SCHIZOPHRENIA: DIATHESIS-STRESS REVISITED D.

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Schizophrenia: Diathesis-Stress Revisited

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The self-medication hypothesis suggests that individuals with schizophrenia may use substances to alleviate distressing psychiatric symptoms (, ) or the uncomfortable neurologic side effects of antipsychotic medications (; ). Despite the appeal of this explanation, studies that have tried to confirm this hypothesis have failed to do so (; ; ; ; ; ; ). Thus, while patients with dual disorders report that use of substances subjectively lessens social problems, insomnia and low mood similar to people with primary substance use disorders, the self-medication hypothesis does not appear to be an adequate causal explanation for the elevated rates of substance use disorder in schizophrenia.

Diathesis stress model and schizophrenia

Despite these intriguing and highly consistent data, however, it must be noted that to this point there are no randomized prospective studies of the effects of clozapine in patients with schizophrenia and co-occurring substance use disorder. Thus, the evidence suggesting that clozapine can decrease substance use remains preliminary.

Diathesis stress hypothesis of schizophrenia – …

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Olanzapine, the second atypical antipsychotic introduced after clozapine, is quite effective in the treatment of psychosis (; ), but is also associated with higher rates of significant metabolic syndrome side effects (including weight gain and elevated blood sugar, cholesterol and triglycerides) than risperidone, aripiprazole, ziprasidone, and the typical antipsychotics. This medication has been used for many patients with co-occurring disorders. An initial study reported by suggested that, like clozapine but unlike typical antipsychotics, olanzapine is efficacious for the treatment of symptoms in patients with schizophrenia whether or not they have co-occurring substance use disorder. Moreover, reported an uncontrolled 12-month open label trial of olanzapine plus psychoeducation and self-help referral in 30 patients with schizophrenia or schizoaffective disorder and co-occurring substance use disorders. Seventy percent of patients achieved early full remission and the remainder achieved partial remission from substance use disorders with olanzapine treatment, and 100% achieved sustained abstinence from cocaine use. Other studies, however, have not supported an advantage for the use of olanzapine compared to typical antipsychotic medications in this population. For example, Noordsy and colleagues reported on a naturalistic follow-up of 105 patients (87% of whom had schizophrenia or schizoaffective disorder and co-occurring substance use disorder) who were switched to olanzapine, and compared them to 49 patients remaining on conventional antipsychotics (, ). While they noted that those patients switched to olanzapine demonstrated significant improvements in alcohol and drug abuse at 6, 12, and 48 months relative to their own baseline, these improvements in the level of abuse did not differ from those who remained on a typical antipsychotic. Moreover, the previously mentioned Veterans Administration study of 249 patients with schizophrenia and co-occurring substance use disorder showed that, after controlling for confounding factors, atypical antipsychotic treatment (mostly risperidone or olanzapine) was not associated with greater improvements on clinical Addiction Severity Index scores of substance use compared to treatment with typical antipsychotics ().

After case reports suggested that risperidone may be helpful in controlling substance use in patients with co-occurring schizophrenia and substance use disorders, studied 18 recently withdrawn inpatients with schizophrenia and cocaine dependence who demonstrated craving while watching cocaine use on videotape. Patients assigned to 6 weeks of risperidone reported reduction in 2 components of cocaine craving (intensity and depression) relative to patients remaining on conventional antipsychotics, and demonstrated a lower rate of relapse to cocaine use at study completion. However, Green and colleagues reported on a 1-year retrospective study among 41 patients with schizophrenia or schizoaffective disorder and comorbid alcohol or cannabis use disorder who were treated with either risperidone (n=8) or clozapine (n=33) (). Only 12% of patients treated with risperidone became abstinent within one year of treatment, as compared to 54% of patients treated with clozapine. Moreover, a larger retrospective chart review study of 249 Veterans Administration patients with schizophrenia and co-occurring substance use disorders showed that, after controlling for confounding factors, atypical antipsychotic treatment (mostly risperidone or olanzapine) was not associated with greater improvements on clinical Addiction Severity Index scores of substance use compared to treatment with typical antipsychotics (). Recently, reported that the new, long-acting, injectable form of risperidone was more effective in improving substance abuse than a depot form of the typical agent, zuclopenthixol (that is not available in the U.S.), but the difference was small and potentially not clinically significant. Further research is required to fully assess the effects of risperidone treatment, including the potential value of the long-acting injectable risperidone (Risperdal Consta) on substance use in this population.

11-10-2017 · Schizophrenia – diathesis stress revisited.

Schizophrenia – diathesis stress revisited

A number of theories have been advanced to explain the frequent association of substance use disorder and schizophrenia. Several groups have proposed that substance use can trigger the onset of schizophrenia in vulnerable individuals (; ; ). A number of reports suggesting that patients with schizophrenia and a history of substance use disorder may have an earlier age of onset of schizophrenia would appear consistent with this possibility (; ; ; ; ; ; ). In addition, most investigators, report that patients with schizophrenia experience negative effects following the use of even small quantities of substances (; ; ; ). Moreover, a recent report () that adolescent cannabis use is associated with the development of psychosis in those who have a “high output” variant of the gene for catechol-o-methyl transferase (COMT) suggests an important gene-environment interaction in this risk.



“Approximately a third did not feel they had freely consented to ECT even when they had signed a consent form.”

Amendments to the Mental Health Act in 2009 made it unlawful to administer ECT to any patient who has the ability to refuse consent. However, it can still be administered against a patient’s will in an emergency and about 2,000 patients annually are still given ECT without consent in the UK.

ECT is very rarely administered in European countries outside of the UK.




Cognitive Behaviour Therapy (CBT)
CBT is currently seen as being the most effective psychological method of treating depression. Originally devised by Aaron T.

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“Schizophrenia: Diathesis-Stress Revisited.”

Loss of Energy

0. I have as much energy as ever

1. I have less energy than I used to have

2. I don’t have enough energy to do very much

3. I don’t have enough energy to do anything

As you can see, each item is rated 0 to 3 and a cumulative total gives an indication of severity of depression.

0–9 indicates that a person is not depressed,

10–18 indicates mild-moderate depression,

19–29 indicates moderate-severe depression and

30–63 indicates severe depression.

Reliability of BDI
Beck et al (1996) gave the test to 26 outpatients during two therapy sessions one week apart. The test-retest concordance was a very high 0.93.

The test is also high on split-test reliability (0.85). Most studies carried out on reliability find that the BDI is a reliable test of depressive severity.


Validity of BDI
The BDI has concurrent validity in that it tends to agree with other measures of depression.

It is also high on construct validity. An obvious way to judge validity of a test is to observe the person in real life situations. If the person scores as suffering severe depression then this should be observable in their behaviour.

BDI-II was introduced specifically to bring it into line with the DSM-IV diagnosis. BDI-II is seen as having higher content validity than its predecessor BDI-1A.

Note: the BDI is not intended to diagnose depression. It was designed by Beck to measure the severity of depression in patients aged 13 and over, who had already been psychiatrically diagnosed with depression. The danger of using it as a diagnostic tool is that the characteristics it is measuring may well be the symptoms of other unknown disorders.




A combination of genetic evidence and discussion of the permissive amine theory is needed here. Remember too that these are not mutually exclusive. A decreased sensitivity to a particular neurotransmitter is likely to be caused by a genetic abnormality!

Genetic explanation
All the usual points need to be borne in mind and spelt out to the examiner. Clearly you will want to mention trends within families, twin studies (MZ and DZ), adoption studies and gene research. These then need to be evaluated in terms of environmental influences and the extent to which they can explain patterns such as sex differences.

Family patterns and studies
Depression does tend to ‘run in families.’ Gershon (1990) found that the incidence of depression is up to three times higher in families with a history of the disorder than it is within the general population as a whole. Others have put this figure even higher. Weissman (1987) looked at the prevalence of affective disorders in general and found that family members with first degree relatives (parent, sibling) with a mood disorder were up to ten times more likely to suffer from one too.

Twin studies
We’ll distinguish here between unipolar and bipolar disorders:

Unipolar or major depression

Allen (1976) reported the following concordance rates:

Suggesting a genetic component to explain the difference between the two.

Bipolar (or manic) depression

It is worth mentioning that different studies have produced varying percentage figures but the overall trend is usually the same.

You must point out however the shortcomings of twin research:

Annual Review of Psychology Vol

are more likely to be similar on both.
Adoption studies

Wender et al (1986) found that the biological parents of adopted children who had developed depression, were eight times more likely to have the disorder than the adoptive parents. As usual, adoption studies like this provide some of the most powerful evidence for a genetic component.

Genes as diathesis
Clearly there are environmental factors involved in depression. A negative environment acting on a person genetically predisposed to depression has more of an impact than a similar environment acting on a person without that predisposition. Kendler et al (1995) found the highest levels of depression in those scoring high on negative life events and having the genetic predisposition.

Identifying specific genes for depression
The first attempt was by Egeland et al (1987) who researched 81 members of the Old Order Amish Community of Pennsylvania. Four families within the community showed a much higher than expected incidence of bipolar (manic) depression. Of the 81 studied 14 were diagnosed with bipolar disorder and all had abnormalities on the tip of chromosome 11. This caused particular interest at the time since this location is adjacent to genes known to be involved in the production of serotonin (see biochemical section below).

However, other studies have failed to replicate the findings suggesting that either this gene is not responsible or more likely; more than one gene is involved. Nemeroff (1998) has implicated a gene on the X chromosome. Recent research has also suggested a possible lo=ink with genes on chromosomes 4,6,11,12,13,15,18,and 22. Clearly genetically complex!

A possible link between genetic and biochemical influences…

Ogilvie et al (1996) found that people with depression were far more likely to have abnormalities on a gene known as SERT that is used to make serotonin-transporter protein. New drugs used to treat depression are believed to act on serotonin-transporter protein.

Biochemical explanations
Noradrenalin and serotonin are the likely candidates. Both are classed as monoamines (as is dopamine).

Background evidence
Schildkraut (1965) found that too high a level of noradrenalin led to mania and too little to depression. The first finding should not come as a surprise if you consider the chemical similarity between noradrenalin and adrenalin! Schildkraut believed that serotonin behaved in the same way. We now know that this is not the case.

Lemonick (1997) found that drugs used to treat depression increased levels of both noradrenalin and serotonin.

Lithium carbonate used to level out some of the mood swings of manic depressives (such as Valerie in the video) decrease levels of noradrenalin and serotonin.

How do these two neurotransmitters work to create depression?

The permissive amine theory:
Kety (1975) believed that fluctuations in noradrenalin levels affect our mood: high levels of noradrenalin leading to heightened mood and eventually mania, low levels to a lowering of mood and eventually to depression. But what about the role of serotonin which is clearly playing an important role too?

Kety concluded that it is serotonin that controls the levels of noradrenalin by restraining the fluctuations.

Evidencefor the permissive amine theory
Teuting etal (1981) examined the urine of depressed patients and found chemicals thatsuggest lowered levels of both serotonin and noradrenalin.

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