Behavior and HPA functioning.

[Guest guest]

HPA hypoactivity is hallmark of CFS and fibromyalgia, and is widely

believed to be a consequence of those conditions, rather than being a

cause. One simple way of testing for HPA functioning is via the

cortisol awakening response test. The following study shows that

self-focused rumination can significantly lower the cortisol

awakening response. CBT attempts to change detrimental behavior

patterns, and self-focused rumination is often one such behavior that

it tries to stop. Thus, can CBT help some people with CFS, by

improving HPA functioning? In any event, here are some quotes from

the study... It's a fun read.

" Decreased cortisol response to awakening is associated with

cognitive vulnerability to depression in a nonclinical sample of

young adults. "

Psychoneuroendocrinology

Volume 32, Issue 2, February 2007, Pages 199-209

Alterations in the hypothalamus–pituitary–adrenal (HPA) axis function

in depression are well documented (Hasler et al., 2004; Antonijevic,

2006). Depression has been linked to altered basal- and stress-

related cortisol responses, and both over- and underactivation of the

HPA axis have been reported, probably depending on subtype and

severity (Stetler and , 2005; Antonijevic, 2006; Oswald et al.,

2006). There is increasing evidence that these alterations are not

merely epiphenomena of the disorder, but may rather be regarded as

endophenotypes, probably playing an important role in causal pathways

of the pathophysiology of depression (Hasler et al., 2004; Oswald et

al., 2006).

With regard to unstimulated HPA-axis activity, the cortisol awakening

response (CAR) has been gaining attention in recent research. The CAR

is a discrete part of the cortisol circadian cycle. In healthy

individuals, it is characterized by a large increase in saliva free

cortisol levels within the first 30 min after awakening (50–60%;

Pruessner et al., 1997; Wuest et al., 2000a; Clow et al., 2004). In

contrast to experimentally stimulated cortisol responses, the CAR

reflects cortisol excretion after a natural stressor (awakening). The

CAR is an easily accessible and reliable means of assessing dynamic

HPA functioning (Pruessner et al., 1997; Rohleder et al., 2004). It

demonstrates moderate to high within-subject stability (Pruessner et

al., 1997; Wuest et al., 2000a; et al., 2001) and—in contrast

to the cortisol profile during the day—appears to be under

substantial genetic control (Wuest et al., 2000b; Bartels et al.,

2003). Furthermore, the CAR seems not to be related to other

parameters of diurnal cortisol secretion or to cortisol responses to

stress, but correlates with the response to standard

adrenocorticotropin stimulation, indicating that it is a marker for

adrenocortical activity (Schmidt-Reinwald et al., 1999; et

al., 2001).

Due to its high intraindividual stability, the CAR may be regarded as

a trait measure of the dynamics of HPA axis activity. In this regard,

it appears ideally suited for investigating possible connections with

psychological vulnerability markers for depression. Investigations of

such kind could contribute important knowledge on the role of

cognitive vulnerability theories within a psychobiological framework

for research on affective disorders (son et al., 2002).

One of the most prominent cognitive vulnerability theories of

depression, the Response Styles Theory by S. Nolen-Hoeksema (2004)

addresses the role of two coping styles, namely perseverative self-

focused rumination versus distraction from negative mood, for the

exacerbation, maintenance, and discontinuation of depressed states.

Ruminative responses are defined as thoughts and behaviours that

comprise passively focusing one's attention on one's dysphoric

symptoms and aspects of the self during low mood and repetitive

thinking about possible causes and consequences of symptoms and

negative self-aspects. Distractive coping is defined as actively

turning one's attention away from one's symptoms on to pleasant or

neutral thoughts and actions (Nolen-Hoeksema, 2004). The theory

postulates that ruminative coping amplifies and prolongs depressed

mood by increasing the likelihood of recalling negative memories, by

interfering with attention and instrumental behaviour, and by

impairing more complex problem solving (cf. Kuehner and Buerger,

2005). There is evidence from observational studies for the proposed

prediction of response styles regarding onset, severity, and duration

of depressed moods (Nolen-Hoeksema, 2000; Kuehner and Weber, 1999).

Furthermore, experimentally induced rumination prolonged depressed

moods, enhanced negatively biased memories, and impaired

interpersonal and complex problem solving, while induced distraction

led to a decline of depressed mood and improved problem solving

(Lyubomirsky et al., 1999; son and Lam, 2004; Joormann and

Siemer, 2004).

The present study investigated associations of basal diurnal cortisol

activity—particularly the CAR—with habitual coping styles in response

to depressed mood and with responsiveness to induced attention

focusing after sad mood induction. In this regard, our study is the

first to connect a measure of dynamic HPA activity to a cognitive

vulnerability marker for depression, the latter assessed both by a

trait measure and by experimental manipulation.

The mood induction procedure used in this study appeared to be

effective. Using a film sequence originally employed by Joormann and

Siemer (2004), levels of mood were lowered significantly from

baseline to post mood induction in the total sample, reflected both

in a decrease of positive and an increase of negative mood.

Participants subsequently induced to ruminate kept their negative

mood whereas participants induced to distract themselves showed a

significant reduction of negative mood along with a significant

increase of positive mood. These results support growing evidence

from the literature showing that actively induced ruminative self-

focused attention prolongs and stabilizes dysphoric mood, while

actively induced distraction attenuates and shortens it (cf.

Lyubomirsky and Tkach, 2004; Nolen-Hoeksema, 2004 for reviews).

Importantly, the present study also revealed that higher levels of

self-focused trait rumination were connected with lower improvement

or worsening of mood after response induction, and these results were

not attributable to interindividual variability in basal levels of

depressive symptoms.

Another key finding of our study was that a low CAR was linked to

high levels of self-focused rumination and to lowered improvement of

mood after induced distraction. This suggests that a decreased CAR is

simultaneously associated with habitual self-related emotional

processing and with a restricted capacity of the individual to lift

negative mood with distractive thoughts. How can this be explained?

There is evidence that depression involves deficient inhibition of

negative information (Goeleven et al., 2006). Research has shown that

depressed individuals show lowered activation in brain regions

responsible for attentional control over emotional interference, such

as the prefrontal cortex and the anterior cingulate (son et al.,

2002; et al., 2004). It has been suggested that impaired

inhibitory function might also be one of the underlying mechanisms of

rumination (Hertel, 1997). For example, self-reported rumination has

been linked to sustained amygdala reactivity to negative words in

depressed individuals (Siegle et al., 2002), with both responses

apparently reflecting difficulties to disengage attention from

negative information. Respectively, in the present response

manipulation task high levels of habitual self-focused emotional

processing appeared to have amplified the negative mood effects of

induced rumination and to have impaired the individual's capacity to

lift mood by switching attention to external cues in the distraction

condition.

In parallel, at the neuroendocrine level, the CAR seems to reflect

the capacity of an organism to focus attention to novel situations or

demands under natural conditions, involving inhibition of task-

irrelevant emotional processing (e.g., kson et al., 2003). It has

been noted that the normal elevation of morning cortisol serves a

variety of functions by mobilizing energy stores, increasing interest

in exploration, and promoting acquisition, attention focusing, and

consolidation in the learning process (Gunnar and Vazquez, 2001).

Similarly, kson et al. (2003) consider moderately enhanced

morning cortisol to reflect a state of heightened attention to the

social environment, which may facilitate the progression of higher

order cognitive mechanisms. Thus, in our opinion, a decreased CAR and

high self-focused rumination appear to share specific vulnerability

qualities involving similar mechanisms. We assume that both hamper

the adaptive shift of attention to external cues during dysphoric

episodes and involve lowered disinhibition of task-irrelevant

negative emotional processing. In this respect, our study revealed

first indications of a possible relationship between a cognitive

vulnerability marker for depression and characteristics of basal

neuroendocrine activity regarding their association with the course

of experimentally induced dysphoric mood.

Within the framework of the present study we are also unable to

determine causal pathways between CAR and self-focused rumination. It

is conceivable that a blunted CAR limits the capacity of an

individual to inhibit interfering negative internal self-evaluating

processes during dysphoric mood. Alternatively, habitual rumination

may promote allostatic load in the individual (cf. McEwen, 2004),

resulting in a long term down-regulation of the stress system as seen

in a number of stress-related conditions (Heim et al., 2000).

Finally, both variables may be influenced by unknown third variables.