While the notion that early trauma may be linked to psychological and behavioral problems in adult life is rather old news, recent work has refined our understanding of this link in two major ways. First, research has shown quite convincingly that early trauma is a major predictor-and causal agent-not only of neurotic-spectrum problems such as anxiety, depression and relationship issues, but also of physiological health outcomes ( Felitti , 2002).
Second, research has begun to disentangle the complex cascade of events that shape the path from the "genotype" of early trauma to the "phenotype" of adult malfunction. At the level of the brain, evidence is accumulating that early trauma may inflict its damage in childhood by adversely affecting the size and functionality of brain structures such as the hippocampus and the corpus calosum, as well as altering neurobiological mechanisms involved in mediating the stress response. These early changes constitute structural vulnerabilities for developing psychological disorders and physical health problems in adulthood.
Looking at environmental influences, we are beginning to understand that, while early adversity appears to have a dose-response relationship with later functioning, the path from early experience to adult outcome is rarely direct. For example, while early trauma is in some cases linked to depression directly, the link is more often mediated by later stress and low self-esteem. Insecure attachment has been found to mediate the links between early trauma and Somatization Disorder in females. While the prevalence of attempted suicide in persons with no experiences of childhood adversity is significantly lower than the prevalence among those with seven or more such experiences, these effects are often mediated, at least in part, by later life events such as drug use, depressed affect, and alcoholism.
Finally, it has become clear that the path from trauma to dysfunction must be examined in the context of current conceptualizations of gene-environment interaction. We realize that while the effects of trauma on brain and behavior depend in part on the individual's genetic susceptibilities, likewise the expression of genetic tendencies depends in part on environmental conditions. In other words, while genes help decide how environmental trauma will affect you, environmental trauma helps decide how your genes will affect you.
Clinical psychologists, of course, are no strangers to the trauma-trouble link. Many patients report chaotic, troubled childhoods and traumatic life experiences. Making the connections between early trauma and subsequent patterns of maladaptive behavior, emotional dysregulation, and distorted perception is part of how therapists help their patients establish a coherent narrative within which to frame their difficulties. However, in light of the emerging understanding of its complex nature, therapists must address the trauma-trouble link thoughtfully in the context of therapy, lest they mislead their patients and themselves.
First, both therapists and patients should resist the temptation to assume that specific current behaviors can be usefully explained by referring to specific early experiences. The temptation is great, because patients often seek such explanations, and psychologists would love to be able to provide them. But there are vast individual differences in the response to early trauma. Those who suffer similar early circumstances rarely share a similar symptom profile in adulthood. For example, despite popular belief to the contrary, adult children of alcoholics do not share a unique and uniform psychological profile.
Teasing apart the various environmental elements that might have produced a certain effect in one individual is quite impossible, particularly in the inherently haphazard context of therapy-where precise mappings of the patient's brain processes and genetic profile are typically absent and accounts of events cannot easily be verified. Traumatic experiences are events in context, and often that context includes multiple risk factors that may operate independently of-or in synergy with-the trauma, rendering difficult the task of knowing whether a certain event acted as a cause, a mediator, a covariant, or a moderator related to later outcome.
Moreover, early environments are not often amenable to rigorous experimental manipulation of the kind science relies on to decipher cause and effect. We can't place a representative sample of children in an environment and then randomly traumatize half of them. Additionally, psychological research on the role of trauma in development relies on comparing outcome variation between individuals. It doesn't tell us much about what happens within each individual. Finding that 50 percent of the variance for some outcome is due to early trauma does not mean that 50 percent of that outcome in the individual patient in front of you is due to trauma.
Thus, even if we figure out the general path from early trauma to later trouble, and a mechanism that explains why more traumatized people end up experiencing some sort of trouble later in life than non-traumatized people, we cannot readily deduce from the group to the individual. Finding that traumatized people are more likely to become depressed does not necessarily mean that the person in front of you is depressed because of his early trauma. There are multiple paths to depression, even for traumatized people.
Understanding the limited prediction value of each specific early trauma is important since many laypersons, as well as some therapists, still assume that they need to know the exact root causes of a condition to fix it. This assumption is incorrect. Perhaps the major contribution of the cognitive-behavioral school of therapy has been to turn the focus of therapy toward the here-and-now and to show empirically how precise knowledge of the historical causes of a problem is not a precondition for overcoming it. Therapists should share that understanding with their patients.
In addition, even as therapists track the possible links between past trauma and present functioning, it is crucial that they understand, and explain to their patients, that what caused a problem in the past is often different from what maintains it in the present. As Allport (1937) famously argued, while adult motives grow out of antecedent systems, they are functionally independent of them. In terms of contemporary therapy, we can say that tracing your current fear of dogs to an early childhood encounter with a scary poodle may plausibly tell us why you became scared of dogs back then. It does not tell us why your fear continues today, after both your childhood and that poodle are long gone. (What causes your fear now is more likely your avoidance. You are afraid of dogs now because you avoid them). Therapists should augment their search for what may have initiated the patient's problems with a more important search for what may be perpetuating the problem in the present. Because, after all, the job of the therapist is to help the patient feel and function better now-not to act as a personal psycho-historical detective.
Finally, even as the therapist probes the trauma-trouble link in therapy, he or she needs to remain aware that the rule of human existence is resilience in the face of adversity. Trauma is linked to heightened risk of disease and disorder, and yet most people who suffer a traumatic experience do not end up diseased and disordered. Most people are resilient in spite of trauma, particularly if they have positive social relationships, if they learn to problem-solve, and if they develop competencies valued by self and society. In other words, therapy patients are wired for survival, recovery, and adaptation. While therapists work to address the sources of their patients' injuries, it is important for them to locate, acknowledge, nurture, celebrate, and capitalize on the patients' reservoirs of strength. Damaged people are never entirely damaged, just as healthy people are never entirely healthy. The patient's assets should be utilized in dealing with the patient's deficits.