Fetal programming of autonomic and HPA function: do people who were small babies have enhanced stress responses?
Fetal programming of autonomic and HPA function: do people who were small babies have enhanced stress responses?
 
  Studies in several species have demonstrated that an adverse early environment can influence the development of the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis. The autonomic nervous system and HPA axis are key components of the neuroendocrine response to stress and many of these animal models show altered biological responses to stress. Recent research now suggests that these processes operate in humans. An adverse early environment, as evidenced by reduced birth or infant weight, is associated with enhanced autonomic and HPA responses to experimental psychological stress. However, there appear to be marked sex differences in the mechanisms involved. Epidemiological studies demonstrate that physiological changes in these neuroendocrine systems may predispose to cardiovascular disease through their influence on risk factors such as plasma glucose and lipid concentrations and blood pressure. Thus the combination of enhanced stress susceptibility and the psychosocial stressors to which people are exposed may be an important component of the disease risk in human populations
  stress response, weight, responses, infant, glucose, fetal, function, birth, development, autonomic nervous system, human, blood, fetal programming, cardiovascular, environment, blood-pressure, cardiovascular-disease, disease, plasma, risk factors, cardiovascular disease, risk, stress, research, blood pressure, pressure, programming, humans
  
  
  45-50
  
    
      Phillips, D.I.
      
        29b73be7-2ff9-4fff-ae42-d59842df4cc6
      
     
  
    
      Jones, A.
      
        bcae84a4-4191-4a3e-b695-1b6e2b0681c7
      
     
  
  
   
  
  
    
      2006
    
    
  
  
    
      Phillips, D.I.
      
        29b73be7-2ff9-4fff-ae42-d59842df4cc6
      
     
  
    
      Jones, A.
      
        bcae84a4-4191-4a3e-b695-1b6e2b0681c7
      
     
  
       
    
 
  
    
      
  
  
  
  
  
  
    Phillips, D.I. and Jones, A.
  
  
  
  
   
    (2006)
  
  
    
    Fetal programming of autonomic and HPA function: do people who were small babies have enhanced stress responses?
  
  
  
  
    The Journal of Physiology, 572 (1), .
  
   (doi:10.1113/jphysiol.2005.104695). 
  
  
   
  
  
  
  
  
   
  
    
      
        
          Abstract
          Studies in several species have demonstrated that an adverse early environment can influence the development of the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis. The autonomic nervous system and HPA axis are key components of the neuroendocrine response to stress and many of these animal models show altered biological responses to stress. Recent research now suggests that these processes operate in humans. An adverse early environment, as evidenced by reduced birth or infant weight, is associated with enhanced autonomic and HPA responses to experimental psychological stress. However, there appear to be marked sex differences in the mechanisms involved. Epidemiological studies demonstrate that physiological changes in these neuroendocrine systems may predispose to cardiovascular disease through their influence on risk factors such as plasma glucose and lipid concentrations and blood pressure. Thus the combination of enhanced stress susceptibility and the psychosocial stressors to which people are exposed may be an important component of the disease risk in human populations
        
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      Published date: 2006
 
    
  
  
    
  
    
  
    
  
    
  
    
     
    
  
    
     
        Keywords:
        stress response, weight, responses, infant, glucose, fetal, function, birth, development, autonomic nervous system, human, blood, fetal programming, cardiovascular, environment, blood-pressure, cardiovascular-disease, disease, plasma, risk factors, cardiovascular disease, risk, stress, research, blood pressure, pressure, programming, humans
      
    
  
    
  
    
  
  
        Identifiers
        Local EPrints ID: 61431
        URI: http://eprints.soton.ac.uk/id/eprint/61431
        
          
        
        
        
          ISSN: 0022-3751
        
        
          PURE UUID: 024d0ef0-c2c3-4e82-aa45-9e3a58e86d12
        
  
    
        
          
            
          
        
    
        
          
        
    
  
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  Date deposited: 09 Sep 2008
  Last modified: 15 Mar 2024 11:26
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      Contributors
      
          
          Author:
          
            
              
              
                D.I. Phillips
              
              
            
            
          
        
      
          
          Author:
          
            
            
              A. Jones
            
          
        
      
      
      
    
  
   
  
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