What is the etiology of depression (Major Depressive Disorder)?

The diathesis-stress model explains the etiology of depression

Question: What is the etiology of depression (Major Depressive Disorder)?
Position‹3 of 3: Depression has a sociocultural etiology
Argument1 of 2›: The diathesis-stress model explains the etiology of depression

The diathesis-stress model of depression posits that depression results from an interaction between inherent vulnerability and environmental stressors. Stress may act as a trigger to activate a biological predisposition to depression, especially when individuals lack resources to cope with stress.

The argument

The diathesis-stress model of depression describes the etiology of depression in terms of the linkage between biological vulnerability and environmental factors. The model assumes that people have different levels of sensitivity for developing depression. In the language of this model, these sensitivities are referred to as diatheses. Diatheses include biological and sociocultural factors. Some people may have more of these factors for developing depression than other people. This model suggests that having a biological sensitivity towards developing depression by itself is not enough to cause the condition. Instead, a person's sensitivities must interact with stressful life events to lead to the condition. Death, relationship difficulties, normal milestones such as puberty, marriage, or retirement are examples of stressful life events. According to this model, the greater a person's biological vulnerability for developing depression, the less environmental stress is needed to cause him or her to become depressed. If someone has a smaller amount of sensitivity for becoming depressed, it will take higher levels of stress for the condition to happen. Until people reach this critical amount of stress, they will generally live their lives normally. Their sensitivity is considered to be hidden. This model has received empirical support. For instance, Arnau-Soler et al. (2019) concluded that gene and environment interaction plays a role in the etiology of depression. Similarly, Patten (2013) empirically tested the diathesis-stress model and concluded that it is valid. Overall, according to the diathesis-stress model, sociocultural factors can explain depression when combined with a biological vulnerability.

Premises

[P1]The diathesis-stress model holds that depression arises from the interaction of a person's underlying vulnerabilities (diatheses) — which include sociocultural as well as biological factors — with stressful life events. [P2] On this model, a biological sensitivity alone is not enough to cause depression; it must combine with environmental stressors such as bereavement, relationship difficulties or life-stage transitions, and studies by Arnau-Soler et al. (2019) and Patten (2013) offer empirical support. [C] Because sociocultural stressors interacting with vulnerability explain the onset of depression, depression has a sociocultural etiology.

Counter-arguments

Gene by environment interaction studies have commonly focused on single loci in candidate genes, with mostly inconsistent or negative results. This approach has limitations because of poor-quality genotyping, inconsistent grouping of genotypes, and publication bias. MDD is a polygenic trait. This implies that it arises from the effect of multiple risk variants of small effect rather than any single genotype of large effect. Several psychologists also stated that the model is “unproductive, either theoretically or empirically.” Monroe and Simons called for more research and more precise measure on the “conceptual essence” of the diathesis-stress premise (“the nature of the interaction between elements in the etiologic process overtime”).

Rejecting the premises

[Rejecting P1] By the argument's own description the diatheses include biological factors, so the model is explicitly interactionist and does not locate the cause in the sociocultural — which is the position it is filed under. As stated, the premise supports the view that no single etiology is sufficient, which cuts against all three sibling positions equally. [Rejecting P2] The empirical support is the weakest part of the case. Gene-by-environment work has leaned heavily on single candidate loci with inconsistent replication and known publication bias, and depression is polygenic — many variants of small effect rather than one interaction of large effect. The framework is also hard to falsify, since any case can be redescribed as high vulnerability with low stress or the reverse, which is why critics have called the premise unproductive absent a more precise measure of the interaction itself.