What Causes Depression?




The Mechanism Of Depression

Emotions are a critical part of the human experience. We laugh and we cry. But sometimes our emotions get out of hand. Sometimes the sadness we feel isn’t just the blues - it’s depression.

It turns out that depression is more than just feeling kind of sad. It’s actually a neurological condition that can really affect your everyday life. Depression is common. It’s actually the leading cause of disability among American adults.

According to the National Institutes for Mental Health, in 2015, about 16 million people had at least one major depressive episode just during that year. That’s almost 7% of the US population.

Depression comes in many forms, but most of those forms have the same symptoms. They just vary in severity and length. Common symptoms of depression include sadness, feeling empty, hopeless, or worthless, fatigue, changes in sleeping patterns, irritability, changes in appetite, and thoughts of suicide.

When a person experiences these symptoms for at least two weeks and it’s interfering with their daily life, it’s called major depressive disorder. This is the one you probably think of when you think of depression. But if those symptoms go on for more than two years, it’s called persistent depressive disorder.

And depression can be brought on by specific situations and life changes. Like postpartum depression, which can occur after a person has a baby. And seasonal affective disorder, when the lack of sunlight in the fall and winter can trigger symptoms.

Because depression can look like normal sadness, and because it’s not always obvious what’s caused it, sometimes it’s hard for people to believe that it’s real. That’s why some people argue that if you just try hard enough, you can break the cycle. You’re in control of your own emotions, so you can choose to feel better.

Anyone who’s suffered from depression knows that that’s not true. We’re still trying to figure out what causes it, and what exactly it does to our brains. And it’s important for doctors and scientists to keep working at understanding the condition so they can patients get back on their feet.

There’s definitely a genetic component to depression. If your parent or sibling has the condition, it’s more likely that you might end up with it too.

But it can also be linked to environmental factors. Things like abusea, neglect, and severe life stressors like financial instability or a death in the family.

Theories Of Depression Mechanism

So what’s actually going on in your brain? Up until recently, scientists were pretty sure that depression was caused by an imbalance of certain chemicals within the brain.

Dubbed the monoamine hypothesis of depression. This theory said that a lack of neurotransmitters like serotonin and dopamine, two chemicals associated with feelings of pleasure and reward, would lead to depression.

This theory is supported by a couple of things.

First, scientists found that people with a particular genetic variation in the gene that codes for the serotonin receptor 5-HTT are more susceptible to depression after stressful life events when compared to people who don’t have that mutation.

This mutation is thought to reduce the production of serotonin receptors in the brain, leading to a decrease in serotonin signaling.

There’s also evidence, mostly from post-mortem brains, that people with depression have changes in the dopamine signaling in their brains.

Some research has found that, in patients with a family history of depression, deliberately reducing levels of the proteins required to make neurotransmitters like serotonin and dopamine, does decrease their mood.

And, finally, there’s the fact that antidepressant medications like selective serotonin reuptake inhibitors, or SSRIs, work. These medications function by altering the release of serotonin at the synapse, adjusting serotonin signaling throughout the brain.

New Theories Of Depression

But scientists are no longer positive that depression is a direct result of a simple chemical imbalance.

Some of the research and treatments have been inconsistent with that idea. And the condition is really complex. So, researchers are also exploring a lot of other possible explanations.

Brain imaging studies have found that patients with depression generally have less grey matter in several different brain regions. Like the cingulate cortex, the hippocampus, and the amygdala. Grey matter, made up mostly of neuronal cell bodies, dendrites, synapses, and glia is the place where most neuronal signaling happens. Changes in grey matter volume can affect all kinds of things like emotions, memory, and decision making.

This has led some scientists to theorize that depression is more related to structural differences than neurochemical ones. Basically, depression shrinks the parts of the brain that are important for controlling our emotions and making choices to take care of ourselves, making it hard for patients to recover from feelings of sadness.

Some scientists think that depression could be related to changes in brain plasticity. That’s the process that lets your neurons change and adapt their signaling in response to new information. It might even be related to a reduction in neurogenesis, the growth of new brain cells.

Even though it’s uncommon in the adult brain, there are some brain regions that create and connect new cells throughout our lives. This theory points out that chronic stress has a negative impact on neuroplasticity. And a similar change in neuroplasticity is seen in patients with depression.

Treating the condition with antidepressants might increase the formation of new brain cells. And depressed patients taking antidepressants have higher levels of BDNF, a chemical that supports neurogenesis.

Yet another theory about depression links it to our immune system. Research has found that patients with depression have unusually high levels of cytokines, small proteins that play a big role in the inflammatory response that kicks off when your body is responding to an injury.

Cytokines are involved in sickness behaviour. You know how, when you’re sick, you’re usually not very hungry, and have trouble concentrating, and really just want to sleep a whole bunch? Hey...those symptoms sound an awful lot like depression, don’t they?

This theory proposes that high cytokine levels, caused by stress, can impact normal neurotransmitter signaling, leading to the symptoms of depression.

This is why some doctors may encourage their patients to take antiinflammatory medications like ibuprofen alongside an antidepressant.

Depression Therapy

Therapy can be very effective at treating depression. About one in every three people will find that cognitive behavioral therapy alone can improve their symptoms.

There are also a number of antidepressants available on the market. Medications like SSRIs, SNRIs and tricyclic antidepressants function by increasing the levels of neurotransmitters like serotonin and norepinephrine at the synapse.

Monoamine oxidase inhibitors, or MAOIs, block the enzymes that break down those same neurotransmitters. In all cases, they’re primarily aimed at enhancing neuronal signaling involving those neurotransmitters.

But not every antidepressant is the same. Even different SSRIs can affect different people in different ways. And it takes a few weeks for the medications to really start having an effect.

Sometimes it takes a while to find the right medication, which can be stressful and frustrating for a patient who’s really needing help.

Because depression is pretty common, and because it’s complex, it could be that the underlying cause of depression varies from person to person.

Whatever the cause, scientists are getting closer and closer to finding better solutions. And luckily, treatments do exist. They’re not perfect, but they can definitely help.

That’s why it’s so important to keep working on answering these questions, even when some medications are already available on the market. If you or a loved one has experienced depression, I hope that this article has helped you understand the condition a bit better.