The delay in PTSD is treated in this study as a continuum in time, where a PTSD onset 2 years after the war, for example, represents a longer delay in onset than a PTSD onset 1 year after the year. Our results indicate that a significant number of veterans reported a delay in PTSD onset. The two study groups that represent a relative delay in PTSD onset (the 1984 onset and 2002 onset groups) comprised 16.5 % of the entire sample and 27 % of those veterans who reported PTSD. The 16.5 % found here is higher than the rate found in most studies employing this method of calculation (e.g., Frueh et al., 2009). However, some studies have found similar rates (e.g., McFarlane, 1988). The 27 % found here seems to represent a midpoint between very low and very high rates that were previously found (Smid et al., 2009). Thus, the present study reveals a relatively high rate of DPTSD cases.

First and foremost, this finding empirically validates the existence of DPTSD, despite the turbulent medicolegal debate regarding the validity of this phenomenon. In recent years, the public discourse surrounding the military campaigns in Iraq and Afghanistan is increasingly becoming centered on the issue of “the hidden costs of war,” from both a financial (Hartung, 2004) and psychological (Coleman, 2007) perspective. The results of the present study clearly support the notion of a delayed PTSD as a hidden cost of war.

The relatively high rate of DPTSD in the present study may be attributed to several factors. First, our results seem to support Prigerson et al.’s contention (2001) that a delayed onset of PTSD symptoms is particularly common among survivors of war trauma. Combat is perhaps the most “masculine” trauma of all. Being tagged as “posttraumatic” following participation in combat often entails a social stigma. This may be especially true in a war-ridden country such as Israel, where the ability to endure the effects of battle is a desirable, even admirable, attribute. A second reason why war trauma may entail relatively high rates of DPTSD may be that during combat, soldiers enter a survival mode that is particularly insistent. The soldier cannot afford to experience psychological breakdown on the battlefield, as his life depends on his functioning. Thus, the psychological scars caused by the war may not manifest themselves on the battlefield or shortly thereafter, but rather remain unseen for a long period of time.

Another possible explanation for the relatively high rate of DPTSD in this study is that it was conducted in Israel, a country that may be viewed as a “stress lab,” where citizens are exposed to ongoing war and terror. DPTSD is known to be associated with external triggers, i.e., events that somehow resemble the index trauma and therefore trigger its recollections (e.g., Green et al., 1995). Thus, the security situation in Israel may provide many opportunities for the early trauma of war to rise to the foreground, even after a long latency period.

Our finding that for some veterans in this study PTSD onset was delayed for 20 years after the war may be attributed to two major factors. First, the third assessment of this study was conducted in 2002, in the midst of the Al-Aqsa Intifada, the violent armed conflict between Israel and the Palestinians. At the time, the Israeli civilian population was under constant terrorist attacks. As expected, studies have shown that this violent atmosphere was also implicated in posttraumatic distress (e.g., Bleich, Gelkopf, & Solomon, 2003). Therefore, it is highly reasonable that the events of that period served as a trigger for DPTSD. The second explanation for DPTSD at 2002 is related to the fact that many of the veterans in this study were approaching midlife, and were already experiencing various aging processes. There is considerable evidence (e.g., Davison et al., 2006) regarding the role of aging processes in the onset of PTSD. Decreased activity during midlife and old age provides one with more opportunities to reminisce and review one’s life, a process often accompanied by the recollection of early traumatic events. In addition, aging often entails many losses and exit events (e.g., retirement, death of loved ones) that may be particularly distressing for previously traumatized individuals (Christenson, Walker, Ross, & Maltbie, 1981).

Previous studies have yielded mixed results regarding the severity of psychopathology in DPTSD (e.g., Bryant & Harvey, 2002; Solomon, Mikulincer, Waysman, & Marlowe, 1991; Watson, Kucala, Manifold, Vassar, & Juba, 1988). Our findings clearly indicate that the longer the delay in onset, the lower the symptom severity. The 1983 onset group was the most vulnerable, followed by the 1984 and 2002 onset groups, who did not differ from one another on most psychopathology measures, and finally the no PTSD group, which, as expected, endorsed the lowest psychopathology levels. Overall, these findings indicate that DPTSD may be considered a unique clinical subtype of PTSD, with an attenuated clinical picture. These findings also suggest that there may be a critical period, potentially a 1-year delay, during which the delay in PTSD onset is particularly related to the severity of psychopathology. However, once this temporal threshold is crossed, further delays in PTSD onset do not significantly affect the level of psychopathology. One possible explanation for our findings is that the initial impact of combat subsides with time, such that when it resurfaces, it takes a less severe form. A second possible explanation may be that veterans with DPTSD were initially more resilient to the effects of combat. This explanation was supported by earlier studies showing that casualties with DPTSD endorsed more psychological resources than those with immediate or chronic PTSD (e.g., Nitto, 2001).