The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.
Given this long history, you may be surprised that experts disagree on what depression is, how to define it, or what causes it.
But many experts agree that depression isn’t a thing. This is a large family of diseases with different causes and mechanisms. This makes it difficult to choose the best treatment for each person.
Reactive vs. Reactive Depression endogenous depression
One strategy is to look for subtypes of depression and see if they might respond better with different types of treatments. An example is to contrast “reactive” depression with “endogenous” depression.
Reactive depression (also called social or psychological depression) is presented as being triggered by exposure to stressful life events. It could be an attack or the loss of a loved one – an understandable reaction to out triggering.
Endogenous depression (also considered biological or genetic depression) is believed to be caused by something insidelike genes or brain chemistry.
Many people working clinically in mental health accept this subtyping. You may have read this online.
But we think this approach is far too simple.
While stressful life events and genes can individually contribute to depression, they also interact to increase a person’s risk of developing depression. And evidence shows that there is a genetic component to exposure to stressors. Some genes affect things like personality. Some affect how we interact with our environment.
What we did and what we found
Our team set out to examine the role of genes and stressors to see if the classification of depression as reactive or endogenous was valid.
As part of the Australian Genetics of Depression Study, people with depression completed surveys about exposure to stressful life events. We analyzed DNA from their saliva samples to calculate their genetic risk for mental disorders.
Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety, and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?
You may wonder why we bothered to calculate the genetic risk of mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, others less. Even people who already have depression may have a low genetic risk. These people may have developed their particular depression from another constellation of causes.
We examined genetic risk for diseases other than depression for several reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. We therefore wanted to cast a wide net to examine a broader spectrum of genetic variants linked to mental disorders.
If the reactive and endogenous depression subtypes are valid, we would expect people with a weaker genetic component to their depression (the reactive group) to report more stressful life events. And we would expect those with a higher genetic component (the endogenous group) to report fewer stressful life events.
But after studying more than 14,000 people with depression, we found the opposite.
We found that people at higher genetic risk for depression, anxiety, ADHD or schizophrenia report exposure to more stressors.
Armed assaults, sexual assaults, accidents, legal and financial problems, and childhood abuse and neglect were all more common among people at higher genetic risk for depression, anxiety, ADHD or schizophrenia.
These associations were not strongly influenced by people’s age, gender, or family relationships. We did not examine other factors that might influence these associations, such as socioeconomic status. We also relied on memory of past events, which may not be accurate.
What role do genes play?
Genetic risk for mental disorders modifies people’s sensitivity to the environment.
Imagine two people, one with a high genetic risk for depression, the other with a low risk. They both lose their jobs. The genetically vulnerable person experiences the loss of their job as a threat to their self-esteem and social status. There is a feeling of shame and despair. They can’t bring themselves to look for another job, for fear of losing it too. For others, job loss concerns them less than the company. These two people internalize the event differently and remember it differently.
Genetic risk for mental disorders could also increase the likelihood that people will end up in environments where bad things happen. For example, a higher genetic risk for depression could affect self-esteem, making people more likely to engage in dysfunctional relationships that then go bad.
What does our study mean for depression?
First, it confirms that genes and environments are not independent. Genes influence the environments we find ourselves in and what happens next. Genes also influence how we respond to these events.
Second, our study cannot distinguish between reactive and endogenous depression. Genes and environment have a complex interaction. Most cases of depression are a mixture of genetics, biology, and stressors.
Third, people with depression who appear to have a stronger genetic component to their depression report that their lives are punctuated by more severe stressors.
So, clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their risk of developing depression. It might also help some people with depression reduce their ongoing exposure to stressors.
This article is republished from The Conversation under a Creative Commons license. Read the original article.