Search PubMed⌕ Search

PubMed · 10074677

Interventions for couples.

Abstract

A substantial body of empirical research has documented both the promise and the shortcomings of psychological interventions for preventing or ameliorating marital distress. Couple therapy reduces relationship distress and may affect individual psychopathology, such as depression. However, some couples are unresponsive and others improve but relapse later. Interventions to prevent marital distress usually produce short-term changes in behavior and relationship satisfaction, but little evidence exists demonstrating a longer-term prevention effect. Furthermore, these interventions have yet to be examined on a diverse population of couples or with a diverse set of outcome criteria (e.g. effects on children). Concern about the negative impact of marital discord and divorce will continue to provide the impetus for research on more effective means of intervening with couples. Future research could benefit from a focus on a more diverse population of couples, treatment in natural settings, the development of more powerful interventions, and the examination of those interventions over longer periods of time and with more comprehensive outcome measures.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Christensen, C L Heavey. 1999. Interventions for couples.. https://doi.org/10.1146/annurev.psych.50.1.165

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Novel and previously reported single-nucleotide polymorphisms in the human 5-HT(1B) receptor gene: no association with cocaine or alcohol abuse or dependence.

Evidence from animal self-administration and human genetics studies suggests that the serotonin(1B) (5-HT(1B)) receptor may be involved in modulating responses to cocaine or alcohol. We hypothesize that polymorphisms, including single-nucleotide polymorphisms (SNPs), in the human 5-HT(1B) receptor gene, may be associated with individual differences in vulnerability to cocaine or alcohol abuse or dependence. A total of 210 subjects were studied, including individuals with a primary diagnosis (DSM-IV criteria) of cocaine abuse or dependence, alcohol abuse or dependence, and controls with no history of previous or current illicit drug or alcohol abuse or dependence. Genomic DNA samples were isolated from each individual. For 157 of the subjects, polymerase chain reaction (PCR) was used to amplify the entire coding region of the 5-HT(1B) receptor gene as well as parts of the 5' and 3' untranslated regions. PCR products were sequenced in forward and reverse directions on an automated sequencer. Amplified DNA from an additional 53 subjects was sequenced in the 5' untranslated region to gain additional data on the frequency of one identified SNP. Seven polymorphisms were identified: one novel SNP in the 5' untranslated region (UTR) of the gene (A-161T); one SNP not reported in any published scientific communication (but found to be recorded in GenBank) in the 3' UTR (A1180G); two novel dinucleotide deletions at positions - 184/- 183 and - 182/- 181; and three previously identified SNPs (T-261G, C129T, G861C). Data were stratified by ethnicity and pooled Relative Risk was calculated for combined alcohol abuse and dependence cases and controls, and also for combined cocaine abuse and dependence cases and controls. No significant differences between cases and controls were found.

Alcoholism↗

Chronic ethanol consumption and liver glycogen synthesis.

Chronic ethanol consumption results in a dramatic decrease in liver glycogen concentrations, which could be related to either a depressed rate of synthesis or an increased rate of breakdown. Earlier studies suggested that there is not an increase in the rate of glycogenolysis as glycogen phosphorylase activities are not elevated. In the present study it was observed that the incorporation of radiolabeled glucose into glycogen was significantly depressed in hepatocytes from ethanol-fed rats under both anaerobic and aerobic conditions. Chronic ethanol consumption decreased the total glycogen synthase (a + b) activity, which correlated closely with a loss in glycogen synthase protein. However, glycogen synthase messenger RNA levels were not depressed, which indicated posttranscriptional modifications affecting both activity and protein levels. The concentration of glucose transporter 1 was also decreased due to ethanol consumption, but glucose transporter 2 levels were not altered. This latter result suggests that glucose transport in the perivenous region of the liver lobule may be decreased in chronic ethanol consumers. The alterations in glucose transport protein and glycogen synthesis observed in this study may contribute to lowered glycogen synthesis, but do not appear to account for the magnitude of the decreases in glycogen levels and rate of synthesis. Indeed, ethanol effects on glycogen metabolism are likely to be exerted at several levels, including posttranslational modulation of enzyme activities.

Alcoholism↗

Alcoholic myopathy: biochemical mechanisms.

Between one- and two-thirds of all alcohol abusers have impairment of muscle function that may be accompanied by biochemical lesions and/or the presence of a defined myopathy characterised by selective atrophy of Type II fibres. Perturbations in protein metabolism are central to the effects on muscle and account for the reductions in muscle mass and fibre diameter. Ethanol abuse is also associated with abnormalities in carbohydrate (as well as lipid) metabolism in skeletal muscle. Ethanol-mediated insulin resistance is allied with the inhibitory effects of ethanol on insulin-stimulated carbohydrate metabolism. It acutely impairs insulin-stimulated glucose and lipid metabolism, although it is not known whether it has an analogous effect on insulin-stimulated protein synthesis. In alcoholic cirrhosis, insulin resistance occurs with respect to carbohydrate metabolism, although the actions of insulin to suppress protein degradation and stimulate amino acid uptake are unimpaired. In acute alcohol-dosing studies defective rates of protein synthesis occur, particularly in Type II fibre-predominant muscles. The relative amounts of mRNA-encoding contractile proteins do not appear to be adversely affected by chronic alcohol feeding, although subtle changes in muscle protein isoforms may occur. There are also rapid and sustained reductions in total (largely ribosomal) RNA in chronic studies. Loss of RNA appears to be related to increases in the activities of specific muscle RNases in these long-term studies. However, in acute dosing studies (less than 1 day), the reductions in muscle protein synthesis are not due to overt loss of total RNA. These data implicate a role for translational modifications in the initial stages of the myopathy, although changes in transcription and/or protein degradation may also be superimposed. These events have important implications for whole-body metabolism.

Alcoholism↗