title: Melatonin suppression by light in euthymic bipolar and unipolar patients.
abstract: BACKGROUND
  Previous studies have suggested that bipolar patients are supersensitive to light suppression of melatonin and that this may be a trait marker for genetic vulnerability. The present study was an attempt to replicate and extend this observation. Propranolol hydrochloride effects were compared with light effects because of the documented influence of beta-adrenergic receptors on melatonin production. Nighttime levels of corticotropin and cortisol were also examined as potential trait vulnerability markers.
  
  
  METHODS
  Melatonin levels in euthymic bipolar patients (n= 29) were tested before and after 500-lux light was administered between 2 and 4 AM and on a separate night in the dark. Results were compared with those of a group of patients with unipolar depression (n= 24) and with those of a group of non-psychiatrically ill control subjects (n= 50). Lithium effects and propranolol effects were tested in subgroups.
  
  
  RESULTS
  No group differences were seen in light suppression among bipolar patients, unipolar patients, and controls; an analysis of the whole group did not reveal differences in propranolol effect, differences in corticotropin or cortisol levels, or evidence for a lithium effect. However, patients with bipolar I affective disorder showed the following: (1) significantly lower melatonin levels on the light night, at baseline and following light exposure; and (2) a later peak time for melatonin on the dark night.
  
  
  CONCLUSIONS
  The general hypothesis of increased light sensitivity in bipolar patients was not supported. However, melatonin secretion abnormalities were confirmed in the subgroup with bipolar I disorder. Further assessments of circadian rhythm disruption as a vulnerability marker in bipolar illness are indicated.
authors.affiliation: Department of Psychiatry, Indiana University School of Medicine, Ind 46202-4887, USA. jnurnber@iupui.edu
authors.forename: J I
authors.initials: JI
authors.lastname: Nurnberger
authors.forename: S
authors.initials: S
authors.lastname: Adkins
authors.forename: D K
authors.initials: DK
authors.lastname: Lahiri
authors.forename: A
authors.initials: A
authors.lastname: Mayeda
authors.forename: K
authors.initials: K
authors.lastname: Hu
authors.forename: A
authors.initials: A
authors.lastname: Lewy
authors.forename: A
authors.initials: A
authors.lastname: Miller
authors.forename: E S
authors.initials: ES
authors.lastname: Bowman
authors.forename: M J
authors.initials: MJ
authors.lastname: Miller
authors.forename: L
authors.initials: L
authors.lastname: Rau
authors.forename: C
authors.initials: C
authors.lastname: Smiley
authors.forename: D
authors.initials: D
authors.lastname: Davis-Singh
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001714:Bipolar Disorder / Q000097:blood* / Q000175:diagnosis / Q000235:genetics*; D002940:Circadian Rhythm / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D003866:Depressive Disorder / Q000097:blood* / Q000175:diagnosis / Q000235:genetics*; D005260:Female; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008027:Light; D008094:Lithium / Q000494:pharmacology; D008297:Male; D008550:Melatonin / Q000097:blood* / Q000378:metabolism; D008875:Middle Aged; D010775:Photic Stimulation; D011433:Propranolol / Q000494:pharmacology; D011863:Radioimmunoassay
chemical_list: D005819:Genetic Markers; D000324:Adrenocorticotropic Hormone; D008094:Lithium; D011433:Propranolol; D008550:Melatonin; D006854:Hydrocortisone