target cells by a different mechanism(s). Nandrolone may interfere with NGF transport and/or utilization by forebrain neurons, causing an altered p75‐NGFr expression and NGF accumulation as a consequence. Since NGF is known to maintain forebrain neurons and to regulate neurobehavioral functions, including memory, learning, and defensive behavior, it is possible to hypothesize that this neurotrophin may play a role in the mechanism of action of anabolic androgenic steroids (AAS) in the brain and be associated with endocrine and behavioral dysfunctions occurring due to AAS abuse. J. Neurosci. Res. 47:198–207, 1997.

Anabolic androgenic steroids and behavioural patterns among violent offenders

Abstract Objective: the purpose of the study is to give an account of psychiatric symptoms, aggressiveness and violent behaviour among users of anabolic androgenic steroids (AAS). The method used is retrospective evaluation based on information from forensic psychiatric evaluations (FPE), police reports and court records. Fourteen violent offenders were evaluated for current or previous use of AAS. The results suggest that AAS may produce violent behaviour and other mental disturbances, including psychosis. Besides previously described AAS-related violence, termed ‘roid rage’, two new patterns are described: (1) the cold-blooded executioner (‘Terminator’), and (2) the temporary AAS-user who takes the drug for the purpose of encouragement shortly before a criminal act (‘Sturmscknapps behaviour’). The effects of AAS on the central nervous system seem to be particularly detrimental to individuals with an inherent psychiatric disorder. It appears that use of AAS may lead to violent acts in vulnerable persons ...

Behavioural Anxiolytic Effects of Low-Dose Anabolic Androgenic Steroid Treatment in Rats

The use of anabolic androgenic steroids (AAS) in supratherapeutic doses has been associated with aggressive behaviour as well as with severe affective and psychotic symptoms. These symptoms usually follow a chronic exposure for several months. However, AAS also may have milder effects with hypomania-like features such as an increase in confidence, energy and self-esteem. We have studied the short-term effects on male rat behaviour in a modified open-field test of the AAS Metenolon administered three times at a low dose (0.01 mg/kg/week x 3). The control rats showed indications of increased timidity and aversive learning following retesting, a reaction that was absent in the AAS-treated rats. The AAS-treated rats showed less fear or anticipatory anxiety compared to control animals. Furthermore, the suppressed marking behaviour and altered morphological allometric relationships were compatible with a modified social and sexual competence in the AAS treated rats.

Alzheimer changes are common in aged drivers killed in single car crashes and at intersections

With increasing age, diseases affecting the cognitive functions are more frequent. These diseases may increase the risk for fatal car crashes. We analyzed the frequency of neuropathological alterations characteristic of Alzheimers disease (i.e. neuritic and diffuse plaques, and neurofibrillary tangles) in two association areas of the brain, parietal and frontal cerebral cortex, from 98 fatally injured aged drivers. In the age groups of 65-75 and over 75 years of age, 50% and 72% of the drivers, respectively, had neuritic plaques in either parietal and/or frontal cortex. In 14% of all killed drivers the number of neuritic plaques reached the Consortium to Establish a Registry for Alzheimers Disease (CERAD) age-related histologic score C, which indicates the diagnosis of Alzheimers disease (AD), and an additional 33% had score B, which suggests the diagnosis of AD. Neuropathological AD changes were most common in the brains of drivers killed in single vehicle crashes, followed by multivehicle crashes at intersections and least common in multivehicle crashes elsewhere, but the differences did not reach statistical significance. In a great majority (80-85%) of cases the killed aged driver was the guilty party of the crash. The results imply, that incipient AD may contribute to fatal crashes of aged drivers, and therefore the forensic autopsy of these victims should include neuropathological examination.

Injuries inflicted on homicide victims. A longitudinal victiminologic study of lethal violence.

For the purpose of studying homicidal violence from a victiminologic point of view, we have examined the number and nature of injuries inflicted on homicide victims examined at the Department of Forensic Medicine in Stockholm during the periods 1976-1978, 1986-1988 and 1996-1998. Evaluation of the total number of injuries (both lethal and non-lethal) revealed a break in the earlier trend during the last of these periods, which demonstrated a clear increase in the number of injuries probably caused by intense and prolonged violence. Thus, there were 14 victims with 40 or more injuries (the maximum being 101 injuries) in the 1996-1998 period, whereas there was only one such victim in each of the two earlier periods. Furthermore, the proportion of victims exhibiting multiple lethal injuries was greater during the last period than during the two preceding periods. These findings indicate a general enhancement in the level of aggression exerted by violent offenders, as well as an increase in the number homicide victims with injuries apparently inflicted by acts of aggression characterized by outrage.