In order to evaluate Lewinsohn’s theory of depression, his three hypotheses will be examined by drawing from empirical research studies and alternative psychological theories. It is proposed that Lewinsohn’s early behavioural theory was revolutionary for our understanding of the aetiology and symptomatology of depression, but overgeneralises the heterogeneity of the disorder.
According to Lewinsohn’s theory, depression is caused by a low, or lack of response-contingent positive reinforcement, meaning that insufficient reinforcement causes a reduction of behaviours as well as dysphoria which characterise the main symptoms of depression.
There are three hypotheses about how a lack of reinforcement arises: Firstly, the environment does not provide sufficient reinforcement; secondly, the individual does not obtain the necessary social skills to receive reinforcement in an environment in which it is actually available; and thirdly, even though the individual obtains reinforcement, they are unable to enjoy it.When one of these antecedents arises, maladaptive behaviours follow, which themselves lead to lack or loss of positive reinforcement or receiving negative reinforcement.
Depression – also known as clinical depression or major depressive disorder (American Psychiatric Association, 2013) – is the most common mental health problem, globally affecting around 300 million people of all ages (World Health Organisation, 2020). It is variable in its causes and presentations, characterised by multivariate symptom complexes – overt behaviour, cognition and somatic symptoms – and an extensive range of functioning (Rehm, 2015). Its comorbidity with various anxiety disorders (Hirschfeld, 2001), behavioural disorders (Daviss & Bond, 2016), and different physical illnesses (Kang et al., 2015) contributes to the disorder’s complexity. This symptomatic and antecedent heterogeneity of depression has only partially been considered by behaviourists. Skinner – ‘the father of behaviourism’ - described depression as an “overt behaviour rather than [a] core affective experience, in line with an operant rather than respondent model” (Kanter et al., 2008, p. 4). This notion became the baseline of Lewinsohn’s (1974a) theory of depression which dominated behaviourist literature for a number of decades (Kanter et al., 2008).
According to Lewinsohn’s theory, depression is caused by a low, or lack of response- contingent positive reinforcement, meaning that insufficient reinforcement causes a reduction of behaviours as well as dysphoria which characterise the main symptoms of depression (Lewinson and Graf, 1973). There are three hypotheses about how a lack of reinforcement arises: Firstly, the environment does not provide sufficient reinforcement; secondly, the individual does not obtain the necessary social skills to receive reinforcement in an environment in which it is actually available; and thirdly, even though the individual obtains reinforcement, they are unable to enjoy it (Abreu & Santos, 2008).When one of these antecedents arises, maladaptive behaviours follow, which themselves lead to lack or loss of positive reinforcement or receiving negative reinforcement. The antecedents, the problem behaviours, and the consequences make up the units of the three-term contingency (Skinner, 1953), which interact with each other in a self-perpetuating cycle, also called chaining (Rehm,
2015); causing and maintaining depression (Segrin, 2000). In order to evaluate Lewinsohn’s theory of depression, his three hypotheses will be examined by drawing from empirical research studies and alternative psychological theories. It is proposed that Lewinsohn’s early behavioural theory was revolutionary for our understanding of the aetiology and symptomology of depression, but overgeneralises the heterogeneity of the disorder.
Lewinsohn’s Theory: A Revolutionary Approach to the Understanding of Depression
In the following, we will critically examine the extent to which Lewinsohn’s theory acted as a revolutionary contribution to our understanding of depression, and whether Lewinsohn’s three hypotheses align with recent empirical research studies.
Lewinsohn’s hypothesis of the environment not providing sufficient reinforcement contributed to our understanding of reactive depression. Rehm (2015) proposed the example of the loss of a job that once served as a positive reinforcer. Indeed, it has been found that both extrinsic and intrinsic reinforcement is positively linked to employees’ impression of doing meaningful work, which in turn has been found to be significantly correlated with employees’ well-being (Fairlie, 2013). Supporting this hypothesis, Andreeva et al. (2015) found job loss to consistently predict subsequent depression in both sexes, confirming the outcomes of various other studies on the matter (Bubonya, Cobb-Clark, & Wooden, 2016; Stolove, Galatzer-Levy & Bonanno, 2017; Navarro-Abal et al., 2018). Nevertheless, the self-reported nature of Andreeva et al.’s (2015) data might have caused method and response biases. Furthermore, there was no control for confounding factors, leading to difficulty in establishing a causal link between job loss and depression. It therefore is unclear whether the lack of reinforcement or other variables - such a financial hardship (=social causation hypothesis) - caused depression
when experiencing job loss. Nevertheless, due to the vast number of studies indicating one’s job has the potential to serve as a positive reinforcer while job loss leads to depression, we can assume that the lack of reinforcement is one factor that leads to depression when facing unemployment. Hence, Lewinsohn’s approach was revolutionary for our understanding of lack of reinforcement being an antecedent “of depression with clear environmental precipitants” (Kanter et al., 2008, p.5).
Lewinsohn’s model also shed light on cases of chronic depression, where an individual experiences “persistently insufficient levels of reinforcement and social skills deficits that prevent the individual from changing the situation” (Kanter et al., 2008, p.5). According to Lewinsohn (1974), individuals with poor social skills have difficulties receiving positive reinforcement from their environment, and experience punishing events from others leading to and maintaining depression. Supporting this hypothesis, Fauziyyah and Ampuni (2018) found “that lower social skills were associated with higher loneliness and in turn contributed to increasing tendency towards depression” (p. 98), and that depression was correlated with the maintenance of loneliness. These findings are supported by Coyne’s (1976) interpersonal theory of depression which posits that individuals’ behaviour can elicit social rejection leading to depression and depressive behaviours that maintain social rejection. While Fauziyyah’s and Ampuni’s (2018) study shows sampling bias due to non-random sampling of college students in a specific cultural context (Indonesia) with gender imbalance (27,91% male, 72,09% female), the vast number of other study outcomes from a variety of samples showing that social skills deficits significantly predict depression (Segrin, 1993, 1996; Cole, Martin, Powers, & Truglio, 1996), and depression significantly predicts social skills deficits (Natale, 1977a, Natale, 1977b) support Lewinsohn’s hypothesis. Hence, this hypothesis contributed to our understanding of how social skills deficits can cause depression and maintain it due to the process of chaining.
Lewinsohn’s hypothesis of depression being caused by a lack of ability to enjoy available reinforcement is based on the idea that social anxiety interferes with the reinforcement, and therefore precedes depression (Lewinsohn, 1974b). Indeed, Schneier et al., (1992) found that social phobia preceded the onset of depression in 69% of their participants, consistent with previous research (Stein et al., 2001). Rodebaugh et al. (2014) discovered that social anxiety leads individuals to report worse friendship quality compared to friend-reports indicating that socially anxious individuals experience less enjoyment from social interactions than their non socially anxious friends. These findings are however limited due to the reliance on self-reports that measured global friendship rather than single friendships. Ratings of specific friendships might have allowed for clearer referents, minimising the possibility of negative attentional biases causing socially anxious participants to focus on less satisfying friendships (Li, Tan & Liu, 2008). Nevertheless, a number of other studies elaborating that characteristic symptoms of social anxiety – such as low self-esteem (Harris & Orth, 2019), negative self-image (Makkar & Grisham, 2011), and underestimation of one’s social performance (Stopa, Brown & Hirsch, 2012) – negatively interfere with the enjoyment normally gained from social relationships, supporting Lewinsohn’s hypothesis.
Lewinsohn’s Theory: An Overgeneralisation of Depression
Although Lewinsohn’s theory highlights important factors which cause and maintain depression, it fails to explain the complexity of its aetiology and symptomatology. In the following, we will critically examine the extent to which his three hypotheses overgeneralise depression, and whether the aetiologies and symptoms of depression can be explained by other theories.
Lewinsohn’s hypothesis regarding depression arising due to insufficient environmental reinforcement is “based on an implicit assumption that a basic minimum ratio of reinforcement to behaviour is required to maintain an adequate level of functioning” (Rehm, 2015, p. 18). While studies show that an increase of engagement in positively-reinforced events results in positive moods in adolescents, the level of autonomy and personal choice in these activities demonstrated to be mediating factors between the two variables (Weinstein & Mermelstein, 2007). This aligns with the self-determination theory (Deci & Ryan, 1985), asserting that “situational factors that satisfy the basic psychological need of autonomy, namely the perception of one’s activities as self-chosen and important, enhance emotional well-being” (Weinstein & Mermelstein, 2007, p. 10). Thus, a simple lack of social activity does not sufficiently explain the development of depression. The factors that contribute to each activity, such as certain associated emotions, might be important variables.
While Lewinsohn’s environmental reinforcement hypothesis applies to some cases of reactive depression, it cannot explain endogenous, none-stimulus-bound depression (Kanter et al., 2008). Costello (1972) argues that not only the loss of reinforcers, but the loss of reinforcer effectiveness causes depression, which can be based on endogenous, neurophysiological changes. Although Costello’s (1972) hypothesis lacks reliability and validity as it is solely based on observations of depressed individuals, various empirical research studies on biological theories support his hypothesis. It has, for instance, been found that age-related alterations of the endocrine system (Clarke & Currie, 2009) and heightened amygdala response to stress caused by genetic predisposition can trigger depression (Dean & Keshavan, 2017). Nevertheless, one’s interaction with “the social environment may influence the development and activity of neural systems, which in turn have an impact on behavioural, physiological, and emotional responses” (Bernaras, Jaureguizar, & Garaigordobil, 2019, p.5).
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