As I am not clinically trained this article is not meant to be any sort of assessment or diagnosis of any individual or the 'cohort' of mothers who seem to experience symptoms of breastfeeding aversion and agitation. It is, rather, a short, unacademic, inquirey into depression and whther BAA is, in fact, post natal depression, or not.
What Is Depression?
We describe depression in radical behavioral terms, emphasizing the occasions on which the term is used and deemphasizing any underlying unitary disease, physiological, or emotional state to which the term refers. Depression comes from the late Latin word depressare and the classical Latin word deprimere. Deprimere literally means “press down”; de translates into “down” and premere translates into “to press.” In essence, the term appears to denote a feeling of heaviness, of being “pressed down,” that is also referred to as “sad,” “blue,” or simply “down.” Depression also refers to a depressed topography or the fact of being pressed down. Depression as a referent to mood or emotional state appeared as early as 1665 and merely meant a lowering of mood or spirits (Simpson & Weiner, 1989). Thus, the core experience of depression appears to be a private event tacted as depressed or in psychiatric terms as dysphoric. However, a minority of individuals will meet criteria for depression and deny depressed mood or present with irritable mood instead. These individuals may have deficits in accurate tacting of private experience, or they may represent diagnostic Type II errors and should not be classified as depressed.
It is important not to associate what is tacted as depression with a specific pattern of physiological responding or reify it as a particular emotional state. The antecedent conditions and underlying physiologies associated with the experience of depression may vary widely, and no core composition can be assumed. Emotional states such as sadness are simply co-occurring behavioral responses (elicited unconditioned reflexes, conditioned reflexes, operant predispositions) that appear to be integrated because the behaviors are occasioned by common discriminanda and are controlled by common consequences (Skinner, 1953). For example, a child with overbearing parents experiences an emotional state of sadness and a co-occurring behavioral response of crying when her parents criticize her. The crying is negatively reinforced when her parents comfort her and stop criticizing her, which may also result in a change of her emotional state.
The particular quality of an emotional state labeled depression should vary with the characteristics of the environmental triggers. For example, private events labeled as depressed may be associated with overworking and receiving little reinforcement for long stretches of time or with grieving the death of a loved partner. In each case the underlying physiology is presumably different, but the experienced phenomena may be sufficiently similar to prompt the tact. More specific discrimination training may be useful (e.g., the first situation may be better labeled as burned out and the second as grieving) but given the problems associated with training the tacting of private events (Moore, 1980) it is not clear that an individual will be able to make these discriminations reliably.
The psychiatric nomenclature emphasizes this core experience and several additional symptoms. Depressed mood or dysphoria is the primary feature of major depressive disorder (MDD), the most common depressive diagnosis. In addition to this core experience, there are several other symptoms of MDD, including loss of interest in activities, sleep and appetite changes, guilt and hopelessness, fatigue, restlessness, concentration problems, and suicidal ideation. As discussed in detail below, the medical model holds that this constellation of symptoms represents a syndrome, but complexity is immediately introduced because the presence and nature of these symptoms vary considerably across clients (Líndal & Stefánsson, 1991). For example, some clients experience vegetative symptoms of depression (decreased appetite and insomnia) whereas, less commonly, others experience reversed vegetative symptoms of increased appetite and hypersomnia. Similarly, psychomotor retardation is more common and agitation is less common, and both may be demonstrated by the same individual at different times.
To account for this complexity, DSM-IV-TR has parsed depression into various additional categories, each with similar and overlapping characteristics, and there are an increasing number of diagnostic categories of depressive disorders or problems involving sad or irritable affect. In fact, Appendix B of DSM-IV-TR lists 17 proposed disorders for further study, six of which deal with disorders of mood. Although detailed review of these subcategories is outside the purview of this paper, it should be noted that although there may indeed be different syndromes with different etiologies and treatment implications, a behavior-analytic view holds that the current proliferation of depressive disorders is largely unnecessary. We see not several distinct disorders but a phenomenon of depression with great variability in time course, symptom severity, and correlated conditions. All the disorders share a depressed mood symptom that parallels the core experience of the problem, and all share several additional criteria with MDD, often differing only in duration or number of symptoms. From an idiographic behavior-analytic perspective, there exists not one or three or several depressive disorders—there are as many depressive disorders as there are depressed individuals.
The constellation of depressive disorders with shared characteristics suggests that the tact depression involves a variety of public and private antecedent stimulating events that vary from occasion to occasion but have sufficient overlapping properties to occasion consistent usage of the term. We view the diversity of additional symptoms represented by these disorders as consistent with the diversity of environmental causes of depression, physiological states labeled depression, and psychological responses to the environmental causes and physiological states. Thus, no overarching depressive syndromes are posited or assumed at this point. Nonetheless, commonalities in history, environmental antecedents, and symptom presentation exist and may guide treatment decisions.
Thus, our understanding of depression must allow for the great variety of stimulus conditions that occasion use of the term. We can discard several classes of use that we can simply label as incorrect. For example, an individual learning a foreign language may simply state the wrong word. Likewise, a person may be diagnosed with depression but later it is determined that the person has a large cancerous tumor that is causing the symptoms. Although a complete behavioral analysis must account for these usages, they are not interesting from a clinical standpoint. More important are instances in which the term is not used but could be. For example, a person visits a psychologist and complains of several symptoms of depression but not depressed mood. Another person would label the private experience as “depressed,” but the current client did not develop adequate private stimulus control over the experience. The psychologist performs a diagnostic interview, and the client falls one symptom short of the diagnosis of MDD. In this case it is advantageous to consider the person depressed even though it is possible that neither the psychologist nor the client will use the term.
Traditional Behavioral Models of Depression
Skinner wrote very little on depression; when he did, he emphasized overt behavior rather than the core affective experience, in line with an operant rather than respondent model. For example, in 1953 he wrote,
If we remove a man from his characteristic surroundings, a large part of his social behavior cannot be emitted and may therefore become more and more probable: he will return to his old surroundings whenever possible and will be particularly “sociable” when he does so. Other parts of his behavior become strong because they are automatically reinforced under the prevailing deprivation; he will talk to anyone who will listen about his old surroundings, his old friends, and what he used to do. This is all a result of deprivation. But nostalgia is also an emotional condition in which there is a general weakening of other forms of behavior—a “depression,” which may be quite profound. We cannot classify this as the result of deprivation because the behavior which is thus affected has not been specifically restrained. (p. 165)
Three aspects of this passage are noteworthy. First, as Skinner typically did, by placing the term depression in quotes he was careful to avoid giving it any special status other than that of a verbal description. As discussed above, this practice of placing such terms in quotes may be awkward and tiresome but serves as a reminder that certain assumptions are not to be made when using them. The quotes also serve as a reminder of an important verbal quality to the term, discussed below. Second, Skinner described the core experience as an “emotional condition,” suggesting an elicited component. Consistent with an operant model, he did not elaborate on this point and instead focused on overt behavioral reductions. Third, Skinner highlighted the centrality of reduced positive reinforcement in depression. Simply put, social behavior depends on a reinforcing environment; change the environment so that responses do not yield reinforcement and one reduces the behavior.
This notion became the foundation of Lewinsohn's (1974) theory and dominated the behavioral literature for several decades. Lewinsohn described depression as characterized primarily by a low rate of response-contingent positive reinforcement (RCPR). In a nutshell, Lewinsohn emphasized environmental events that produce losses of major sources of RCPR, such as a divorce or the loss of a job, and social skills deficits that limit an individual's ability to reobtain RCPR once it has been lost. Thus, his model focused on the behavioral reductions often seen in depression. Lewinsohn assumed the core experience to be an elicited by-product of these situations, but he did not detail this process. Other symptoms of depression (e.g., fatigue, somatic symptoms, and cognitive symptoms) were assumed to be evoked or to be secondary elaborations of other symptoms.
We hold that Lewinsohn's (1974) characterization of the core affective experience of depression as an elicited by-product of losses of or reductions in positive reinforcement is fundamental to understanding depression. Some cases of depression clearly are described best by Lewinsohn's model, such as single, discrete episodes of depression with clear environmental precipitants and with symptom profiles that emphasize behavioral reductions that resolve when the environments are reinstated. For example, a person may become depressed after a divorce or loss of job, and the depression resolves when the person finds a new relationship partner or a new job. With cases of chronic depression, Lewinsohn's model emphasizes persistently insufficient levels of reinforcement and social skills deficits that prevent the individual from changing the situation, and this model also seems to be adequate for some cases. For example, a person who becomes depressed after a divorce, resulting in a net reduction in positive reinforcement, and does not have adequate social skills for initiating new romantic relationships will likely become chronically depressed until the necessary social skills are learned.
All of this is nothing new. However, Lewinsohn's (1974) model vastly underestimated the variety and complexity of factors that can reduce behavior. Indeed, the field of behavior analysis, if nothing else, has demonstrated functional processes that can increase or decrease behavior. All functional processes that decrease behavior are potentially relevant, if the behavioral reductions produced are large and generalized and a dysphoric reaction occurs concomitant with the behavioral reductions. For example, extreme persistent and uncontrollable punishment may lead to substantial behavioral reductions, elicited negative affect, and depression as per Seligman's early learned helplessness model (Overmier & Seligman, 1967).
Further consideration of this complexity is provided by Hopko, Lejuez, Ruggiero, and Eifert (2003) and Lejuez, Hopko, and Hopko (2001), who analyzed depression in terms of the matching law (Herrnstein, 1970). Briefly, this suggests that the behavioral reductions seen in depression are not accurately seen as the simple product of reductions in positive reinforcement but rather as the product of ratios of reinforcement for depressed relative to nondepressed (or healthy) behavior. In other words, the sum total of reinforcement available in a person's environment must be taken into consideration, not just reinforcement for target behaviors. As a simple example, a depressed person may not get out of bed due to loss of a job (loss of positive reinforcer for getting out of bed), but positive reinforcers for staying in bed (e.g., spouse who now takes care of the person or makes the person breakfast) must also be considered. The bottom line is that the situation is complicated, and nothing less than a complete functional analysis of the individual's environment is required if one is to attempt a full functional analysis of depression.
Aversive Control in Depression
Skinner also suggested that depression may be an emotional response to aversive controlling practices, especially aversive social control (1953, pp. 360–363). Similarly, Ferster (1973) suggested that depression is characterized as much by increased escape and avoidance repertoires as by reduced positive repertoires. In fact, research indicates that more cases of depression are characterized by the accrual of multiple chronic mild stressors, such as work-related stress, homemaking demands, and financial trouble than by major losses such as divorce or the loss of a job (Billings & Moos, 1984; Kessler, 1997; Mazure, 1998; Monroe & Depue, 1991; Paykel, 1982). In these cases we suggest that the core elicited affective experience of depression is as much a product of increased aversive control as it is reduced appetitive control.
It is important to recognize, however, that the two sources of control are often intimately related. Ferster (1973) suggested that the depressed escape and avoidance repertoire is largely passive, which also leads to a decrease in positive reinforcement relative to what an active repertoire would provide. For example, consider a client who stayed in bed all day and did not go to work, thereby avoiding a stressful meeting with his boss where he believed he was going to be reprimanded. Staying in bed successfully avoids this outcome, but it also prevents contact with other contingencies that might function to ameliorate depression—for example, if the client was wrong and no reprimand was forthcoming. Similarly, an individual with social phobia, which is highly comorbid with depression (Mineka, Watson, & Clark, 1998), may be negatively reinforced by successfully avoiding situations that may result in social humiliation or embarrassment, but avoidance of such situations also reduces opportunities for contact with positive social reinforcement. In other words, an increase in aversive social control here almost guarantees a decrease in appetitive social control. These aversive environments evoke and maintain behavior that is immediately effective as a response to these contingencies but maladaptive over the long term in that access to positive reinforcers is diminished.
Such aversive situations may elicit anxiety rather than depression per se, but the point is that a repertoire characterized by excessive escape and avoidance behavior (and elicited affect labeled anxiety) will undoubtedly result in decreased contact with positive reinforcement (and elicited affect labeled depression) over time. Thus, anxiety should precede and then become comorbid with depression, and this pattern appears to characterize many comorbid cases (Mineka et al., 1998). In fact, the well-established comorbidity of anxiety and depressive disorders should be a function of the degree to which anxious avoidance also results in a loss of positive reinforcement. Hayes, Wilson, Gifford, Follette, and Strosahl (1996) have provided a convincing review showing that avoidance may underlie a host of psychological problems, including depression, and the specific relation between avoidance and depression has received empirical support as well (reviewed by Ottenbreit & Dobson, 2004). Finally, research indicates that over the course of treatment for social phobia, change in anxiety predicts change in depression, but change in depression does not predict change in anxiety (Moscovitch, Hofmann, Suvak, & In-Albon, 2005), suggesting that symptoms of depression are at least partially maintained by a social environment that has aversive functions.
To summarize our analysis to this point, there are many pathways to depression. Depression is not a precise, technical term and has no essential composition. It is not a syndrome. The term refers to a chronic experience of feeling sad or down and to associated symptoms that vary widely. This symptomatic heterogeneity is due to the heterogeneity of historical and environmental controlling variables. That said, some processes may be more common in depression, and awareness of these processes would help to limit what could be a vast assessment of many potentially irrelevant variables (Hayes & Follette, 1992). Two broad processes have been highlighted here: (a) losses of, reductions in, or persistently insufficient levels of positive reinforcement as per Lewinsohn (1974), and (b) increases in environmental aversive control (negatively reinforcing and punishment contingencies). When chronic, both processes may be seen as functioning as enduring motivating operations for depression (Dougher & Hackbert, 2000). Of course, multiple sources of control are probable.
An Adaptive Syndrome or Maladaptive Response? Genetics and Evolutionary Theories
In contrast to an idiographic functional analysis of depression, the medical disease model posits that depression is a syndrome or multiple syndromes and one inherits risk for this syndromal response. The model relies to a considerable degree on research indicating at least some genetic involvement in depression (Wallace, Schneider, & McGuffin, 2002). However, the family, twin, and adoption studies on which this conclusion is based point to a larger environmental contribution than genetic contribution in all but the most severe cases of depression (Wallace et al., 2002). Furthermore, researchers and theorists from a variety of perspectives have highlighted methodological flaws and unsubstantiated assumptions of this research (Ceci & Williams, 1999; Hayes, 1998; Turkheimer, 1998) that have the collective effect of lowering heritability estimates even further as well as questioning their very basis. Nonetheless, it seems likely that some inherited vulnerability to depression exists in some cases, and a full behavior-analytic account can include this possibility.
A typical behavioral argument against the medical disease model of depression is to accept that depression is a syndrome but posit that it is adaptive, the product of contingencies of survival (Skinner, 1953). In fact, many evolutionary explanations for depression have been offered (e.g., Bowlby, 1980; Gilbert, 1992; Leahy, 1997; Price, Sloman, Gardner, Gilbert, & Rohde, 1994; P. J. Watson & Andrews, 2002; see McGuire & Troisi, 1998, for a review), and such evolutionary accounts are important to consider and are consistent with behavioral theory (Corwin & O'Donohue, 1995). There are three broad themes under which these theories fall: resource conservation, social competition, and attachment (Allen & Badcock, 2003).
Theories of resource conservation posit that depression permits the conservation of resources and disengagement from unsuccessful goal-directed activity by decreasing appetite, energy levels, and motivation (Leahy, 1997; Nesse, 2000). For instance, when in a new environment with unknown contingencies, such as traveling to a foreign country, one is more likely to be functioning in a way to avoid negative reinforcement or punishment while trying to learn the rules of the new environment. If one were to engage in a goal-directed activity, such as trying to obtain a job, one would likely not be successful. Social-competition theories view depression as a deescalation or yielding reaction to a defeat. This is said to be adaptive because it signals submission to the victor and allows acceptance of social subordination and the avoidance of unnecessary conflict (Price, 1967, 1998; Price et al., 1994). An example of this can be seen in a boxing match, when one fighter is knocked down for a full 10 counts. The loser typically displays behaviors including sloped posture, decreased eye contact, and avoidance (all depressed behaviors) as opposed to getting back up and continuing to fight. Finally, attachment theories of the adaptive nature of depression claim that a depressive reaction is an adaptive response to the loss of interpersonal relationships that helps to maintain the proximity of caregivers or reestablish an attachment by signaling a need for assistance from others and eliciting that assistance (Averill, 1968; Bowlby, 1980; Frijda, 1994). This can easily be seen by a lost boy in a busy mall. When the child begins to cry, passersby typically attend to him, try to find the boy's parents, and comfort him during the search.
We suggest that depression is neither a syndrome nor adaptive. Any theory of depression as an adaptive syndrome has to overcome two primary hurdles inherent in the phenomenon. First, given the variability in symptom profiles in depression, one has to pick which set of symptoms of depression comprises the syndrome, or alternately posit multiple syndromes with different symptom sets (M. C. Keller & Nesse, 2006). For example, are both melancholic and atypical depression adaptive syndromes? Given that some of symptoms associated with melancholic depression (insomnia and loss of appetite) are the opposite of those associated with atypical depression (hypersomnia and increased appetite), it is impossible for the same theory to account for both presentations.
Second, the nature and chronicity of depressive symptoms seem to be maladaptive. For example, a transient sad mood in response to a loss certainly seems adaptive in that it elicits empathy and evokes helping behaviors in others. If this is true, then such an affective respondent reaction may have evolved due to contingencies of survival. It would be expected to have certain losses as antecedents and to resolve when support is acquired. However, in clinical depression the sad mood is often chronic and unresponsive to helping behaviors. In fact, although the evolutionary account suggests that the response should garner social support, research is clear that depressive behaviors result in decreased social support (Coyne, 1976; Gotlib & Lee, 1989; Joiner & Metalsky, 2001) and worse psychosocial functioning in general (Barnett & Gotlib, 1988). Suicide is another example. Although suicidal gestures may be seen as operant attempts to garner support (Linehan, 1993), completed suicide is difficult to conceive of as an operant (i.e., learned) behavior (Hayes, Strosahl, & Wilson, 1999) and is clearly not adaptive in terms of survival.
A more likely scenario is that depression itself is not adaptive, but the core experience represents a variation of an adaptive affective response (Nettle, 2004; also see Nesse, 2000). In other words, the capability to experience moderate low mood or sadness in appropriate situations (but not become clinically depressed) may have many of the same short-term benefits that have been used to support the claim that depression is adaptive. Support for this view comes from personality researchers, who have posited the temperamental trait of negative affectivity as a trait that is selected for and normally distributed (Nettle, 2004; D. Watson & Clark, 1984), and considerable research suggests that this trait may be a vulnerability factor for both depression and anxiety (L. A. Clark & Watson, 1991; L. A. Clark, Watson, & Mineka, 1994).
Although the notions of temperament or traits are unnecessary, it is reasonable to suggest that there may be a range in the duration and magnitude of affective reactions that are adaptive. A depressed individual could represent a deviation from that range in that he or she experiences negative affect longer and to a greater extent in response to an environmental event. In other words, the propensity to experience mild and appropriate levels of negative affect may be adaptive and thus appear on a continuum; those at one of the extreme ends of this continuum may be quite sensitive to fluctuations in reinforcement contingencies, suffer from chronic negative affect, and be at risk for clinical depression.
It is important to remember that we are proposing a scenario in which there is a genetic contribution to the likelihood of the core affective experience in depression but the remaining symptoms are potentially free to vary and should be described in terms of antecedents and consequences. Of course, there may be an adaptive, normally distributed range in the sensitivity of these additional behaviors (e.g., sleep) to environmental stimuli that represent separate inherited vulnerabilities. This view of depression is consistent with recent biological findings that suggest that depression is likely a product of multiple genes and a complex gene–environment interaction (Wallace et al., 2002), as well as neuroscientific findings of mixed and variable structural and functional abnormalities in several brain regions, with few depressed individuals displaying the complete package of deficits, leading researchers to conclude that depression refers to a heterogeneous group of disorders as well (Davidson, Pizzagalli, Nitschke, & Putnam, 2002). Thus, other scientific fields are taking tentative steps away from a syndromal view of depression and toward an idiographic analysis.
The Shift From Adaptive to Maladaptive Behavior
As discussed above, elicited affective experiences are normal, adaptive, and not disordered. Depression appears to be a maladaptive dysregulation or extension of this adaptive experience. Genetic vulnerabilities aside, it is important to identify the historical and environmental processes responsible for this shift from a normal, adaptive experience of elicited affect to a disordered experience of depression.
Obviously, chronically maladaptive environments may produce chronically maladaptive behavior. Perhaps the simplest and ultimate example of this is a concentration camp (Frankel, 1984). Such an environment, almost completely lacking in positive reinforcers and abundant in stable and salient aversive stimuli, may result in rather consistent depressed behavior and negative affect. However, it is safe to say that most depressed people do not live in such environments. Processes through which environments characterized by variable positive and negative reinforcers and punishers result in relatively stable experiences of depression need to be identified. For example, consider a person who has a handful of close friends with whom she interacts with on a regular basis, men who are showing interest in her romantically, good career prospects including an upcoming promotion (all opportunities for positive reinforcement), but still cannot sleep at night and considers herself to be depressed. The question remains, why do so many people engage in repertoires that are more consistent with impoverished environments than with those environments in which they live? Below we consider two processes: avoidance of aversive private events and the role of verbal behavior.
Avoidance of Private Events
Two similar processes by which an adaptive elicited response can lead to chronic and maladaptive depression in the absence of chronically maladaptive environments recently have been proposed and linked to treatment techniques: Martell, Addis, and Jacobson's (2001) theory behind behavioral activation (BA) and Hayes et al.'s (1999) model of experiential avoidance for acceptance and commitment therapy (ACT). The two models differ in several respects (see Kanter, Baruch, & Gaynor, 2006, for a full comparison).
Both models argue that problematic avoidance in depression is not always a response to the environment per se, but is a response to the core aversive experience of depression (which is in turn a response to the environment). Both models suggest that the core affective experience, once elicited, may play a functional role in maintaining, exacerbating, and creating the additional symptoms of depression. Specifically, if we allow that the initial elicited private response is functionally aversive, it may evoke behavior designed to avoid and escape the private response. For example, after a difficult breakup, a man may experience an increase in feelings of anxiety and negative self-referential thoughts. Although this individual now may avoid public stimuli based on formal stimulus properties (e.g., romantic relationships), he also may avoid the newly elicited thoughts and feelings in a variety of ways (e.g., heavy drinking). The key to understanding how this applies to depression is the notion that avoidance of private events, even when it works in the short term, produces additional long-term problems. In the example above, the man feels better in the short run after drinking, but the long-term consequences would likely include an even more impoverished environment. Through this process, flexible repertoires of problem solving and repertoires based on stable positive reinforcement are either extinguished, depotentiated, or never developed.
BA interventions have focused on disrupting how aversive private events can function as discriminative stimuli or motivating operations for avoidance behavior. For example, consider a client who stayed in bed all day because she felt depressed and thereby was able to avoid the additional stress and fatigue associated with her unpleasant work situation. Although she may experience her work situation as aversive to some extent at all times, the heaviness and fatigue experienced upon awakening in the morning and tacted as “feeling depressed” may signal that working would be experienced as especially aversive on that particular day. According to BA, staying in bed in this situation is negatively reinforced through avoidance of an especially aversive work day. However, it creates more long-term problems and solves none in that it does nothing to address the aversive work situation proactively (Kanter et al., 2006).
ACT offers additional theoretical elaborations that suggest a more prominent role for verbal behavior in avoidance processes. First, ACT suggests that experiential avoidance repertoires are maintained over long periods of time because they are rule governed or verbally controlled (Hayes & Ju, 1998). In other words, individuals develop rules that dictate experiential avoidance, and these rule-governed avoidance repertoires may persist in the face of histories of reinforcement to the contrary. For example, a depressed man may tell himself, “If bad things happen in my life, I will take it like a man.” Such self-talk may lead to denial of certain private events such as sadness or grief (e.g., after his father died) despite an environment that would shape more effective behavior (e.g., a loving wife who wants to discuss his feelings), were it not for verbal control.
There may in fact be no way to distinguish a rule-governed avoidance repertoire (i.e., ACT) from a directly conditioned avoidance repertoire (i.e., BA) in a clinical setting, in that the topographies may look similar, the relevant reinforcement histories are distal, and reporting on them accurately will be unreliable. At issue is the degree to which a depressed individual's avoidance is rule governed. In fact, Rehm (1979, 1989) has argued that depressed individuals demonstrate deficits in the ability to generate and follow rules, and his self-management therapy program attempts to improve self-monitoring, self-evaluation, and self-reinforcement skills. In accord with these views are findings that depressed individuals demonstrate increased self-reported preferences for immediate over delayed reinforcement compared to nondepressed individuals, suggesting less rule following in depressed individuals (Rehm & Plakosh, 1975). Two additional studies have shown that dysphoric individuals demonstrate greater schedule sensitivity and less rule-governed behavior compared to nondepressed individuals (Baruch, Kanter, Busch, Richardson, & Barnes-Holmes, 2007; Rosenfarb, Burker, Morris, & Cush, 1993). However, these studies demonstrate significant variability in schedule sensitivity, and McAuliffe (2003) found the opposite (increased rule-governed behavior in depressed adolescents), again highlighting the need for idiographic analysis and acknowledging both increased rule-governed behavior and decreased rule-governed behavior to be problematic in depression.
To reiterate the important themes at this point, it bears repeating that an idiographic analysis is required. Some cases of depression may be adequately conceptualized in terms of Lewinsohn's (1974) traditional model of reductions in response-contingent positive reinforcement, whereas others may be more accurately conceptualized in terms of ACT's or BA's models of avoidance. In both the traditional model and the new conceptualizations, the core experience is seen as an elicited response to environmental events that produce reductions in positive reinforcement. However, the new conceptualizations speculate how one's reaction to that experience may in fact perpetuate and exacerbate it, and in some cases this may be the case.
The Functions of Private Events in Behavior Analysis
Allowing that a private response is functionally aversive creates some problems for behavior analysis. Simply put, the classic exhortation to focus functional analyses on manipulable environmental variables may lead some to conclude that private events are simple respondent by-products and have no functional value. This stance on the nonfunctional value of private events is one of the great perplexities of behavior analysis. It is a perplexity because, to most humans, thoughts and emotions—as we have come to label them—are not only felt quite strongly at times but it feels as if they control our behavior (Schnaitter, 1978). This is especially true regarding avoidance behavior, which is often described as negatively reinforced by a reduction in aversive emotional experience (e.g., Barlow, 2002). In other words, it seems as if we avoid not only the conditions that occasion depression but also feeling depression itself. It may have been behavior analysts' rigid adherence to this simple view of private events, which runs counter to common sense for many researchers, therapists, and clients, that bolstered the cognitive revolution and the subsequent obsolescence of behavioral approaches to treatment of depression, as well as adult outpatient psychotherapy in general, which is dominated by “feeling” talk.
Skinner presented a much more nuanced and complex view. On the one hand, he consistently defined reinforcers and discriminative stimuli as environmental stimuli on pragmatic rather than ontological grounds (Skinner, 1945, 1953). Simply put, reinforcers are labeled as such only if functional analysis has determined, or at least in principle could determine, that a manipulable event evidences such a function. Private events in general are not manipulable in this sense and thus have been typically defined as dependent rather than independent variables. Put differently, Skinner consistently argued that emotions are not causes.
However, in other places Skinner allowed private events to participate, partially, in the control of behavior. For example, he wrote,
Emotional responses may be interpreted as in part an escape from the emotional components of anxiety. Thus we avoid the dentist's office, not only because it precedes painful stimulation and is therefore a negative reinforcer, but because, having preceded such stimulation, it arouses a complex emotional condition which is also aversive. The total effect may be extremely powerful. (1953, p. 179)
In this example, the emotional components of anxiety clearly have taken on functional stimulus properties. Likewise, Skinner's analysis of self-knowledge (1957, 1974) depended heavily on the supposition that private events exert discriminative control over tacting. In this case, the use of the term private event rather than private behavior may have been Skinner's acknowledgment of the complexity, but the complexity is not resolved simply by changing the term. In these cases, although the private events in question are assumed to have acquired at least partial control over other behavior, environmental variables are important for the historical development of the control (see also Hayes & Brownstein, 1986). For example, in the case of the tact of “sad,” the private stimulation involved is seen as the discriminative stimulus for the resulting tact, and that stimulation has obtained functional significance through social mediation (Moore, 1980). Thus, it is consistent with behavior analysis (or at least, with behavior analysis's inconsistency) to allow functionally salient private events to evoke avoidance behavior.
The Role of Verbal Behavior in Depression
Perhaps the biggest obstacle for traditional behavioral theorists to overcome when discussing depression is the role of language. In general, an extremely large and unquestionable body of research establishes the presence of negative cognitive content during depressive episodes, leading cognitive researchers to assume a causal role for cognition in depression (D. A. Clark, Beck, & Alford, 1999). Although longitudinal research has failed to establish negative cognitive biases as independent predictors of depression (Ingram, Miranda, & Segal, 1998), it is clear that thinking influences feeling on a moment-to-moment basis. Cognitive researchers see this influence as sufficiently causal, but behavior analysts instead search for environmental conditions responsible for such behavior–behavior relations (Hayes & Brownstein, 1986). Regardless, it is clear that negative thinking predominates in many depressions, and such thinking may elicit aversive affect.
Research on stimulus equivalence (e.g., Sidman, 1994) readily accounts for the relation between cognition and mood. Simply put, through participation in equivalence relations with nonverbal stimuli, verbal stimuli may obtain eliciting functions. Although there are many examples of this effect, perhaps the clearest example is work by Dougher and colleagues on the transfer of aversive elicitation and avoidance functions through equivalence classes. Using match-to-sample procedures, Dougher, Augustson, Markham, Greenway, and Wulfert (1994) taught 8 subjects two four-member equivalence classes, paired one member of one class with electric shock, and then demonstrated transfer of elicited arousal to other members of the class that had not been directly paired with the shock. Augustson and Dougher (1997) subsequently demonstrated that avoidance responding similarly transfers through equivalence classes. After pairing one member of one class with shock, subjects were taught that they could avoid this member by repeatedly pressing a key on the keyboard. Subjects then demonstrated transfer of avoidance response functions to other class members.
Growing research on relational frame theory (RFT; Hayes, Barnes-Holmes, & Roche, 2001) extends these findings. According to RFT, verbal behavior (including thinking) is technically seen as the behavior of framing events relationally: responding to one stimulus in terms of its given or inferred relation to other stimuli. For example, a woman caught speeding receives a ticket. If that person thinks that people who get speeding tickets are bad drivers, she may then consider herself a bad driver. RFT views equivalence as just one type of relation (i.e., sameness) and views deriving relations among stimuli in the absence of direct conditioning as a generalized operant (Barnes-Holmes & Barnes-Holmes, 2000).
Responding in accordance with other derived relations has also been demonstrated, including relations of sameness, opposition, and difference (Roche & Barnes, 1996, 1997; Steele & Hayes, 1991; Whelan & Barnes-Holmes, 2004), more than and less than (Dymond & Barnes, 1995; O'Hora, Roche, Barnes-Holmes, & Smeets, 2002; Whelan, Barnes-Holmes, & Dymond, 2006), and before and after (O'Hora, Barnes-Holmes, Roche, & Smeets, 2004; see also Barnes & Roche, 1996; Hayes & Barnes, 1997). Evidence is mounting that these relations may result in the transformation of functions in accordance with the relations trained, akin to the transfer of function seen with equivalence relations (for a review, see Dymond & Rehfeldt, 2001). Thus if that same woman who received a speeding ticket has a history of avoiding authority figures who reprimanded her in the past (e.g., teachers and supervisors), she may then begin to avoid police officers as well. These stimulus functions may be quite arbitrary and unrelated to current environmental features. Thus, the behavior of relational framing has a potentially transformative effect on the environment; environmental stimuli that would otherwise control behavior may not do so and new stimuli, idiosyncratic to the individual's verbal learning history, may exert control.
The importance of these findings to depression, and other psychological disorders, cannot be overstated. To the extent that stimulus equivalence and RFT present a behavior-analytic model of language and cognition, these theories provide behavior analysts with a vocabulary and theory with which cognitive variables can be conceptualized and understood. Negative self-statements so often seen in depression acquire their meanings and functions through transformations of function that occur in relational framing. For verbal stimuli to obtain these specific functions, previous specific-exemplar training involving the specific stimuli participating in relational frames is not necessary. All that is necessary is a history that establishes relational framing as a generalized operant and a history in which the specific stimuli at issue are related in a relational network.
There appear to be two uses of the term relational network, and a brief diversion on this issue is necessary because one of the usages may be potentially confusing to behavior analysts. First, a relational network may refer to a sentence or another unit of speech that sets the context for relational activity (Barnes-Holmes, Hayes, Dymond, & O'Hora, 2001)—there is no issue with this usage. Second, a relational network may be used to graphically depict the full set of relations between specific stimuli and the transformations of function that are relevant to a particular stimulus. Such networks are often displayed in RFT or stimulus equivalence experiments to depict the specific relations trained, but a network may also be employed more loosely when the history can only be assumed. For example, Blackledge (2003) displayed a network to account for a person taking a walk in the woods that elicits fear due to a verbal history in which it was learned that snakes are to be found in woods. This usage bears considerable resemblance to nonbehavioral entities such as schemas and requires clarification. One has to be careful to maintain that the network, unlike a schema, is the not the cause of behavior. The network is a description of a history, and it is this history, along with the current environmental and verbal events, that functions as the cause. The history is described in terms of a network to emphasize how the functions of any term in the network may be transformed in accordance with the network, but such transformations are a product of a history of verbal behavior described as a network, not the network per se. It is easy to lose sight of behavior analysis at this point; thus, it is important to remember that these functions of relational framing were obtained through a history of interaction with the social and verbal community. Historical environmental factors result in the transformation and reduction of control by the current environment. These effects are easily described in terms of relational networks and stimulus functions that are transformed across members of the network.
The important point is that verbal behavior can dysregulate and extend normal adaptive experiences of aversive elicitation into disordered experiences. Consider an individual who has received a poor work evaluation. This naturally elicits aversive affect that, if transient, can be considered normal and adaptive. However, this individual may begin to think about the event, and the content of thinking will be a complex product of multiple historical and current antecedents. Given a history that has established high-strength relational networks of “loss,” “failure,” “helplessness,” or similar networks, a transient setback such as a poor job evaluation can become functionally overwhelming. The key point is that the core experience of depression, the elicited affect, was normal and adaptive without verbal elaboration. With verbal elaboration, however, the experience is magnified and extended, and may become disordered.
Examples of verbal elaborations of potentially normal experiences abound in the clinical literature on depression. In fact, cognitive therapy for depression (Beck, Rush, Shaw, & Emery, 1979) assumes challenging these unrealistic verbal elaborations to be the primary task of therapy. Discussion of whether such cognitive interventions are successful, for the reasons cognitive therapists say they are, is beyond the scope of this paper. Rather, we simply highlight the finding that many depressed individuals appear to have become depressed in the absence of environmental histories that would indicate such a response to be adaptive, and point to verbal behavior to account for the elaboration of such histories into a disorder. Language vastly expands the range of situations that can function as depression-eliciting and depression-maintaining stimuli, because the functions of the stimuli largely may be determined by one's idiosyncratic verbal learning history.
As an example, a depressed individual may respond to all social events as participating in a verbal relation with a host of other aversive stimuli (e.g., the words fake, small-talk, embarrassment, boring, stressful, idiot, foolish, exposed and the words for a range of aversive private sensations germane to escape, panic, etc.). Although another individual may respond to the relation between the stimuli party and stressful on occasion, there is flexibility in responding based on other historical and contextual features. For the depressed individual, however, this verbal class may be so well formed through a fairly idiosyncratic history of verbal and nonverbal pairings of these stimuli, and so negatively reinforced through past derived escape and avoidance experiences, that there may be few or no contexts in which the term party does not elicit the functions of other aversive stimuli or function as a derived discriminative stimulus for escape or avoidance. This rigid avoidance repertoire vastly narrows the range of behavioral options available and most likely will lead to rather stable reductions in response-contingent social reinforcement.
What are the signs or symptoms of post-natal depression, and are they similar to Breastfeeding / Nursing Aversion and Agitation (BAA)?
Below we will explain the signs of postpartum depression and anxiety, but in what we call “plain mama English.” We won’t use words like hypomania or dysthymia—the kind of confusing terms you might see elsewhere. We will use the words thousands of other moms have used who have already been through this. Words that make sense. After that, we’ll give you some links to some really helpful resources and information. You are not alone. Here at Postpartum Progress we understand and we’re happy to help.
When you read the two different symptoms lists below, one for postpartum depression and the one after it for postpartum anxiety and OCD, please remember a few very important things:
You may not be experiencing all of the symptoms listed below or even most of them. Postpartum depression and anxiety are not “one-size-fits-all” illnesses. Your experience may include just a few of the symptoms and you may not have others at all.
Many people have a feeling like the ones listed below every now and then, for a day or two. We all have bad days. Postpartum depression and anxiety are not just bad days. Women with PPD or anxiety have symptoms like these most of the time, for a period of at least 2 weeks or longer, and these symptoms make it feel very hard to live your life each day.
Postpartum depression and anxiety are sometimes “comorbid.” This means you can have a bit of both, or all of both. If you have symptoms on both lists, that’s not unusual.
Postpartum Depression Symptoms
Okay. Here we go. You may have postpartum depression if you have had a baby within the last 12 months and are experiencing some of these symptoms:
You feel overwhelmed. Not like “hey, this new mom thing is hard.” More like “I can’t do this and I’m never going to be able to do this.” You feel like you just can’t handle being a mother. In fact, you may be wondering whether you should have become a mother in the first place.
You feel guilty because you believe you should be handling new motherhood better than this. You feel like your baby deserves better. You worry whether your baby can tell that you feel so bad, or that you are crying so much, or that you don’t feel the happiness or connection that you thought you would. You may wonder whether your baby would be better off without you.
You don’t feel bonded to your baby. You’re not having that mythical mommy bliss that you see on TV or read about in magazines. Not everyone with postpartum depression feels this way, but many do.
You can’t understand why this is happening. You are very confused and scared.
You feel irritated or angry. You have no patience. Everything annoys you. You feel resentment toward your baby, or your partner, or your friends who don’t have babies. You feel out-of-control rage.
You feel nothing. Emptiness and numbness. You are just going through the motions.
You feel sadness to the depths of your soul. You can’t stop crying, even when there’s no real reason to be crying.
You feel hopeless, like this situation will never ever get better. You feel weak and defective, like a failure.
You can’t bring yourself to eat, or perhaps the only thing that makes you feel better is eating.
You can’t sleep when the baby sleeps, nor can you sleep at any other time. Or maybe you can fall asleep, but you wake up in the middle of the night and can’t go back to sleep no matter how tired you are. Or maybe all you can do is sleep and you can’t seem to stay awake to get the most basic things done. Whichever it is, your sleeping is completely screwed up and it’s not just because you have a newborn.
You can’t concentrate. You can’t focus. You can’t think of the words you want to say. You can’t remember what you were supposed to do. You can’t make a decision. You feel like you’re in a fog.
You feel disconnected. You feel strangely apart from everyone for some reason, like there’s an invisible wall between you and the rest of the world.
Maybe you’re doing everything right. You are exercising. You are taking your vitamins. You have a healthy spirituality. You do yoga. You’re thinking “Why can’t I just get over this?” You feel like you should be able to snap out of it, but you can’t.
You might be having thoughts of running away and leaving your family behind. Or you’ve thought of driving off the road, or taking too many pills, or finding some other way to end this misery.
You know something is wrong. You may not know you have a perinatal mood or anxiety disorder, but you know the way you are feeling is NOT right. You think you’ve “gone crazy.”
You are afraid that this is your new reality and that you’ve lost the “old you” forever.
You are afraid that if you reach out for help people will judge you. Or that your baby will be taken away.
Postpartum Anxiety & OCD
You may have postpartum anxiety or postpartum OCD if you have had a baby within the last 12 months and are experiencing some of these symptoms:
Your thoughts are racing. You can’t quiet your mind. You can’t settle down. You can’t relax.
You feel like you have to be doing something at all times. Cleaning bottles. Cleaning baby clothes. Cleaning the house. Doing work. Entertaining the baby. Checking on the baby.
You are worried. Really worried. All. The. Time. Am I doing this right? Will my husband come home from his trip? Will the baby wake up? Is the baby eating enough? Is there something wrong with my baby that I’m missing? No matter what anyone says to reassure you, it doesn’t help.
You may be having disturbing thoughts. Thoughts that you’ve never had before. Scary thoughts that make you wonder whether you aren’t the person you thought you were. They fly into your head unwanted and you know they aren’t right, that this isn’t the real you, but they terrify you and they won’t go away. These thoughts may start with the words “What if …”
You are afraid to be alone with your baby because of scary thoughts or worries. You are also afraid of things in your house that could potentially cause harm, like kitchen knives or stairs, and you avoid them like the plague.
You may feel the need to check things constantly. Did I lock the door? Did I lock the car? Did I turn off the oven? Is the baby breathing?
You may be having physical symptoms like stomach cramps or headaches, shakiness or nausea. You might even have panic attacks.
You feel like a captive animal, pacing back and forth in a cage. Restless. On edge.
You can’t eat. You have no appetite.
You’re having trouble sleeping. You are so, so tired, but you can’t sleep.
You feel a sense of dread, like something terrible is going to happen.
You know something is wrong. You may not know you have a perinatal mood or anxiety disorder, but you know the way you are feeling is NOT right. You think you’ve “gone crazy.”
You are afraid that this is your new reality and that you’ve lost the “old you” forever.
You are afraid that if you reach out for help people will judge you. Or that your baby will be taken away.
Now that you’ve gone through these lists, are you thinking, “How the heck does this lady know me? Is there a hidden camera in here?” Nope. What this should tell you is that you are not alone and you are not a freak and you are not highly unusual. If you are having these feelings and symptoms then it is possible you are experiencing common illnesses that 15 to 20% of new mothers have, and they are completely treatable. We’re happy to be here to support you.
Postpartum Depression Help
Postpartum Progress is a nonprofit created by moms for moms with maternal mental illness. We know what it’s like and we know how hard it is. Here are some of our best resources for moms with postpartum depression, postpartum anxiety and related illnesses:
List of postpartum depression treatment specialists and programs. We find that if possible it helps to see someone who has more experience treating women with these illnesses.
List of postpartum depression support groups.
Our description of the six stages of postpartum depression, or what it feels like as you progress through this illness.
A list of some of our top postpartum depression stories, organized in categories so you can find and read stories about moms just like you.
What recovery from PPD does NOT look like, so you know what to focus on and what not to focus on as you get better.
To learn more about how Postpartum Progress can help you, click here.
Other Things You Should Know
If you are pregnant and are having symptoms similar to those listed above, you should know that you aren’t unusual either. You may have depression or anxiety during pregnancy, which is just as common.
If you are having the symptoms listed above, call your doctor. There is no need to suffer alone. Don’t try to wait this out. Perinatal mood and anxiety disorders are temporary and treatable with professional help.
If you are already past the first year postpartum and still suffering, you could still have postpartum depression or anxiety. Perhaps you never reached out for help in the first year and you are still struggling. Call your doctor. You can still get help for this.
One last but very important thing: If you are having moments where it seems like you can see or hear things no one else does, if you are feeling paranoid as if others are out to get you, if you are feeling that you or your baby are somehow related to the devil or God in some way, or if you are having thoughts of harming yourself or others, it’s important to reach out for help right now. These symptoms require immediate attention as they could be signs of postpartum psychosis. If you have these symptoms, your illness has the potential to take over and lead you to do things that you wouldn’t normally do. In order to avoid that it is important to reach out for help right away so that trained professionals can help you get stabilized and healthy.
So what if BAA is part of depression, so what? The question is why isn't it being identified and what specific interventions can help