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Sleep debt and serotonin. A response to a comment on my hypothesis Pires et al. made a comment [1] on my hypothesis entitled ‘‘More sleep will bring more serotonin and less suicide in Japan’’ [2]. In their critique, Pires et al. (in press) argue that sleep deprivation can actually increase the activity of serotonergic system. However, the evidence cited by the authors is a study of paradoxical sleep deprivation [3], which differs substantially from total sleep debt. As such, the hypothesis that total sleep debt is related to suicide remains plausible. During wakefulness, the serotonergic system is activated not only through exposure to morning light [4] but also through rhythmic movements, such as gait, chewing, and respiration [5]. It is widely recognized that poor sleep habits in humans can induce mood and motivational disturbances, reduce attention, vigilance, and concentration, and increase daytime fatigue or sleepiness [6]. In addition, behaviorally-induced insufficient sleep syndrome is believed to be associated with the development of anergia, fatigue, and malaise [6]. When people are exhausted or sleepy, they are unlikely to perform sufficient physical activity to activate serotonergic activity to a desirable level. However, I strongly agree with Pires et al. [1] that a possible relationship between sleep debt and suicide cannot be decisively attributed to a single neurotransmitter system at this point in time [7]. Conflict of interest statement
References [1] Pires GN, Andersen ML, Kahan V, Araujo P, Galduróz JC, Tufik S. Is serotonin responsible for the relationship between sleep debt and suicide? A comment on Kohyama’s hypothesis. Med Hypo (in press). doi:10.1016/j.mehy.2010. 07.015. [2] Kohyama J. More sleep will bring more serotonin and less suicide in Japan. Med Hypo 2010;75:340. [3] Machado RB, Tufik S, Suchecki D. Chronic stress during paradoxical sleep deprivation increases paradoxical sleep rebound: association with prolactin plasma levels and brain serotonin content. Psychoneuroendocrinology 2008;33:1211–24. [4] Cagampang FR, Yamazaki S, Otori Y, Inouye SI. Serotonin in the raphenuclei: regulation by light and an endogenous pacemaker. Neuroreport 1993;5: 49–52. [5] Jacobs BL, Azmitia EC. Structure and function of the brain serotonin system. Physiol Rev 1992;72:165–229. [6] American Academy of Sleep Medicine. The international classification of sleep disorder, 2nd ed. Westchester; 2005. [7] Kohyama J. Sleep, serotonin and suicide in Japan. J Physiol Anthropol, in press.
Jun Kohyama Tokyo Bay Urayasu/Ichikawa Medical Center, 3-4-32 Toudaijima, Urayasu 279-0001, Japan Tel.: +81 47 351 3101; fax: +81 47 352 6237. E-mail address:
[email protected]
Jun Kohyama served as a consultant and speaker for Johnson & Johnson. doi:10.1016/j.mehy.2010.11.027
Biological resilience of older adults versus frailty
In a recent issue of Medical Hypotheses, Conti and Conti welcomed increasing use of the term resilience in medicine, as a complement to the term frailty [1]. We made similar considerations [2] in the field of geriatric medicine, recommending specific attention to biological resilience. Medline research reveals many papers on frailty but few on the possibility of measuring and recognizing resilience in clinical experience. Interest in the definition and recognition of frailty is aimed at promoting prevention and care to modify adverse outcomes in vulnerable elders. Resilience indicates the ability to cope with stress and catastrophe and regain health by learning and adaptation, a well-known capacity of the human mind. We proposed that biological resilience could be identified to recognize the protective factors (genetic, demographic, environmental, gender-linked, social, humoral, psychological and functional) that may contribute to positive outcomes in the very elderly [2]. Our advice was to shift the accent from a negative (frailty) to a positive aspect (resilience), which could have benefits for medical practice. The terms frailty and resilience are related but certainly not opposites. Frailty is common in elderly persons and a focus for geriatricians, but there is no consensus on its definition, recognition criteria, long-term dynamic development and lifetime determinants. Despite its ‘‘slippery’’ meaning, it is a useful concept, referring to a state of increased vulnerability to stressors due to age-related decline in physiological reserves. Frailty may initially be clinically silent and its development may only be recognized by clinical, functional, behavioural and biological signs. These in-
clude wasting, nutritional status, subjective health perception, cognitive and physical performance, current care, sensory and physical impairment, and certain biological markers. Evidence of a phenotype [3] in older adults is a reliable tool for predicting adverse outcomes and an indication for prevention; it is less problematic than conceptualizing frailty as physiological decline caused by cumulative effects of disease-related, psychosocial and environmental changes, applicable to functionally limited or disabled elders. If an old person is not frail, he/she is robust and no specific treatment is necessary, apart from the usual therapeutic and lifestyle measures. On the other hand, the term resilience is widely used in many fields (ecology, soil science, organization, homeland security, computer networking, technology, psychology and dentistry), meaning competence under stress. Our original proposal was to use it in a biological sense to explain the amount of change a patient can undergo in the case of severe acute illness, without losing functional and structural control [2]. The proposal arose from the observation that geriatricians often make the right decision for severely disabled, comorbid elderly patients suffering from severe, acute, unstable diseases with high risk of complications and death, because they are aware that certain patients respond well to treatment, regardless of age. If biological resilience were demonstrated and measured, it would facilitate decision-making for clinicians and especially geriatricians (for example in patients over 80 with multiple severe impairment requiring aggressive treatment) [2]. Frail and robust elderly patients may or may not be resilient and recover from acute illness. We recently conducted a study on the capacity of functional recovery during hospital stay for acute diseases. This capacity