The Kindling Phenomenon: What Doesn't Kill You Makes You Weaker
The differential activation hypothesis (DAH) was first proposed by J.D. Teasdale in 1988. He later elaborated on it to include the phenomenon of kindling. This process explains why some people become weaker after several depressive episodes. Curiously, it contradicts one of the myths of popular wisdom that says that “what doesn’t kill you, makes you stronger “.
The kindling effect explains that, when you’re faced with new stressors, you’re conditioned by previous internal and external experiences. For example, if you’ve experienced various job failures, each time you subsequently try to do a job well and fail, you’ll feel more frustrated and less motivated than the first time you tried.
As a matter of fact, this “negative job information node” is easily activated by any new work experience. Like the node itself, many similarities and differences exist in each individual.
Therefore, we all have nodes of negative information that are activated by stressors and different information. Teasdale tried to explain with his differential activation hypothesis how these negative nodes are activated in human beings.
Teasdale’s differential activation hypothesis (DAH)
Teasdale’s differential activation hypothesis has been proposed as an explanation for cognitive vulnerability to depression.
Influenced by Aaron T.Beck and G. H.Bower, Teasdale put forward the idea that each emotion is represented in memory by a specific node. Each of these nodes is connected to associated cognitions or traits. In the case of depression, cognitions are negative. When a node is activated, the corresponding emotion is experienced and the activation propagates through the node’s connections.
The author argued that the factors that determine whether the initial depression becomes more persistent are the degree of activation and the patterns of behavior of these nodes.
Teasdale’s theory is a stress-vulnerability model. It assumes that the type of events that cause clinical depression in certain individuals may only produce a dysphoric or mild mood in others.
The onset of depressive symptoms results from the activation of the depression node after the occurrence of a stressful event. This activation spreads to the associated (negative) cognitive nodes or constructs. However, if the cognitive activity reactivates the depressive nodes through a cyclical mechanism, a vicious cycle is established. Hence, it causes the initial depression to intensify and remain.
Unlike Aaron T. Beck, Teasdale didn’t believe that the match between the type of event (type of stressor) and type of nodes or cognitive constructs is a necessary requirement. In fact, he believed that, as the personal experiences of episodes of major depression increase, environmental stressors of lesser magnitude are able to provoke relapse.
Research on cognitive models of depression has frequently neglected the relationships between different levels of cognitive and personality variables, person interaction, and event factors. However, Teasdale’s theory is a perfect example of an explanation of how the person accepts an experience, but, at the same time, also constructs it.
The kindling phenomenon: pain is triggered less yet spreads faster
Teasdale’s hypothesis was reviewed by Segal, Williams, Teasdale, and Gemar in 1996. In fact, they proposed a further elaboration of this hypothesis. Indeed, it was then that they suggested the application of the concepts of kindling and sensitization.
- The kindling phenomenon assumes that the continuous reactivation of negative cognitive structures causes the associative networks between depressotypic constructs to be strengthened. Thus, a wide range of stimuli can favor the activation of the network simply by activating one element.
- The sensitization effect is explained by a decrease in the activation threshold of depressotypic constructs produced by the repeated activation of these structures.
These aspects add difficulties to the already problematic definition of stressors in the vulnerability-stress model. According to this theory, the importance of the stressor would decrease as a person’s cognitive awareness increases. Therefore, a minimal stimulus could cause an activation of the depressogenic network in a person, without having to be a great stressor.
Depression: experiences and how they’re interpreted
Vulnerability to depressive relapse is determined by the increased risk of negative information patterns being activated in depressive states. The kindling-sensitization studies explain the reason for this increased risk of activation of negative thought patterns.
The appearance of a depressive episode facilitates cognitive familiarity. Therefore, the individual can resort to already familiar negative processing in the face of a new stressor. This dependence on negative nodes for their strength and accessibility is the kindling phenomenon.
In turn, this dependence facilitates that any future activation is achieved on the basis of increasingly less intense signals. In other words, it facilitates awareness. Hence, the patient’s pain threshold is lowered.
This model suggests that the processes related to relapse/recurrence and the onset of the depressive episode may not be isomorphic. For this reason, further research and psychological interventions are required that are aimed at optimizing relapse prevention strategies.
It should be clarified that this form of negative processing supposes a tendency to depressive episodes, but not a certainty or immutability. Indeed, certain experiences can accentuate or reduce the tendency.