virus (Cohen, 2005). Therefore, using a more complex study design, Cohen, Doyle
and Skoner (1999) investigated whether psychological stress influenced cytokine
production in participants after receiving an influenza virus. Specifically, they tested
whether stress had the capacity to interfere with the body’s ability to regulate cytokine
production. Normally, when a virus is detected, the body produces enough cytokines
to remove the virus. However, Cohen et al. 1999 found that stress short-circuited the
body’s ability to switch off the cytokine response. Individuals who had previously
experienced high stress prior to receiving the virus were found to have higher IL-6
(cytokine) levels and greater symptom scores in response to the viral challenge. In a
subsequent study, these researchers replicated their findings and demonstrated that
prolonged stress influences susceptibility to infectious illness by decreasing cortisol’s
effectiveness in regulating the pro-inflammatory cytokine response, leading to increased
production of IL-6 and greater illness expression (Miller, Cohen and Ritchey , 2002).
Taken together, these findings bring us to a surprising conclusion: psychological stress
does not influ ence upper respiratory illness by suppressing the immune system. On
the contrary, stress experienced over an extended period of time results in the immune
system over-responding, which in turn activates and extends the symptoms of upper
respiratory infections.
There have been a number of exciting new developments in the area of stress and
the common cold. Of particular note is the investigation of the relationship between
telomeres and the development of upper respiratory infections (Cohen et al., 2013a,
2013b). Telomeres are ‘caps’ at the end of chromosomes, which get shorter as we get
older and it has been suggested that these are biomarkers (or indicators) of good or
bad aging. For example, shorter telomeres have been linked with the development
of diseases such as cardiovascular disease and cancer. Moreover, a recent study has
shown that people with shorter telomeres were at greater risk of developing an upper
respiratory infection after receiving the common cold virus in the laboratory (Cohen
et al., 2013a). In addition, in a related investigation, these authors also found that
participants from lower socio-economic backgrounds were also more likely to be
infected by the cold virus and that this was explained, in part, by having shorter
telomeres (Cohen et al., 2013b).
Stress and wound healing
In 1995, Janice Kiecolt-Glaser and colleagues from Ohio State University published
a seminal study that provided evidence, for the first time, that psychological stress
slowed wound healing. Similar to Cohen and his co-investigators, Kiecolt-Glaser and
her colleagues developed an unusual research design to investigate the links between
stress and immune functioning. Using a punch biopsy, a 3.5 mm full thickness wound
was created on the non-dominant forearm, approximately 4 cm below the elbow, in
each of the study participants. Levels of perceived stress were then measured using
questionnaires and the wound was photographed every day until it completely healed.
A wound was considered fully healed when it no longer foamed after hydrogen
peroxide was applied! In this study the researchers were interested in the effects of
chronic stress on immune function and wound healing. Therefore, participants who
were caring for a relative with Alzheimer’s disease (high stress group) were com-
pared to control participants (low stress group) matched for age and family income.
BIOPSYCHOSOCIAL PATHWAYS 35