How can we prevent depression?

We know a lot about treating depression — research incentivized by a competitive $14 million dollar antidepressant industry. But what do we know about preventing it?

Depression is best understood within the larger context of human mood (or emotional) regulation, as a specific pathology of the homeostatic process. To define depression, we must first exclude low mood in a healthy individual.

“I don’t like when I can’t control what reality is doing. Which is unfortunate because reality works independently of the things I want, and I have only a limited number of ways to influence it, none of which are guaranteed to work. I still want to keep tabs on reality, though. Just in case it tries to do anything sneaky. It makes me feel like I’m contributing. The illusion of control makes the helplessness seem more palatable. And when that illusion is taken away, I panic.”

— Allie Brosh, Hyperbole and a Half: Unfortunate Situations, Flawed Coping Mechanisms, Mayhem, and Other Things That Happened

What Depression Is Not

In the healthy human body, mood varies from day to day, and from moment to moment within a range, similar to other homeostatic processes in the body (Carstensen et al., 2000). According to Beck’s cognitive model, which has persisted for 50 years, a healthy individual’s mood responds to subjective cognitive interpretation of external or internal experiences. Internal mood deflects “down” to a sad mood in response to an experience the individual interprets as negative, and “up” to happy mood in response to an experience the individual interprets as positive. The “magnitude” of the deflection is influenced by the degree of positivity, or negativity the individual assigns to the experience (see Figure 1). (Beck, 1974; Beck and Haigh, 2014).

Now, for the first time in human history, we can measure objective evidence for this theory by mapping emotional variation in the human brain using functional MRI (Ochsner et al., 2002).

An important facet of healthy emotional regulation is the return to baseline mood after the stimulus has passed. As Brickman demonstrated in his study of paraplegics and lottery winners, individuals return to their baseline level of happiness after a stimulus, regardless of whether it is positive or negative (Brickman et al., 1978). However, the length of time it takes to reestablish equilibrium may depend on the magnitude of the stimulus (see Figure 1). (Chen et al., 2013; Parker, 2013)

Current evidence in the field of positive psychology suggests that although personality and choice are factors in the establishment of a “contentment with life” baseline for mood, this baseline is not entirely subjective. In accordance with Maslow’s hierarchy of needs model, evidence suggests that a minimum level of basic human needs must be satisfied in order to achieve contentment (ie a “good-enough environment”), after which individual variation in interpretation of stimulus becomes a significant determining factor in baseline mood (Maslow, 1943; Veenhoven, 1991; Cloninger et al., 2006; Drakopoulos and Grimani, 2013).

**Figure 1:** Pictorial representation of homeostatic model of mood variation in healthy individual, in a “good-enough” environment. ©Todreamalife, 2022

When defining depression, it is essential to differentiate between low mood due to grief, low mood due to past or current trauma, and low mood due to a pathology of homeostatic mood regulation. (O’Donnell et al., 2004; Association and Psychiatric, 2013; Parker, 2013; Gambrill, 2014)

Grief is defined here as: low mood due to an experience that a healthy individual interprets as severely negative (e.g. losing a limb, losing a loved one, being diagnosed with a terminal disease, or experiencing a rape).

**Figure 2:** Pictorial representation of low mood in healthy individual, due to grief. ©Todreamalife, 2022

Grief may take a significantly longer period of time to return to baseline mood due to the magnitude of the stimulus. Grief is an inescapable facet of human existence, and the healthy individual follows a natural process of recovery from such an event, which includes low mood for at least two months by DSM-V definitions (see Figure 2). (Association and Psychiatric, 2013; Larson, 2014)

Trauma is defined here as: low mood due a recurring series of experiences which a healthy individual interprets as severely negative, (e.g. living in a concentration camp, being a victim of domestic abuse, experiencing childhood sexual abuse.

Trauma may take a significantly longer period of time to return to baseline mood due to the duration of the stimulus. Trauma is a severely disruptive experience. The healthy individual survives a traumatic situation by adopting a specific set of mental coping mechanisms (often described as “stoicism”), which can be maladaptive when the stimulus is removed (Peterson and Seligman, 1983; Frankl, 1985; Herman, 2015). Thus, low mood due to past trauma may require an alternate treatment approach (O’Donnell et al., 2004) including therapy for post-traumatic stress disorder.

**Figure 3**: Pictorial representation of low mood in healthy individual, due to trauma. ©Todreamalife, 2022

It is also important to recognize that individuals seeking treatment for low mood may be living with past “hidden grief”, or current “hidden trauma” which is unrecognized in the prevailing culture. These are health disparities that may be compounded by the pathologization of low mood in a healthy individual (Braveman et al., 2000; Parker, 2013; Gambrill, 2014).

Examples of hidden grief include stillbirth and miscarriage (Turner, 1989; Scott, 2011); caregivers of loved ones with dementia (Dempsey and Baago, 1998), adoption, and other forms of disenfranchisement (Kamerman and Doka, 1991)

Examples of unrecognized trauma include intergenerational trauma (Cole, 2006; Gorman, 2010); living with prejudice or discrimination (Cox et al., 2012) living with a non-visible mental disability or giftedness (Beljan et al., 2006; Arnold and Fisch, 2011), and being transgender (“Unable to find information for 7716660,” n.d.)

Low mood may also be a symptom of many other disorders including substance use (e.g. ecstasy), recreational or prescribed medication (e.g. Accutane, estrogens, statins, etc.), and disease in other areas of the body (e.g. Alzheimer’s disease, hypothyroidism), brain injury (Jeffrey S. Kreutzer, Ronald T. Seel, 2001; American Psychiatric Association, 2013).

In addition, low mood is a co-occurring symptom in many mental conditions including bipolar disorder, ADHD, PTSD, and schizophrenia (Bleich et al., 1997). As any professional working with depression can attest - it remains difficult to differentiate low mood from recurring trauma versus underlying pathology (O’Donnell et al., 2004).

What Depression Is

There are many diseases that affect different regulatory mechanisms in mood homeostasis. However, depression as a disease is best conceptualized as an inability to return to baseline mood after a negative stimulus.

At the neurochemical, biological, emotional and behavioral levels, depression can best be described as an “inability to recover” (see Figure 4) (Kramer, 2006; Brosh, 2013).

**Figure 4:** Top, pictorial representation of healthy homeostasis of mood. Bottom, depression. ©Todreamalife, 2022

Although any negative stimuli may produce depression in a susceptible individual, severely negative stimuli (such as grief or trauma) are more likely to produce depression in those who have difficulty recovering. Thus past grief, and past trauma, as negative stimuli, may result in depression but are not equivalent to it.

In addition, current hidden grief and trauma in maintaining low mood may mimic symptoms of depression. (O’Donnell et al., 2004; Yehuda et al., 2006), If depression persists, it can also include anhedonia, or the inability to benefit from a positive stimulus.

To conceptualize depression as a chronic disease it is helpful to use the model of heart disease. Depressive symptoms can be compared to high blood pressure (many patients suffer from depression for many years before seeking treatment and the symptoms are often not visible). Suicide attempts can be likened to angina, or non-fatal heart attacks, (indicators of worsening disease). Fatal suicides are the mortality measure, for the end-point of untreated or unresolved depression (Kessler et al., 2003; Richards, 2011).

Within this context, suicide prevention is a tertiary preventive care measure for depression, treatment of depression to prevent suicide is a secondary preventative care measure, and prevention of the onset of depression is a primary preventative treatment for depression (Rose, 2001).

Primary prevention for depression is underresearched and under-deployed, primarily because of significant financial interests in the treatment of the pathology. (Fani Marvasti and Stafford, 2012)

How to prevent depression

While there are venture capital firms who propose the entire US population adopt prophylactic antidepressant therapy, we advocate for non-medical interventions for coping with what will likely be for all of us a grief, trauma, and low-mood ridden life.

Currently there are three main primary treatments for depression, each targeting a specific point in the development of depression. They are as follows (see Figure 5):

Modulating individual interpretation of unavoidable negative events as they arise, thus reducing the magnitude of a negative stimulus with techniques such as cognitive behavioral therapy (CBT) and logotherapy (Burns, 1981; Frankl, 1985; Robinson and Sirard, 2005; Goodkind et al., 2011; Ameli and Dattilio, 2013; Wexler, 2014).
Enhancing the ability to recover from negative stimuli by developing and fostering resilience and grit and by facilitating emotional processing (Teasdale, 1999; Yehuda et al., 2006; Duckworth and Quinn, 2009; Kleiman et al., 2013; Wright et al., 2013).
Increasing the intensity of positive stimuli as they arise with techniques such as learned optimism and gratitude (Reker, 1997; Desrosiers and Miller, 2007; Seligman, 2011).

**Figure 5:** Primary preventative treatment targets for the prevention of depression. ©Todreamalife, 2022

Written by Drea Burbank, MD. This article is adapted from a whitepaper produced for Stanford Health4All Science of Prevention course, March 17, 2014. Collaborators included Dr. Maile Jachowski and Nicole Jeffrey.