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Depression

10 Common Causes of Depression

Genetics, sleep disruption, life crises, comorbidities, and more.

Key points

  • Depression is more complicated than a bad day or one-size-fits-all chemical imbalance.
  • Seasons, gestation, other mental illnesses, and medical issues can encourage depression.
  • Depression can look different depending on what ingredients are at play, and may require unique interventions.
Tiyowpresetyo/Pixabay
Source: Tiyowpresetyo/Pixabay

“I’ve got everything someone could ask for. Why do I feel like this?” has escaped the lips of more than one patient. True, some may not seem to have anything to be depressed “about,” although they nonetheless suffer. It’s important to remember that depression isn’t necessarily “about” anything and that there are many avenues to depression.

If you’ve googled “depression,” you’ve probably encountered those canned statements that “scientists aren’t sure what causes depression…” It’s as if the world is waiting for some researcher to stumble upon a yet-unmapped cortical region with a switch labeled “depression mode” that can be flicked on and off.

Further, it implies that depression is a homogenous experience. The truth is that depression has many faces and disguises, as detailed in "The Many Faces of Depression." Further, there is no one route to depression. Different types of depression present strong evidence of different contributors. These include physiological, environmental, and psychosocial components, and the various presentations spurring from these require their own unique clinical considerations.

Forget the deceptively-simplistic popular concept of mere "serotonin imbalance," which has lately been challenged scientifically (i.e., Montcrieff, et al., 2022). And forget the more sinister idea that someone is "psychologically weak." The reality is that the following 10 items, whether individually or in combination, are what we know to be strong contributors to depression.

1. Bipolar disorders. Bipolar disorder is not simply a moody person, as pop culture may dictate. There are significant, sustained mood alterations, and depression is the "South Pole," or low, of the condition. As written about in "Can Bipolar Disorder Be Detected Early?" major depressive episodes that seem spontaneous, intense, and long-lasting, especially in teens and young adults, are not unusually the initial mood episode of a bipolar disorder.

2. Circadian rhythm disruption. Sleep disturbance has always been a notable characteristic of depression. Now, modern researchers are uncovering a complicated relationship between our synchronicity with natural rhythms and depression. In 2009, Kalman and Kalman released a paper called "Depression as Chronobiological Illness" and since then, the topic has gained a lot of interest. Researchers Vadnie and McClung (2017), and Lamont et al., (2022) noted it seems that disruption in circadian rhythm engenders significant sleep disturbance and/or other hormonal imbalances, the downstream effect being mood complications. If depression seems treatment-resistant, especially if the person has worked third shift, a referral for a chronobiology study is ideal.

3. General medical conditions. Underlying medical conditions should be ruled out as causes of mental illness symptoms, as they can encourage mimicry of psychogenic pathology. Medical mimicry is especially suspect if the person has no personal/family history of symptoms, they come on quickly, and there's no triggering event. Common culprits are thyroid disease, especially hypothyroidism (APA, 2022); low iron, Lyme disease, and Cushing's Disease. Clearly, a physician specialist, not psychotherapy or an antidepressant, would be the first-line intervention.

4. Genetics. Modern researchers have discovered that depression has a 30 to 50 percent heritability rate. Further, over 100 specific gene locations have been implicated in major depressive disorder (Kendall et al., 2021), clearly indicating genetic influence.

However, it's likely that the sprouting of depression is often a matter of nature and nurture. Researchers like Park et al. (2019), for instance, note, "Growing evidence suggests that epigenetic [how experience alters genes] changes are a key mechanism by which stressors interact with the genome leading to stable changes in DNA structure, gene expression, and behavior."

Depression can also be a response to inflammation, vulnerability to which may also be influenced by genetics (Beurel et al., 2020). Interested readers are directed to Dr. Edward Bullmore's The Inflamed Mind (2018) for an easily digested, expansive understanding of inflammation and depression.

5. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction. HPA complications have long been known to influence depression (e.g., Fink & Taylor, 2007; Parker, et al., 2010; Juruena et al., 2018). This is particularly true regarding melancholic major depressive disorder, as written about in an earlier post, "The Darkest Mood."

Melancholic depression is marked by a palpable darkness/heaviness to the sufferer's mood, severe feelings of guilt, loss of appetite/weight loss, early morning awakening, and psychomotor agitation or retardation. Clearly, more biological interventions are necessary, and, as written in the aforementioned post, tricyclic antidepressants, electroconvulsive therapy, and transcranial magnetic stimulation are often successful.

6. Life events. It's no secret that less-than-desirable life events can take the wind from our sails. For some, especially if there is genetic proneness to depression, a hard time can become a shipwreck. Adverse life events are highly correlated to depression onset (e.g., Shrout et al., 1999; Kendler et al., 1999; APA, 2022) even in the absence of obvious genetic influence. I've worked with many people who, in midlife, had major changes like divorce, and, despite no other personal or family history of depression, met the criteria for major depressive episodes.

7. Perinatal matters. This is an expansive topic, involving the intersection of genetic proneness to depression, natal-related hormonal changes, and parenting anxieties.

8. Psychiatric comorbidities. Depression is not unusually a downstream effect of another psychiatric condition. For example, people with social anxiety disorder want relationships but are debilitatingly fearful of scrutiny. Thus, they can become very lonely and just watch life go by, a fertile breeding ground for depression.

Those with personality disorders (PDOs) tend to have tumultuous interpersonal relationships, make poor decisions, and/or have ingrained self-images of ineptness and undesirability. If this is one's baseline of existence, it's easy to see how depression can settle in. Major depressive disorder is a well-documented comorbidity of PDOs (e.g. Millon, 2011; APA, 2022). Given it is encouraged by another condition, resolving the in this case, social anxiety or PDO, will likely have the most lasting effects on managing the depression.

9. Seasonal changes. Seasonal depression is most often associated with decreased sunlight, but it can also occur as daylight increases. As noted in "3 Seasonal Depression Myths," seasonal depression is more prevalent in females and is highly correlated to significant vitamin D sensitivities disrupting healthy neurotransmitter transporters. Light therapy, dietary supplements, and pharmacology and therapy during the problematic season are successful interventions.

10. Substances. Like general medical conditions, providers should consider if psychological symptoms are influenced by drug/alcohol abuse, prescriptions, or environmental toxin exposure. Substance-induced depression may be considered if the onset or worsening of depression symptoms coincides with a change in medication(s), initiation of or decreased/increased use of alcohol/illicit substances, or perhaps working in an environment where there is regular exposure to neurotoxins (APA, 2022), like a chemical factory. If suspected, immediate pharmacological re-assessment or pointed substance abuse or toxicity treatment must be considered.

Disclaimer: The material provided in this post is for informational purposes only and is not intended to diagnose, treat, or prevent any illness in readers or people they know. The information should not replace personalized care or intervention from an individual’s provider or formal supervision if you’re a practitioner or student.

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References

American Psychiatric Association, (2022). Diagnostic and statistical manual of mental disorders (5th ed, text revision.)

Beurel, E., Toups, M., & Nemeroff, C.B. (202). The bidirectional relationship of depression and inflammation: Double trouble. Neuron, 107 (2), 234-256.

Bullmore, E. (2018). The inflamed mind: A radical new approach to depression. Picador.

Fink M., Taylor M.A. (2007) Resurrecting melancholia. Acta Psychiatr Scand. 115, (Suppl. 433), 14-20.

Juruena, M., Bocharova, M., Agustini, B., and Young, A. (2018). Atypical depression and non-atypical depression: Is HPA axis function a biomarker? A systematic review. Journal of Affective Disorders, 233, 45-67.

Kalman, S. & Kalman, J. (2009). Depression as chronobiological illness. Neuropsychopharmacologia Hungarica, 11(2), 69-81.

Kendall, K.M., Van Assche, E., Andlauer, T.F.M., Choi, K.W., Luykx, J.J., Schulte, E.C., & Lu, Y. (2021). The genetic basis of major depression. Psychological Medicine, 51 (13), 2217-2230.

Kendler, K., Karkowski, L., & Prescott, C. (1999). Causal relationship between stressful life events and the onset of major depression. The American Journal of Psychiatry. https://doi.org/10.1176/ajp.156.6.837

Lamont, E.W., Legault-Coutu, D., Cermakian, N., & Boivin, D.B. (2007). The role of circadian clock genes in mental disorders. Dialogues in Clinical Neuroscience, 9(3), 333-342.

Millon, T. (2011). Disorders of personality: Introducing a DSM/ICD spectrum from normal to abnormal (3rd ed). Wiley.

Moncrieff, J., Cooper, R.E., Stockmann, T., Amendola, S., Hengartner, M.P., & Horowtiz, M.A. (2022). The serotonin theory of depression: A systematic umbrella review of the evidence. Molecular Psychiatry. https://doi.org/10.1038/s41380-022-01661-0

Park, C., Rosenblat, J., Brietzke, E., Pan, Z., Lee, Y., Cao, B., Zuckerman, H., Kalantarova, A., & McIntyre, R. (2019). Stress, epigenetics and depression: A systematic review. Neuroscience and Biobehavioral Reviews, 102, 139-152.

Parker G., Fink M., Shorter E., et al. (2010). Issues for DSM-5: Whither melancholia? The case for its classification as a distinct mood disorder. American Journal of Psychiatry, 167 (7), 745-747. doi:10.1176/appi.ajp.2010.09101525

Shrout, P. E., Link, B. G., Dohrenwend, B. P., Skodol, A. E., Stueve, A., & Mirotznik, J. (1989). Characterizing life events as risk factors for depression: The role of fateful loss events. Journal of Abnormal Psychology, 98(4), 460–467. https://doi.org/10.1037/0021-843X.98.4.460

Vadnie, C.A. & McClung, C.A. (2017). Circadian rhythms in regulation of brain processes and role in psychiatric disorders. Neural Plasticity, 2017. https://www.hindawi.com/journals/np/2017/1504507/

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