Earlier this month, I wrote about inflammation and a possible cause of mental illness and, in the process, mentioned some of the theories about what causes depression. Now I want to revisit the debate and the pros and cons of the various possible explanations.
The leading suggested causes are emotions (anger turned inward), genetics, trauma, brain chemistry, and now bodily causes such as cell disruptions and inflammation.
Anger turned inward and other emotional mechanisms never made a lot of sense to me, though in the course of my depression (later revealed to be the depressive phase of bipolar disorder), I certainly experienced a lot of anger that I wasn’t able to express. In fact, I denied that it even existed. The emotions most associated with depression for me at that time were guilt, shame, and hopelessness. There was a veritable stew of emotions I had turned inward, including anger, but it was far from the only one. Everyone who’s depressed has their own stew of emotions, which may also include fear, self-hatred, blame, and/or resignation. Any of those could turn inward as well, punishing their sufferers with depression.
Genetics makes more sense when you consider that depression and other mental disorders can run in families. But it also arises in families with no history of depression. Statistics say that if one family member experiences major depression, other family members—parents, children, and siblings—are 30% to 50% more likely to have it too. It’s even higher in twins.
Depression’s heritability is complicated, however. There’s not a specific depression gene, but some combination of elusive genes that combine to foster that tendency. What genes they are and how they interact with each other are among the problems still to be solved. And if genetics cause depression, what to do about it is still a mystery.
Trauma, PTSD, and C-PTSD have also been implicated in depression. That really rings true. Experiencing personal trauma or witnessing it again creates a stew of emotions, many long-lasting, which could easily cause depression. If you’re living with the after-effects. potentially for years, it’s easy to see how depression might result. The science of epigenetics may explain how the genes themselves change or how they are passed on to family members. The answers may involve several different mechanisms.
Brain chemistry is the most controversial of the hypotheses for the cause of depression. The theory is that certain neurotransmitters, such as serotonin, are deficient or not properly taken up by their receptors. However, Harvard Health Publishing has noted that “It’s often said that depression results from a chemical imbalance, but that figure of speech doesn’t capture how complex the disease is. Research suggests that depression doesn’t spring from simply having too much or too little of certain brain chemicals.” The major treatment has been to try to restore the balance with medication.
Part of the problem with this theory, however, is that no one is quite sure how these drugs work, only that they do—but not for every person with depression and not reliably. The most popular antidepressants are thought to work by improving the uptake of these brain chemicals. Until recently, improving these chemical “imbalances” was the primary treatment for depression, and it did a lot of good for a lot of people. But if the receptors are flooded with neurotransmitters right away, why do they take six weeks or more to take effect? Why do the results lessen over time to the point where antidepressants quit working for some patients? Why do they have no effect on others (treatment-resistant depression)?
Neurons/Cellular Interactions and Immune Disruptions are the latest avenues being explored. Research has focused on specific areas of the brain, such as the hippocampus, which is associated with both emotion and memory. Excitatory neurons, which change gene functions, and microglia, which microglia, the brain’s immune cells, become dysregulated and cause ongoing inflammation, which can affect the brain..
Also, Columbia University has shown for the first time that neurogenesis stalls in the brains of adults with major depressive disorder. They have identified the molecular programs that control neurogenesis, which may help researchers develop new therapies.
These new theories, while they present hope for understanding depression and the brain, are still a long way from reaching a consensus, or even agreement on the causative factors. That means they’re also a long way from developing new treatments for depression. Until they do, selective serotonin reuptake inhibitors (SSRIs) will likely continue to be the front line of therapy for major depression.
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Janet Coburn
Bipolar Me 
Comments on: "Causes of Depression: The Debate Continues" (1)
Perhaps we have made depression far more complicated than it needs to be.
We use the word depression as though it identifies a thing that exists independently inside a person, a disorder that causes someone to feel sad, withdraw, lose motivation, sleep differently, lose their appetite or experience a lack of pleasure. But perhaps we have reversed the relationship between the word and the behaviour.
A person does not necessarily behave in a particular way because they have depression. We observe a collection of behaviours, emotions and experiences and give that collection a name: depression.
The label describes what we see; it does not necessarily explain why it is happening.
If somebody becomes withdrawn, stops enjoying things, sleeps excessively, loses motivation and feels miserable, we call those behaviours “depressive symptoms.” But those behaviours are not inherently abnormal. Human beings naturally experience periods of sadness, withdrawal, exhaustion, hopelessness, frustration and disinterest. They are part of the enormous range of ways in which human beings respond to life.
Perhaps what we call depression is therefore not something that causes the behaviour, but a word we have created to categorise a particular pattern of behaviour and experience.
Consider the difference between saying:
“He is depressed, therefore he behaves this way.”
and:
“He is behaving and feeling this way, therefore we describe his condition as depression.”
The first treats depression as the explanation. The second treats depression as the description.
That distinction is important.
If depression is simply the name we give to a particular collection of experiences, then saying that depression causes those experiences can become almost circular. Someone is withdrawn because they are depressed; how do we know they are depressed? Because they are withdrawn, alongside the other recognised characteristics. The label can end up explaining nothing beyond the behaviour it was originally created to describe.
This does not mean the suffering is imaginary. Quite the opposite.
The person’s suffering can be completely real without depression having to be treated as a separate entity that causes it.
Perhaps sadness, hopelessness, exhaustion, loss of motivation and withdrawal are sometimes natural reactions to circumstances, thoughts, relationships, experiences or simply the fluctuating nature of being human. The reaction itself can produce further symptoms: sleeping more can produce lethargy; withdrawing can produce loneliness; losing activity can reduce stimulation and pleasure; hopeless thoughts can reinforce hopeless feelings.
A chain of completely natural human responses can therefore become self-perpetuating.
At some point we give the resulting pattern a name.
Depression.
But naming the pattern does not necessarily mean that we have discovered its fundamental cause.
This is why I think there is value in questioning the assumption that depression must be something causing a person to behave differently. Perhaps the person isn’t behaving differently because an illness has taken control of them. Perhaps they are behaving exactly as a human being can naturally behave when confronted with whatever their mind and circumstances are presenting to them.
The word depression may therefore be useful. It allows people to communicate, clinicians to categorise experiences and society to recognise that somebody is suffering.
But usefulness does not necessarily make a label an explanation.
Depression may describe the experience without explaining its origin.
And perhaps that is the more interesting question:
Are we treating depression as a cause when it may simply be the name we have given to a particular way human beings can naturally feel, think and behave?
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