Somatic symptoms can stem from heightened awareness of normal body sensations alongside a tendency to interpret those sensations as abnormal. Studies suggest that risk factors of somatic symptoms include
childhood neglect,
sexual abuse, and substance abuse.
Psychosocial stressors, such as unemployment and poor job performance, may also be risk factors. There could also be a
genetic element: A 2010 study of
monozygotic and
dizygotic twins found that genetics explained 7% to 21% of participants' risk for somatic symptoms, with the remainder related to
environmental factors. In another study, various
single-nucleotide polymorphisms were linked to somatic symptoms. In addition, evidence suggests that negative psychological factors have a significant impact on the impairments and behaviors of people suffering from somatic symptom disorder, as well as the long-term stability of such symptoms.
Psychosocial Psychosocial stresses and
cultural norms influence how patients present to their
physicians. American and Koreans engaged in a study to measure
somatization within the
cultural context. It was discovered that Korean participants used more body-related phrases while discussing their connections with stressful events and experienced more
sympathy when asked to read texts using somatic expressions when discussing their emotions.
Physiological The
hypothalamo pituitary adrenal axis (HPA) has a crucial role in
stress response. While the
HPA axis may become more active with depression, there is evidence of
hypocortisolism in somatization. In somatic disorder, there is a negative connection between elevated pain scores and
5-hydroxy indol acetic acid (5-HIAA) and
tryptophan levels.
Proinflammatory activation and
anterior cingulate cortex activity have been shown to be linked in those who experienced stressful life events for an extended period of time. It is further claimed that increased activity of the anterior cingulate cortex, which acts as a bridge between attention and emotion, leads to increased sensitivity of unwanted stimuli and bodily sensations.
Pain is a multifaceted experience, not just a sensation. While
nociception refers to afferent
neural activity that transmits
sensory information in response to stimuli that may cause
tissue damage, pain is a conscious experience requiring
cortical activity and can occur in the absence of nociception. The term "
central sensitization" has been created to describe the
neurobiological notion that those predisposed to somatization have an overly sensitive
neural network. Harmless and mild
stimuli stimulate the
nociceptive specific
dorsal horn cells after
central sensitization. As a result, pain is felt in response to stimuli that would not typically cause pain.
Genetic Genetic investigations have suggested modifications connected to the
monoaminergic system, in particular, may be relevant while a shared genetic source remains unknown. Researchers take into account the various processes involved in the development of somatic symptom disorder as well as the interactions between various
biological and psychosocial factors. Another study found that the
glucocorticoid receptor gene (
NR3C1) is
hypomethylated in those with somatic symptom disorder and in those with depression. ==Diagnosis==