Secretion of a stress hormone called cortisol and activation of the sympathetic nervous system are components of the classic "fight or flight" response to danger. A common source of cortisol release and increased cardiovascular activity is public speaking. A study in the June issue of Alcoholism: Clinical & Experimental Research builds upon previous work by comparing the cardiovascular responses of alcoholics and nonalcoholics to the psychological challenge of public speaking in relation to the physical challenge of standing (orthostasis).
"Since cortisol is central to our ability to handle stress," said William R. Lovallo, Director of the Behavioral Sciences Laboratories at the Veterans Affairs Medical Center, Oklahoma City and corresponding author for the study, "we were surprised several years ago when we found that patients with alcohol dependence had cortisol responses that were absent or greatly attenuated. It didn’t matter if the patient was asked to hold a hand in ice water, squeeze a hand-exercise device until it hurt, do mental arithmetic problems, or perform in a public-speaking simulation. Due to this cortisol response deficit, we suspected that these patients might also have a reduced fight or flight response. Most persons see public speaking as socially threatening, and they respond with the primitive fight or flight mechanism."
Before testing alcoholics for their responses to a public-speaking task, researchers first needed to establish if their sympathetic nervous system was able to respond at all. "This would tell us if their blunting was specific to psychological stressors like public speaking," said Lovallo, "or due to a generalized autonomic deficit."
He and his colleagues examined 20 alcohol-dependent subjects, abstinent for 21 to 28 days, and 10 age-matched nonalcoholics. All subjects were males between the ages of 22 and 55 years. The researchers used impedance cardiography and dinamap blood pressure monitoring to assess the participants’ heart rate, stroke volume, cardiac output, total peripheral resistance, mean arterial pressure, systolic blood pressure, and diastolic blood pressure during orthostasis and public speaking. Self-reported mood was also assessed during these two tasks.
Cardiovascular responses to orthostasis were similar for the two groups. However, the alcoholics had blunted heart-rate responses to public speaking even though they reported similar anxiety responses to the nonalcoholics. This suggests a disconnection between perception of threat and resulting physiological responses among the alcoholics.
"The similar cardiovascular responses to orthostasis among the alcohol-dependent patients indicate that their autonomic nervous systems were working normally," said Lovallo. "Yet when we asked them to prepare and memorize a short speech and then deliver the speech to a video camera, the patients reacted with little or no change in heart rate, and of course, they failed to have a cortisol response. The patients reacted as if the social challenge of public speaking had no special meaning for them. So, the sympathetic nervous system in the patients looked normal, but their response to a psychological stressor was almost absent. When faced with a socially meaningful stressor, neither part of their fight-flight mechanism was working."
"Emotion is the product of cognitive and physiological processes," observed Ralph E. Tarter, professor of pharmaceutical sciences and psychiatry at the University of Pittsburgh. "Although speculative, the results of this study point to a physiologic-cognitive disconnection as a potential mechanism underlying the disturbed emotional experience of alcoholics. For example, although speculative, it could perhaps help explain why alcoholics appear outwardly unconcerned about their alcoholism when in fact their life is chaotic. This is commonly referred to as ‘denial.’ However, we need further research to delineate the extent to which deficient interpretation of cognitive and physiological processes is responsible for certain of the emotional tendencies of alcoholics."
"The significance of this finding comes in part from understanding how and why a normal person has a stress response to a social event," said Lovallo. "Psychological stressors are usually events in our environment that have no ability to hurt us directly, in the way that cold, hunger, or a predator can hurt us. So, why do we react as if we were in real danger when we are only giving a talk to an audience, and a fake audience at that? We process these kinds of events in our frontal cortex, the part of the brain that allows us to imagine things and to project ourselves into the future. This brain region has extensive connections with our limbic system, the primitive brain areas responsible for emotions and stress responses. The frontal-limbic connections are how we generate a threat response to such things as embarrassment if we fail to speak well before an audience. Such events are only meaningful to us because we are social beings that value the esteem of our peers. However, if these frontal-limbic connections are disturbed, then we may either fail to psychologically comprehend a potential threat when we encounter it, or we may fail to respond even if we recognize the threat. Our results suggest that some aspect of this frontal-limbic connection has been altered in patients recovering from severe alcohol dependence, which has implications for their social functioning and comprehension."
Funding for this Addiction Science Made Easy project is provided by the Addiction Technology Transfer Center National Office, under the cooperative agreement from the Center for Substance Abuse Treatment of SAMHSA.
Articles were written based on the following published research:
Panknin, T.L., Dickensheets, S.L., Nixon, S.J., Lovallo, W.R. (June, 2002). Attenuated heart rate responses to public speaking in individuals with alcohol dependence. Alcoholism: Clinical & Experimental Research 26(6), 841-847.
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