neuropeptide-y and Fatigue

The high prevalence of osteoporosis, observed in multiple sclerosis (MS) patients, has been attributed to reduced mobility and or the use of disease-modifying drugs. However, MS-impaired cardiovascular autonomic nervous system (ANS) function has the potential of reducing bone mass density (BMD) by altering the expression and/or function of the neuronal, systemic, and local mediators of bone remodeling. This review describes the complex regulation of bone homeostasis with a focus on MS, providing evidence that ANS dysfunction and low BMD are intertwined with MS inflammatory and neurodegenerative processes, and with other MS-related morbidities, including depression, fatigue, and migraine. Strategies for improving ANS function could reduce the prevalence of MS osteoporosis and slow the rate of MS progression, with a significant positive impact on patients' quality of life.

Topics: Adiponectin; Autonomic Nervous System; Bone Density; Bone Remodeling; Brain; Cardiovascular System; Depression; Endocannabinoids; Fatigue; Humans; Inflammation; Leptin; Migraine Disorders; Multiple Sclerosis; Nerve Degeneration; Neuropeptide Y; Osteocalcin; Osteopontin; Osteoporosis; Osteoprotegerin; Parathyroid Hormone; RANK Ligand; Serotonin; Vitamin D

Define covariates of cerebrospinal corticotropin-releasing hormone (CRH) levels in normal humans. CRHCSF was measured in 9 normal subjects as part of an intensive study of physiological responses stressors in chronic pain and fatigue states. CRHCSF was first correlated with demographic, vital sign, HPA axis, validated questionnaire domains, baseline and maximal responses to pain, exercise and other stressors. Significant factors were used for linear regression modeling.. Highly significant correlations were found despite the small number of subjects. Three models were defined: (a) CRHCSF with blood glucose and sodium (explained variance = 0.979, adjusted R2 = 0.958, p = 0.02 by 2-tailed testing); (b) CRHCSF with resting respiratory and heart rates (R2 = 0.963, adjusted R2 = 0.939, p = 0.007); and (c) CRHCSF with SF-36 Vitality and Multidimensional Fatigue Inventory Physical Fatigue domains (R2 = 0.859, adjusted R2 = 0.789, p = 0.02).. Low CRHCSF was predicted by lower glucose, respiratory and heart rates, and higher sodium and psychometric constructs of well being. Responses at peak exercise and to other acute stressors were not correlated. CRHCSF may have reflected an overall, or chronic, set-point for physiological responses, but did not predict the reserves available to respond to immediate stressors.

Topics: Adult; Blood Glucose; Confidence Intervals; Corticotropin-Releasing Hormone; Demography; Fatigue; Female; Heart Rate; Humans; Male; Models, Statistical; Neuropeptide Y; Pain; Radioimmunoassay; Regression Analysis; Respiration; Sex Factors; Sodium; Statistics as Topic; Stress, Physiological