Has Everything We Know About Depression Changed?

The pastor seemed uncertain. He might normally talk with the discouraged congregant about spiritual endurance or encourage him with a psalm, but today he was relatively silent. He was compassionate but offered no hopeful connections to Christ’s redeeming work or the Savior’s present help. Why? This pastor was concerned that any spiritual encouragement he gave might be misguided or unhelpful because the congregant had recently been diagnosed with depression.

Most people believe depression is caused by a chemical imbalance, but this assumption has been challenged by a recent medical study titled “The Serotonin Theory of Depression.” The project, led by Dr. Joanna Moncrieff of the University College of London, was an umbrella review, a survey of the major psychiatric research on the link between depression and serotonin, the neurotransmitter psychiatrists have long cited as the most likely chemical cause of depression. After reexamining and collecting much of the relevant and reliable research, the study concluded there is “no convincing evidence that depression is caused by serotonin abnormalities.”

Since that conclusion first appeared in Molecular Psychiatry on July 20, 2022, it’s made waves and has garnered some critique. At the very least, the study’s publication provides us with a fresh opportunity to assess what we know (and don’t know) about the experience of depression. Here are four questions the study raises and how we’d answer them as biblical counselors.

1. Does this new research mean depression is only a spiritual matter?

The discrediting of the serotonin hypothesis doesn’t mean the body and brain are now marginalized players in depression. Years ago, Charles Spurgeon described his depression as a physical event largely beyond his control. He wrote, “A sluggish liver will produce most of those fearsome forebodings, which we are so ready to regard as spiritual emotions.” Our brains and bodily fallenness are complex. The present research study only suggests that clinicians would be inaccurate to say that medication treats an underlying serotonin deficit, not that there’s no physical culprit contributing to depression.

2. Will the serotonin study affect the amount and type of medication prescribed for depression?

As groundbreaking as the recent metastudy may sound, the conclusion isn’t surprising. Voices within traditional psychiatry have always urged interpretive caution regarding medication and theories of chemical imbalances. Direct real-time measurement of neurotransmitter levels in the human brain has proven nearly impossible. No one found a neurotransmitter deficit and then set out to fix it. Instead, the earliest classes of antidepressants, like many psychoactive medications, were discovered fortuitously: drugs created for other purposes had some level of ameliorative effect on those suffering with depression. And while SSRIs (selective serotonin reuptake inhibitors) such as fluoxetine (Prozac) were proactively developed to address the hypothesized serotonin deficit, their exact effects on the human brain remain unclear.

The discrediting of the serotonin hypothesis doesn’t mean the body and brain are now marginalized players in depression.

SSRIs will remain the most common treatments for depression for one very simple reason: they regularly work. At this point, general physicians and psychiatrists don’t prescribe them because of the strength of neurobiological research but because of their clinical experience.

If a depressed person is helped by a medication the Food and Drug Administration approved through clinical trials (and that help isn’t outweighed by the side effects), that’s enough. The chemical mechanism for that help doesn’t need to be fully understood, and it certainly isn’t. The present study doesn’t mean patients taking antidepressants for depression should discontinue that form of treatment. Rather it reminds us that the factors that make existing antidepressants effective are, as yet, very poorly understood.

3. If it’s not serotonin, what causes depression?

The brain is a complex web of interdependent networks. We’d be naive to think depression can be reduced to the action of one neurotransmitter system when there are dozens. The research on serotonin hoped to identify one link in a complex chain of events by focusing on one prominent neurotransmitter. But while serotonin is less and less likely to be that significant link, other neurotransmitters may be more promising.

Yet whatever neurotransmitters may be involved, their involvement doesn’t necessarily point to causation. Instead, we can only say that neurotransmitter changes coexist with depression. A common analogy is that fires and fire trucks occur together, but the fire truck doesn’t necessarily cause the fire. To demonstrate that a problem with a neurotransmitter is the cause of depression isn’t yet within the bounds of what brain research can accomplish.

If there was a trend in the present literature on depression, it would be the connection between traumatic events and subsequent depression. Notice, for example, how the recent COVID-19 lockdown, and the upheaval around it, is beginning to reveal its mental health effects on many people. It’s as if we marshal all our energies to make it through a crisis, then, when the crisis wanes, the body collapses and emotional changes are prominent in those physical breakdowns. We can assume neurotransmitter networks are part of that process, even if our understanding is quite limited. But what we know is that global rates of anxiety and depression have skyrocketed during the pandemic, and this should mobilize pastors to love sufferers well.

4. What should we do about it?

The review study doesn’t mean that, with evidence lacking for a chemical imbalance, we can assume depression results from sinful or foolish choices! The sadness, fatigue or exhaustion, altered sleep and eating patterns, loss of pleasure, decreased concentration, and feelings of being physically drained or lacking energy and momentum aren’t sinful in themselves. To assume a person suffering with a deep and lasting feeling of darkness and discouragement must be sinning is to follow the lead of Job’s discredited counselors. Many of the psalms capture the righteous experience of being greatly downcast. The stark words of Psalm 88 stand out. There the psalmist declares, “Darkness is my closest friend” (v. 18, NIV).

While there are certainly instances where depression is driven by sin (e.g., being discovered in an affair and resenting the loss of a secret idolatrous escape), depression is not necessarily sin.

Depression, however, is always suffering.

When you listen to someone who’s depressed, you’ll hear her pain. Sometimes we know the causes of suffering—the death of a loved one or a chronic disease— and sometimes we don’t. The genius of Scripture is that we can help sufferers without knowing all the precise causes of their suffering, because God does know. While we’re still interested in causes, we don’t have to find them to bring his comfort to bear. We can hold out the hope of God’s presence in suffering (Ps. 23:4), whether it’s the product of a painfully fallen world, a faulty body, faulty choices, or a combination of them all. We can help the sufferer know God cares about their suffering and speaks with words that offer trustworthy hope no matter how strong the storm rages about them.

The genius of Scripture is that we can help sufferers without knowing all the precise causes of their suffering, because God does know.

Jesus meets people in seasons of darkness with faithful and sustaining provision. And sometimes with significant deliverance from the darkness as well. As experienced counselors, we can safely say there are more people taking antidepressant medication in our churches than most imagine. You may not understand all that goes on in their bodies or their hearts, but you can offer encouragement in their suffering that isn’t trite in holding out faith as a quick fix but that also refuses to stand to the side as if only medication were needed.

Our goal when ministering to someone with depression is to seek to understand the person’s experience, plumb the depths of God’s counsel expressed in the Scripture to find words to fit the occasion, and skillfully give grace to those who hear (Eph. 4:29). Perhaps this news about serotonin will be an invitation for us to redouble our efforts in biblical care. So we join hands with other potential helpers (friends, pastors, physicians, counselors). As we do this, we’re confident we have all we need for life and godliness in our knowledge of Christ (2 Pet. 1:3).

Ed Welch

Published by Intentional Faith

Devoted to a Faith that Thinks

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