wear and tear. If such differences exist, then they may explain why some people are
more likely to become ill as a result of stress and others do not. These exciting
developments are considered in the next section.
Stress reactivity
The central idea linked to the ‘stress reactivity hypothesis’ is that individuals who have
large emotional and physiological responses to stress may be more likely to develop
health problems in the future (Kamarck and Lovallo, 2003). In particular, people who
are prone to having dramatic increases in heart rate and/or blood pressure after stressful
situations may be at greater risk of developing high blood pressure and cardiovascular
disease. Over the last 25 years, evidence has accumulated in support of this hypothesis
from animal as well as human studies. In a sample of monkeys, Manuck, Kaplan and
Clarkson (1983) found greater evidence of heart disease in monkeys who were
previously identified as being high reactors to stress compared to the low reactors. The
high reactors were also found to be more aggressive than the low reactors. In a human
study, the results from the Kuopio Heart Study in Finland showed that men who had
a greater cardiovascular response to stress were more likely to develop hypertension
(i.e. high blood pressure) and stroke (Everson et al., 1996a, 2001). In another
longitudinal study known as the Coronary Artery Risk Development in Young Adults
(CARDIA) study, Matthews et al. (2004) found that cardiovascular reactivity to stress
at the beginning of the study was associated with higher blood pressure levels 13 years
later!
However, not all studies have been supportive with several researchers suggesting
that the mixed findings may be associated with methodological inconsistencies (e.g.
using different laboratory stress challenges; time of testing, Nebel et al., 1996; Linden,
Rutledge and Con, 1998; Kamarck and Lovallo, 2003) and with individual differences
(e.g. cynical hostility (see Chapter 6), morningness-eveningness; Kamarck and Lovallo,
2003; Willis, O’Connor and Smith, 2005) which may obscure the effects. For
example, Willis et al. (2005) found that stress reactivity levels were moderated by
morningness-eveningness (i.e. the extent to which you are a ‘lark’, who prefers doing
tasks in the morning, or an ‘owl’ who prefers the evening). They found that ‘owls’
had higher heart rate generally and in response to stress in the afternoon compared to
the morning. Therefore, it seems that the research into the impact of stress reactivity
is far from clear-cut. In addition, a number of researchers have begun to argue that
low or blunted reactivity (and not just high!) may also be associated with negative
health outcomes (Phillips, Ginty and Hughes, 2013). These authors have suggested
that departures from the norm in either direction may indicate that the bodily systems
are ‘operating in a biased state’ (Phillips et al., 2013: 4). Overall, it seems that there is
fairly strong evidence showing that people who have large or small responses to stress
may be at greater risk of becoming ill following the long-term effects of stress.
Stress recovery
More recently, researchers have turned their attention to exploring the impact on
health outcomes of the amount of time it takes the body to return to normal after
STRESS THEORY AND RESEARCH 63