JULS
NEWS@UOFT
A Negative Inheritance: Children Mimic
Parents With Bipolar Disorder in Cortisol
Overproduction
Nothando Swan
Slowing the increasing incidence of mental health disorders
has been difficult in part because no single etiological agent is
responsible for their onset. However, researchers have reported
that in people suffering from affective mood disorders, the relay
system between the hypothalamus, anterior pituitary gland, and
adrenal glands (HPA axis) is hyperactive [1]. Normally, the HPA
axis releases cortisol in response to stressful situations. Thus, abnormally high cortisol levels indicate dysregulation of the HPA
axis’ response to stress.
Recently, Ostiguy and colleagues have linked high levels of interpersonal stress with increased cortisol levels among children whose
parents suffer from bipolar disorder [2]. Interestingly, their work
assessed how both chronic and episodic stress might affect the probability of affective disorder progression, whereas most research to
date has focused only on the effects of episodic “negative life events”
[2]. Ostiguy et al.’s findings indicate that HPA axis abnormalities may
accompany other symptoms of affective disorders. Furthermore,
they suggest that these abnormalities may be markers for the future
onset of mental health disorders given stressful lifestyles.
In their longitudinal study, Ostiguy et al. recruited parents suffering from bipolar disorder and parents with no previous history
of mental illness from the same Québec neighborhoods. Ten years
later, 62 of the offspring of parents with bipolar disorder (OBD)
and 60 offspring with no family history of affective disorders
(OFH-) agreed to be interviewed and to produce salivary samples.
Clinical psychologists conducted UCLA Life Stress Interviews in
order to grade each participant’s levels of chronic and episodic
interpersonal stress.
The associations between these stress scores and cortisol levels
after waking were particularly noteworthy. Radioimmunoassays
of the salivary samples showed that cortisol response after waking
and daytime cortisol levels were constant among the OFH- group,
regardless of their levels of either type of stress. In contrast, OBD
with high chronic stress scores had higher cortisol responses after waking than OBD with low chronic stress scores. In terms of
episodic stress, OBD who scored in the severe range had higher
daytime cortisol levels than OBD who scored lower, although this
result was measured with 92% confidence of statistical significance,
rather than the conventional 95%. This shortcoming cannot be ignored in light of work by Havermans and colleagues who reported
no significant difference in daily cortisol levels between people suffering from bipolar disorder and those who are not [3].
The link between interpersonal stress and high cortisol levels
identified by Ostiguy et al. indicates that children of parents who
suffer from bipolar disorder have a pronounced physiological response to stress. This increased response supports genetic-based research which reports increased HPA axis reactivity in offspring with
a short allele for the serotonin transporter gene [4]. Recognizing
increased sensitivity to stress as a marker for increased susceptibility for developing an affective disorder opens the door for new epidemiological and public health research. Public health campaigns
aimed at educating youth about the effects of stress might help
to decrease the incidence of youth, and subsequently adults, who
need treatment for mood disorders. This research also justifies the
increased emphasis on behavioural modifications such as meditation and mindfulness to prevent stress and increase overall wellbeing. These interventions, and others like them, may be effective
strategies in preventing the onset of affective disorders, particularly
among those who are most vulnerable to developing them.
References
1. Pariante CM, Lightman SL. The HPA axis in major depression: classical theories and new
developments. Trends Neurosci. 31(9), 464 – 468 (2008).
2. Ostiguy CS, Ellenbogen MA, Walker CD, Walker EF, and Hodgins S. Psychol. Med. 41(11),
2447 – 2457 (2011).
3. Havermans R, Nicolson NA, Berkhof J, and deVries MW. Patterns of salivary cortisol secretion and responses to daily events in patients with remitted bipolar disorder.
Psychoneuroendocrinology. (36), 258 – 265 (2011).
4. Goodyer I, Bacon A, Ban M, Croudace T, and Herbert J. Serotonin transporter genotype,
morning cortisol and subsequent depression in adolescents. Br. J. Psychiatry. (195), 39 – 45
(2009).
Journal of Undergraduate Life Sciences • Volume 6 • Issue 1 • Spring 2012
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