Supersensitivity to melatonin suppression by light in young people at high risk for affective disorder A preliminary report

Nürnberger, John I.; Berrettini, Wade H.; Tamarkin, Lawrence; Hamovit, Joel; Norton, James A.; Gershon, Elliot S.

doi:10.1016/0893-133x(88)90020-6

Cited by 103 publications

(50 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast patients with MDD did not demonstrate significantly different suppression of nocturnal plasma melatonin concentrations following light exposure when compared to controls. The findings are similar to that of Lewy et al (1981Lewy et al ( , 1985 and Nurnberger et al (1988) who likewise found a supersensitivity in bipolar patients, and Cummings et al (1989) who found no difference in the light sensitivity between controls and patients with MDD. However, the study does not agree with a more recent study that showed more suppression in the controls than in a group of patients with MDD or BD (Lam et al 1990), and the study of Whalley et al (1990) showing no differences in sensitivity to 500 lux between euthymic (recovered) bipolar patients and control subjects.…”

Section: Discussionsupporting

confidence: 90%

“…Early reports suggested bipolar disorder patients were supersensitive to the effects 500 lux of light (Lewy et al 1981) and that this may be a trait marker for the illness (Lewy et al 1985). Nurnberger et al (1988) have taken this hypothesis further and investigated familial sensitivity as a possible genetic marker. It was reported that the supersensitivity in the melatonin response to light was more likely amongst those with a parent with bipolar disorder.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Melatonin Sensitivity to Dim White Light in Affective Disorders

Nathan

Burrows

Norman

1999

Neuropsychopharmacology

107

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Melatonin Sensitivity to Dim White Light in Affective Disorders

Nathan

Burrows

Norman

1999

Neuropsychopharmacology

107

View full text Add to dashboard Cite

“…If replicated in larger sample sizes, the data would suggest that PMDD patients may be more sensitive than NC subjects to the acute suppressive effects of light on melatonin secretion as were the depressed vs. control subjects reported in initial studies by Lewy et al (1981) and Nurnberger et al (1988).…”

Section: Premenstrual Dysphoric Disordermentioning

confidence: 91%

Chronobiological Basis of Female-Specific Mood Disorders

Parry

Newton

2001

Neuropsychopharmacology

112

View full text Add to dashboard Cite

Women have twice the incidence of major depression compared with men. They are prone to develop episodes of depression during times of reproductive hormonal change at puberty, with use of oral contraceptives, during the premenstrual phase of the menstrual cycle, postpartum and during the perimenopause (see review: Parry 1995a). WirzJustice (1995) In women, hormonal changes associated with the reproductive cycle may provoke affective changes in predisposed individuals. Examples include depression associated with oral contraceptives (Parry and Rush 1979), the luteal phase of the menstrual cycle (Hamilton et al. 1984;Endo et al. 1978;Halbreich and Endicott 1985), the postpartum period (Parry and Hamilton 1990), and menopause (Winokur 1973). Sex differences in the rates of depression begin to appear after puberty (Weissman et al. 1984;Angold et al. 1998), a time of major change in the neuroendocrine reproductive axis. From this time onward, women have a greater lifetime risk for major depression than men. Women predominate with respect to unipolar depression (Weissman et al. 1984), the depressive subtype of bipolar illness (Angst 1978), and cyclical forms of affective illness such as rapid cycling manic-depressive illness (Wehr 1984) and seasonal affective disorder (Rosenthal et al. 1984). Furthermore, the risk for major depression in both men and women appears to be increasing in recent generations (Weissman et al. 1984;Klerman and Weissman 1989).The fluctuation of ovarian steroids during specific phases of the reproductive cycle may bear some relationship to the particular vulnerability of women for mood disorders. The ovarian hormones could exert their effects on mood directly or indirectly by their effect on neurotransmitter, neuroendocrine, or circadian systems (McEwen and Parsons 1982;Albers 1981;Albers et al. 1981;Thomas and Armstrong 1989; Parry 1995a,b). Although each of these systems has been implicated in the pathogenesis of depressive illness, the circadian basis of these disorders has received the least attention. We have designed our studies with their particular chronobiological focus because the predisposition of women for major depression has not been investigated systematically with respect to the interaction of Chronobiology, Women and Depression S103 the unique cyclic reproductive neuroendocrine axis in women and circadian physiology. Although chronobiological disturbances have been described in depression (Kripke et al. 1978;Wehr and Goodwin 1980), the characterization of chronobiological disturbances in reproductive-related mood disorders in women remains to be elucidated. Below we review the circadian rhythm abnormalities that we have observed in premenstrual dysphoric disorder, pregnancy and postpartum depression and menopause. As reproductive hormones modulate the synchrony or coherence between different components of the circadian system (Thomas and Armstrong 1989), we hypothesize that these changing hormones during the premenstrual, postpartum and menopausal periods may destabilize circ...

show abstract

“…At ¢rst sight, there is a con£ict between our suggestion that the primary defect is a reduction in cationic channels and the many ¢ndings of increased cellular and neuronal sensitivity in bipolar disorder, as cationic-channel reduction would have the general e¡ect of decreased neuronal sensitivity. Documented examples of increased neuronal sensitivity in bipolar disorder include: (i) elevated levels of G proteins (Mitchell et al 1997); (ii) increased responsiveness of cAMP processes (Andreopoulos et al 1997); (iii) increased sensitivity to light-induced melatonin suppression (Nurnberger et al 1988); and (iv) increased sensitivity to cholinergic REM sleep induction (Nurnberger et al 1983). We suggest that these apparent contradictions can be resolved if the primary e¡ect on the timing of the oscillator is distinguished from the`downstream' e¡ects on other parts of the brain, such as the cerebral hemispheres, where compensatory mechanisms may be used to restore normal levels of excitability in the face of reduced cationicchannel function.…”

Section: Discussion (A) Geneticsmentioning

confidence: 99%

A ‘sticky’ interhemispheric switch in bipolar disorder?

Pettigrew

Miller

1998

Proc. R. Soc. Lond. B

146

205

View full text Add to dashboard Cite

Despite years of research into bipolar disorder (manic depression), its underlying pathophysiology remains elusive. It is widely acknowledged that the disorder is strongly heritable, but the genetics are complex with less than full concordance in monozygotic twins and at least four susceptibility loci identi¢ed. We propose that bipolar disorder is the result of a genetic propensity for slow interhemispheric switching mechanisms that become`stuck' in one or the other state. Because slow switches are also`sticky' when compared with fast switches, the clinical manifestations of bipolar disorder may be explained by hemispheric activation being`stuck' on the left (mania) or on the right (depression). Support for this sticky' interhemispheric switching hypothesis stems from our recent observation that the rate of perceptual alternation in binocular rivalry is slow in euthymic subjects with bipolar disorder (n 18, median 0.27 Hz) compared with normal controls (n 49, median 0.60 Hz, p50.0005). We have presented evidence elsewhere that binocular rivalry is itself an interhemispheric switching phenomenon. The rivalry alternation rate (putative interhemispheric switch rate) is robust in a given individual, with a test^retest correlation of more than 0.8, making it suitable for genetic studies. The interhemispheric switch rate may provide a trait-dependent biological marker for bipolar disorder.

show abstract

Supersensitivity to melatonin suppression by light in young people at high risk for affective disorder A preliminary report

Cited by 103 publications

References 0 publications

Melatonin Sensitivity to Dim White Light in Affective Disorders

Melatonin Sensitivity to Dim White Light in Affective Disorders

Chronobiological Basis of Female-Specific Mood Disorders

A ‘sticky’ interhemispheric switch in bipolar disorder?

Contact Info

Product

Resources

About