Neuroendocrine Abnormalities in CFS Deserve More Comprehensive Study

CFIDS Association, CDC Scientific Panel Issues Consensus Statement

On Research Issues



Apr 23, 2001, 01:00 ET from CFIDS Association of America

    WASHINGTON, April 23 /PRNewswire Interactive News Release/ -- Research on
 the neuroendocrine system, which involves interactions between the brain and
 glands that secrete hormones, could help explain many of the symptoms of
 chronic fatigue syndrome (CFS).  This was one conclusion reached by a panel of
 experts that convened in March for the second in a series of scientific
 symposia on CFS.  The symposium was sponsored by The Chronic Fatigue and
 Immune Dysfunction Syndrome (CFIDS) Association of America and the U.S.
 Centers for Disease Control and Prevention (CDC).
     Several studies have suggested a neuroendocrine component to CFS, but the
 exact role these abnormalities play is still a mystery.  For example, studies
 have found that some CFS patients have low levels of cortisol, a hormone
 produced by the hypothalamic-pituitary-adrenal (HPA) axis that plays a key
 role in sleep and fatigue, but more recent research has not confirmed those
 findings.
     "CFS is a multisystem disorder, and needs a multidisciplinary approach,"
 said Dimitris Papanicolaou, MD, assistant professor of medicine, Emory
 University, and panel chair.  "Researchers from diverse areas of study need to
 collaborate to answer questions about neuroendocrine involvement in CFS and
 drive treatment strategies to improve patients' daily lives."
     Following a day of presentations by experts from around the world, an
 independent panel composed of researchers and practitioners in the fields of
 biostatistics, endocrinology, epidemiology, immunology, internal medicine,
 neurology, psychiatry, and sleep disorders developed a consensus statement on
 the key issues surrounding the role of the neuroendocrine system in CFS.
     The panel agreed that:
 
     * The nature of HPA function in CFS needs to be clarified.  There is
       evidence of HPA axis dysfunction in CFS patients, but testing has
       yielded inconsistent results.  This may be due in part to the relapsing-
       remitting nature of the illness and to differences in research study
       designs.  The panel suggested that studies comparing CFS patients with
       and without HPA axis dysfunction should be conducted.
     * Cytokine abnormalities, neuroendocrine abnormalities, orthostatic
       intolerance, and CFS may be interconnected.  Cytokines are chemical
       messengers that stimulate the HPA axis when the body is under stress or
       experiencing an infection.  A number of them, including tumor necrosis
       factor alpha (TNF-alpha) and interleukin-6 (IL-6), have been implicated
       in CFS.  The panel noted these findings are intriguing in view of
       research connecting CFS and a family of blood pressure-related disorders
       called orthostatic intolerance (OI).  There is evidence that excessive
       secretion of inflammatory cytokines such as TNF-alpha may induce OI,
       although more studies delineating the links between these abnormalities
       are needed.
     * CFS is not synonymous with depression.  The panel agreed that CFS should
       be differentiated from major depression.  Individuals with major
       depression have an activated HPA axis, but HPA axis studies in CFS
       patients have been contradictory.  Studies have shown that
       corticotrophin releasing hormone (CRH) levels in the cerebrospinal fluid
       are normal or even low in CFS patients, while they may be increased in
       depressed individuals.  As a group, persons with CFS also demonstrate a
       diminished cortisol response compared to persons with depression.  The
       panel suggested that these data may point toward a potential biological
       marker for persons with CFS compared to persons with depression.
     * No link has been established between CFS and stress.  Past research has
       suggested that stressors such as viral infections, traumatic life
       events, physical abuse, and automobile accidents may cause CFS symptoms.
       However, the panel agreed that there is not enough evidence to date to
       establish a link between specific stressors and neuroendocrine
       abnormalities in CFS and related disorders.
     * Sleep abnormalities may contribute to CFS symptoms.  Sleep disturbances
       have been shown to cause increased production of IL-6 and TNF-alpha, and
       some researchers believe that they contribute significantly to excessive
       daytime sleepiness in CFS.  However, the panel pointed out that studies
       of the association between HPA axis alteration, cytokine secretion
       patterns, and sleep abnormalities have not yet been conducted in CFS
       patients.
     * More research is needed to define the neuroendocrine aspects of CFS.
       The panel outlined future research needs, including studies to: evaluate
       stressors previously hypothesized to cause CFS; test treatment
       strategies, including drugs to affect HPA axis activity; and identify
       neuroendocrine activity in larger populations of persons with CFS,
       including those that fit specific subtypes of the disease.  Panelists
       also suggested ways to overcome potential research barriers, such as
       conducting long-term studies to capture the fluctuations in symptom
       severity most CFS patients experience and developing human experimental
       models that temporarily recreate the symptoms of CFS to identify
       potential biological markers for the illness.
 
     The CFS assessment symposia series is designed to examine the role of the
 neurological, endocrine, circulatory, and immune systems in CFS.  The symposia
 gather experts to evaluate research findings, identify the most promising next
 steps for research, define research and funding priorities, and create
 research collaboration teams.
     The CFIDS Association of America, which developed the symposia series, is
 the nation's leading organization working to conquer this illness.  Since
 1987, the Association has invested nearly $12 million in education, public
 policy, and research programs in its efforts to bring an end to the suffering
 caused by CFS.
     The CDC protects people's health and safety by preventing and controlling
 diseases and injuries, enhances health decisions by providing credible
 information on critical health issues, and promotes healthy living through
 strong partnerships with local, national, and international organizations.
 The agency conducts a CFS research program under the auspices of the National
 Center for Infectious Diseases.
 
     CFS, also called chronic fatigue and immune dysfunction syndrome (CFIDS),
 is a debilitating and complex disorder characterized by profound fatigue,
 pain, and cognitive problems that are not improved by bed rest and may be
 worsened by physical or mental activity.  For more information, call
 1-800-442-3437 or visit www.cfids.org.
 
                     MAKE YOUR OPINION COUNT -  Click Here
                http://tbutton.prnewswire.com/prn/11690X19137977
 
 

SOURCE CFIDS Association of America
    WASHINGTON, April 23 /PRNewswire Interactive News Release/ -- Research on
 the neuroendocrine system, which involves interactions between the brain and
 glands that secrete hormones, could help explain many of the symptoms of
 chronic fatigue syndrome (CFS).  This was one conclusion reached by a panel of
 experts that convened in March for the second in a series of scientific
 symposia on CFS.  The symposium was sponsored by The Chronic Fatigue and
 Immune Dysfunction Syndrome (CFIDS) Association of America and the U.S.
 Centers for Disease Control and Prevention (CDC).
     Several studies have suggested a neuroendocrine component to CFS, but the
 exact role these abnormalities play is still a mystery.  For example, studies
 have found that some CFS patients have low levels of cortisol, a hormone
 produced by the hypothalamic-pituitary-adrenal (HPA) axis that plays a key
 role in sleep and fatigue, but more recent research has not confirmed those
 findings.
     "CFS is a multisystem disorder, and needs a multidisciplinary approach,"
 said Dimitris Papanicolaou, MD, assistant professor of medicine, Emory
 University, and panel chair.  "Researchers from diverse areas of study need to
 collaborate to answer questions about neuroendocrine involvement in CFS and
 drive treatment strategies to improve patients' daily lives."
     Following a day of presentations by experts from around the world, an
 independent panel composed of researchers and practitioners in the fields of
 biostatistics, endocrinology, epidemiology, immunology, internal medicine,
 neurology, psychiatry, and sleep disorders developed a consensus statement on
 the key issues surrounding the role of the neuroendocrine system in CFS.
     The panel agreed that:
 
     * The nature of HPA function in CFS needs to be clarified.  There is
       evidence of HPA axis dysfunction in CFS patients, but testing has
       yielded inconsistent results.  This may be due in part to the relapsing-
       remitting nature of the illness and to differences in research study
       designs.  The panel suggested that studies comparing CFS patients with
       and without HPA axis dysfunction should be conducted.
     * Cytokine abnormalities, neuroendocrine abnormalities, orthostatic
       intolerance, and CFS may be interconnected.  Cytokines are chemical
       messengers that stimulate the HPA axis when the body is under stress or
       experiencing an infection.  A number of them, including tumor necrosis
       factor alpha (TNF-alpha) and interleukin-6 (IL-6), have been implicated
       in CFS.  The panel noted these findings are intriguing in view of
       research connecting CFS and a family of blood pressure-related disorders
       called orthostatic intolerance (OI).  There is evidence that excessive
       secretion of inflammatory cytokines such as TNF-alpha may induce OI,
       although more studies delineating the links between these abnormalities
       are needed.
     * CFS is not synonymous with depression.  The panel agreed that CFS should
       be differentiated from major depression.  Individuals with major
       depression have an activated HPA axis, but HPA axis studies in CFS
       patients have been contradictory.  Studies have shown that
       corticotrophin releasing hormone (CRH) levels in the cerebrospinal fluid
       are normal or even low in CFS patients, while they may be increased in
       depressed individuals.  As a group, persons with CFS also demonstrate a
       diminished cortisol response compared to persons with depression.  The
       panel suggested that these data may point toward a potential biological
       marker for persons with CFS compared to persons with depression.
     * No link has been established between CFS and stress.  Past research has
       suggested that stressors such as viral infections, traumatic life
       events, physical abuse, and automobile accidents may cause CFS symptoms.
       However, the panel agreed that there is not enough evidence to date to
       establish a link between specific stressors and neuroendocrine
       abnormalities in CFS and related disorders.
     * Sleep abnormalities may contribute to CFS symptoms.  Sleep disturbances
       have been shown to cause increased production of IL-6 and TNF-alpha, and
       some researchers believe that they contribute significantly to excessive
       daytime sleepiness in CFS.  However, the panel pointed out that studies
       of the association between HPA axis alteration, cytokine secretion
       patterns, and sleep abnormalities have not yet been conducted in CFS
       patients.
     * More research is needed to define the neuroendocrine aspects of CFS.
       The panel outlined future research needs, including studies to: evaluate
       stressors previously hypothesized to cause CFS; test treatment
       strategies, including drugs to affect HPA axis activity; and identify
       neuroendocrine activity in larger populations of persons with CFS,
       including those that fit specific subtypes of the disease.  Panelists
       also suggested ways to overcome potential research barriers, such as
       conducting long-term studies to capture the fluctuations in symptom
       severity most CFS patients experience and developing human experimental
       models that temporarily recreate the symptoms of CFS to identify
       potential biological markers for the illness.
 
     The CFS assessment symposia series is designed to examine the role of the
 neurological, endocrine, circulatory, and immune systems in CFS.  The symposia
 gather experts to evaluate research findings, identify the most promising next
 steps for research, define research and funding priorities, and create
 research collaboration teams.
     The CFIDS Association of America, which developed the symposia series, is
 the nation's leading organization working to conquer this illness.  Since
 1987, the Association has invested nearly $12 million in education, public
 policy, and research programs in its efforts to bring an end to the suffering
 caused by CFS.
     The CDC protects people's health and safety by preventing and controlling
 diseases and injuries, enhances health decisions by providing credible
 information on critical health issues, and promotes healthy living through
 strong partnerships with local, national, and international organizations.
 The agency conducts a CFS research program under the auspices of the National
 Center for Infectious Diseases.
 
     CFS, also called chronic fatigue and immune dysfunction syndrome (CFIDS),
 is a debilitating and complex disorder characterized by profound fatigue,
 pain, and cognitive problems that are not improved by bed rest and may be
 worsened by physical or mental activity.  For more information, call
 1-800-442-3437 or visit www.cfids.org.
 
                     MAKE YOUR OPINION COUNT -  Click Here
                http://tbutton.prnewswire.com/prn/11690X19137977
 
 SOURCE  CFIDS Association of America