Why We Don't Need the Concept of Repression

People don’t remember their earliest experiences, right? Unless you’re a member of the Association for Pre- and Perinatal Psychology and health (APPPAH), you probably agree with Freud that there is a normal “infantile amnesia”. (If you belong to APPPAH, you may think babies remember their births and can tell you about them.) So why is there “amnesia” for the early years? Some have argued that unless we have the words to encode memories, we can’t later access them in verbal form, and since there is little language ability until after age two years, this would explain why we don’t remember those early experiences.

Other people claim that we cannot remember early experiences, even (or especially) dramatic ones, because we have repressed them. The idea of repression is that human beings have the capacity to defend themselves against anxiety by becoming unable to know or remember frightening events. Proponents of the repression concept usually also posit that repressed memories continue to exist in a way inaccessible to the conscious mind, and that they can have a variety of impacts on both mental and physical life.

J.F. Kihlstorm has summarized these beliefs as “the trauma-memory argument” (see http://socrates.berkeley.edu/~kihlstrm/Tsukuba05.htm). Here are the elements of Kihlstrom’s summary:

1. Traumatic experiences can cause the activation of mental defenses that result in amnesia for the stressful event.

2. Only explicit memory is affected, but there may remain implicit memories like “body memory”.

3. If there are “body memories”, this is evidence that there was a traumatic event.

4. The traumatic memory may be recovered in explicit form spontaneously, or as a result of guided imagery, hypnosis, or sedation with barbiturates.

5. It can be inferred that the recovered memory is correct if it seems to explain the person’s symptoms, or if he or she gets better after the memory is recovered.

6. Without recovering the memory, the person cannot cope with the traumatic event.

(Please note that this is Kihlstrom’s summary, not his own position.)

The trauma-memory argument and the concept of repression assume that all experiences are remembered, no matter when they occurred, and a failure to have an explicit memory is due to the activation of a mechanism that defends against trauma. Infantile amnesia presumably occurs because there are so many traumatic experiences young children undergo. (Of course, we get into some interesting side issues when we think about other forms of forgetting. Does my husband really forget to mail the letter because he found it so traumatic when I asked him to do it? Do students fail exams because they were traumatized by the material they were trying to study—or even found it linked mentally to some already-repressed memories? We do seem to need some other explanations of forgetting, in addition to--  or instead of--  repression.)

A recent study on memory has supplied a likely candidate for explanation of the forgetting of frightening or painful events. This candidate is a normal process, neurogenesis, the creation of new neurons. And while I am usually the first to query generalization from a study using mice to conclusions about humans, I do think there are interesting implications here.

Katherine Akers and her colleagues published in the May 9 issue of Science an article entitled “Hippocampal neurogenesis regulates forgetting during adulthood and infancy” (pp. 598-602). Neurogenesis occurs at a high rate during infancy, but it continues to occur in adulthood. Also, it can be speeded up or slowed down by drug treatment or by exercise like forced running in a wheel. Mice easily learn fear of a place when they receive electric shocks to the feet in that place, and they later show their learned fear by “freezing” rather than running around exploring when put back in that place. Adult mice remember their frightening experience over time and continue to “freeze” after as much as 28 days after the original learning. Infant mice, on the other hand, have already forgotten their experience and do not “freeze” a day later.

Akers and her co-authors showed that adult mice forgot their painful experience more quickly when they exercised—an event that leads to increased neurogenesis. And, drug treatments that slowed neurogenesis in infant mice also made them less likely to forget the experience, as they showed by being more likely to “freeze” in the situation where they had experienced shock. The investigators also compared their results with mice to a similar study using guinea pigs and degus, rodents that unlike mice are “precocial”, or capable of caring for themselves soon after birth, and that have a relatively slow rate of neurogenesis in infancy. These animals showed the same level of memory for a shock in infancy and in adulthood, but could be made more “forgetful” by forced running (again, this increases neurogenesis).

These results did not explain all events of memory or forgetting, but did explain events related to the hippocampus, which supports explicit, declarative memories.

The real difficulties in moving from this work to treatment of problem memories of trauma in human beings are obvious, and Akers and her colleagues certainly did not suggest in their article that PTSD patients should be given an exercise wheel to run in. However, their evidence clearly shows a mechanism for restructuring memories that leads to genuine forgetting and that does not require repression to make traumatic memories inaccessible; those memories cannot be accessed because they are actually no longer there. Many years of argument to the effect that memories are not repressed and recovered are now buttressed by systematic evidence about neural mechanisms that support forgetting of traumatic events.