Annotation: culture and family therapy

This annotation considers the importance of understanding culture for the theory and practice of family therapy. A number of theoretical approaches are described. Some are concerned with ubiquitous and universal family processes like the family life cycle, while others are concerned with the particularity of family life such as the content of myths and rituals. Some practical implications for the participants of the therapy, and the choice of therapeutic approach is discussed.     

Family therapy for bulimia nervosa in adolescents: an exploratory study

Family therapy has only rarely been reported as a treatment for bulimia nervosa and not specifically’for adolescents. This account describes family therapy with eight adolescents who suffered from bulimia nervosa. Change was measured by assessing symptomatic behaviours and global measures of family and social function prior to treatment and again one year later. At reassessment there was a significant reduction in bulimic behaviours although many had some continuing symptoms. Some aspects of the therapy are described and implications for further study of treatment for adolescent bulimia are discussed.     

Structural therapy for a West African family

In West Africa kinship is a very important aspect of social organization; it is a hierarchical system which functions as the domestic group and in the wider realm of politico-jural and economic relations. The individual is constituted through the kinship group. It is suggested that family therapy, especially structural family therapy, may be suitable as a treatment technique in such non-individualistic societies. A case example is given to illustrate how this understanding can lead to successful therapy.     

Stress, Glucocorticoids, and Damage to the Nervous System: The Current State of Confusion

An extensive literature demonstrates that glucocorticoids (GCs), the adrenal steroids secreted during stress, can have a broad range of deleterious effects in the brain. The actions occur predominately, but not exclusively, in the hippocampus, a structure rich in corticosteroid receptors and particularly sensitive to GCs. The first half of this review considers three types of GC effects: a) GC-induced atrophy, in which a few weeks' exposure to high GC concentrations or to stress causes reversible atrophy of dendritic processes in the hippocampus; b) GC neurotoxicity where, over the course of months, GC exposure kills hippocampal neurons; c) GC neuroendangerment, in which elevated GC concentrations at the time of a neurological insult such as a stroke or seizure impairs the ability of neurons to survive the insult. The second half considers the rather confusing literature as to the possible mechanisms underlying these deleterious GC actions. Five broad themes are discerned: a) that GCs induce a metabolic vulnerability in neurons due to inhibition of glucose uptake; b) that GCs exacerbate various steps in a damaging cascade of glutamate excess, calcium mobilization and oxygen radical generation. In a review a number of years ago, I concluded that these two components accounted for the deleterious GC effects. Specifically, the energetic vulnerability induced by GCs left neurons metabolically compromised, and less able to carry out the costly task of containing glutamate, calcium and oxygen radicals. More recent work has shown this conclusion to be simplistic, and GC actions are shown to probably involve at least three additional components: c) that GCs impair a variety of neuronal defenses against neurologic insults; d) that GCs disrupt the mobilization of neurotrophins; e) that GCs have a variety of electrophysiological effects which can damage neurons. The relevance of each of those mechanisms to GC-induced atrophy, neurotoxicity and neuroendangerment is considered, as are the likely interactions among them.