Biological Explanations of Depression (Unipolar Disorder)

There is some evidence to suggest that depression may be due to heredity factors. Most research into this area looks at first degree biological relatives.

- Having a first-degree relatives with depression appears to be risk factor for depression.

- Family studies select people who already have depression (the probands).

- If there is a genetic link, the probands' relatives should show a higher rate of depression than the rest of the population.

- Harrington et al (1993), found 20% of such relatives have depression compared to around 10% of the population.

Gershon (1990) 

- Carried out a review of 10 family studies and found that the rates of unipolar depression in first degree relatives ranges between 7 and 30%, this range being higher than the incidence in the general population 

- This study suggests that there is a genetic link for depression as the % found is higher than that of the general population.

Ao2

- The % found is no higher than 30%, yet first degree relatives share 50% of thei genes. If depression was truly inhereted via genes the % found should be higher than this range.

- The findings from the meta-analysis do vary greatly, and perhaps cast doubt on the reliability of the 10 studies, as they lack consistency.

- A major problem with family studies is that the individuals being studied not only have a % of genes in common, but also share the same environment.

McGuffin et al (1996)

- Studied 109 monozygotic (MZ) and dizygotic (DZ) twins who had been reared apart. They found a concordance rate of 46% in MZ (identical) twins and 20%in DZ (unidentical) twins for depression.

- These findings offer partical support for the Genetic explanation of depression as the % are so much higher than that of the general population, and rising as the genetic link increases.

AO2 

- Even so, as MZ twins share 100% genes we would expect a much higher concordance rate than that found in the McGuffin study. However, the 46% found does partially support the genetic approach.

- Another negative criticism is that although there was no evidence of shared environment, all twins sahre the same environment in the womb, and it is this shared environment, which could have an impact on the later onset of depression and the high concordance rate

AO2 Further Supporting Evidence for McGuffin et al

Allen (1976)

- carried out a meta-analysis for MDD, finding a concordance rate of 40% in MZ twins and 11% in DZ twins.

- These findings compliment the McGuffin study, however there is a slight contradiction found in the statistics.

Bierut et al (1999) 

- Carried out a study of 2662 twin pairs in Australia and found a concordance rate of 36-44%. 

- Even with this reasonably high % the researchers concluded their study with the belief that environment factors played a larger role in the onset of depression than heredity factors.

Family studies such as Gershon and twin studies such as McGuffin, can't say genes are the only reason for depression, because they didn't separate genes from environment.

Adoption studies are an improvement and the most concrete evidence, because they eliminate the influence of the family environment from the genetic factors.

Wender et al (1986)

- Looked at the incidence of depression in people who had been adopted then looked at whether there was a depression to be found in their biological parents and the adopted parents. 

- They found that biological parents where 8 times more likely to suffer from MDD when compared to the statistics found in the adopted parents. 

- This statistic therefore suggests that the casual factors of derpression may lie within the genes and not the environment.

Overall, these three different types of studies give an indication that heredity factors may contribute to the onset of depression, or atleast give sometype of rpedisposition/vulnerability to the disorder. 

- One negative criticism is that there has yet to be a gene, which has been implicated in the onset of the disorder.

- A further negative criticism is that it is a rather reductionist approach, as is reduces complex human behaviour to an over-simplified explanation of depression being inherited through genes and fails to recognise the impact of other factors on the inset of depression e.g. learning, cognitive thought processes and environmental.

- Another negative criticism is the argument of Nature vs Nurture, is depression completely biological or is it a behaviour which is learned through our environment. This is something the studies, apart from adoption, do not take into account.

Neurotransmitters 

In 1960s, it was proposed that depression stems from a deficiency of the neurotransmitter norepinephrine in certain brain circuits. 

Serotonin - link between low levels of serotonin and depression

McNeal (1986) - treated patients with prozac. Symptoms were relieved but not cured.

Delgado (1990) 

- Gave patients who were receiving antdepressants a specific diet that lowered levels of the precursor of serotonin, tryptophan. 

- Majority of patients experienced a return of depressive symptoms.

- This shows that there is definitely a link between serotonin and depression.

AO2 Further Supporting Evidence

Ruhe (2007)

- In recorded depressed patients withdrawn from medication (in remission), trytophan depletion (TRD) in a high proportion of patients caused a transient but striking return of depressive symptomatology.

- This suggests that in those with risk factors of depression, lowering the brains 5-HT function can indeed cause depression.

HOWEVER 

- Ruhe also found in a different study, healthy volubteers with no vulnerability factors for the development of depression, TRD does not produce consistent changes in mood.

- This suggests that lowering the brain 5-HT is not of itself sufficient to cause depressive symptoms.

Aan Het Rot et al (2009)

- Depressive episodes alter the serotonin system in such a way that a person becomes more vulnerable to the effects of future changes in serotonin levels.

- This could explain why in Ruhe's findings the patients who were in remission had a return of the depressive symptoms, therefore showing that there is a clear link between low levels of serotonin and depression.

Commentary and AO3 

- Effects are not immediate. Antidepressants raise serotonin levels immediately, however, it takes several weeks for these effects can be detected; low levels of neurotransmitters therefore cannot be the simple explanation for depression.

- Cause or effect? We cannot be sure that the low levels of neurotransmitters cause depression or it is infact that depression is the cause for the low levels of neurotransmitters. Miller et al found low levels of norepinephrine after dogs experienced learned helplessness. This suggests that depression caused low levels of neurotransmitters. Although this research was carried out on dogs and cannot be generalised to the human populations.  

- Individual differences. Not everyone who has depression can be helped by serotonin-based drugs, which suggests that there are other causes to this disorder.