The prevailing belief regarding the cause of depression in the brain is centered around some form of chemical imbalance. Pharmaceutical companies often claim in their marketing that antidepressants work by addressing this imbalance. This notion was also embraced by mental health activists aiming to demonstrate that depression isn’t uniform across all individuals, but rather has a “real” biological root.
While many antidepressants do impact various chemical levels in the brain, particularly neurotransmitters like serotonin, dopamine, noradrenaline, and glutamic acid, most experts now acknowledge that attributing depression to chemical imbalances is an oversimplified view.
The absence of a standard for defining the “correct” levels further complicates this theory. A significant review of literature published in 2023 has even asserted that there is insufficient evidence supporting a biochemical foundation for depression. While this review generated controversy, some critics argue it’s a far-reaching claim.
Other aspects of brain function also seem to influence a person’s susceptibility to depression and its onset. For instance, overactivation of the hypothalamus-pituitary-adrenal (HPA) axis has been implicated in this condition. The HPA axis is a network of brain regions responsible for regulating responses to stress.
Individuals with depression often exhibit an overactive HPA axis, potentially stemming from early life stress, and show elevated cortisol levels. Dysfunction in the HPA axis can also disrupt levels of other mood-related brain chemicals like serotonin.
Additionally, signs of dysfunction in the brain’s immune system are linked to depression. People with depression tend to have increased levels of proinflammatory cytokines in both the body and brain, with neuroinflammation posing a risk factor for depression.
There is evidence suggesting that stressful experiences can trigger this immune dysfunction, contributing to a higher risk of developing depression.
It’s evident that there isn’t a single cause of depression in the brain, but rather a complex interplay of factors. One plausible framework is the idea that depression results from a lack of neuroplasticity. Chronic stress and trauma seem to diminish the brain’s adaptability, leading to a negative bias in memory and thought processes.
Factors like altered brain chemicals, an overactive HPA axis, and neuroinflammation can all contribute to this inflexible state. Various treatments such as antidepressants, brain stimulation, therapy, and exercise can enhance neuroplasticity by promoting new neuron growth and better communication between pleasure and reward centers in the brain.
This article addresses the query “What actually causes brain depression?” from Chloe Reynolds in Bath.
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