Association of adverse childhood environment and 5-HTTLPR Genotype with late-life depression.
OBJECTIVE
Neurobiological and clinical studies suggest that childhood maltreatment may result in functional and structural nervous system changes that predispose the individual to depression. This vulnerability appears to be modulated by a polymorphism in the serotonin gene-linked promoter region (5-HTTLPR). Little is known, however, about the persistence of this vulnerability across the life span, although clinical studies of adult populations suggest that gene-environment interaction may diminish with aging.


METHODS
Depressive symptomatology and adverse and protective childhood events were examined in a population of 942 persons aged 65 years and older, taking into account sociodemographic characteristics and proximal competing causes of depression (widowhood, recent life events, vascular and neurologic disorder, and disability). Subjects were recruited between March 1999 and February 2001 and were diagnosed as depressed if they met 1 of 3 criteria: a diagnosis of major depression on the Mini-International Neuropsychiatric Interview, a score higher than 16 on the Center for Epidemiologic Studies-Depression Scale, or current treatment with an antidepressant.


RESULTS
Exposure to traumatic events in childhood doubled the risk of late-life depression and increased the risk of repeated episodes. Not all events were found to be pathogenic; significant risk was associated with excessive sharing of parental problems, poverty or financial difficulties, mental disorder in parents, excessive physical punishment, verbal abuse from parents, humiliation, and mistreatment by an adult outside the family. Interactions were observed between the 5-HTTLPR long (L) allele, poverty, and excessive sharing of parental problems.


CONCLUSIONS
Certain types of childhood trauma continue to constitute risk factors for depression in old age, outweighing more proximal causes. Gene environment vulnerability interaction is linked in older age to the L-carrying genotype, modulating the effects of general environmental conditions rather than aggressive acts on the individual, perhaps due to increased cardiac reactivity.
Ritchie
Karen
K
Inserm, U888, Montpellier, France. karen.ritchie@inserm.fr
Jaussent
Isabelle
I
Stewart
Robert
R
Dupuy
Anne-Marie
AM
Courtet
Philippe
P
Ancelin
Marie-Laure
ML
Malafosse
Alain
A
D000328:Adult; D054523:Adult Survivors of Child Abuse / Q000523:psychology* / Q000706:statistics & numerical data*; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D002648:Child; D016241:Child of Impaired Parents / Q000523:psychology / Q000706:statistics & numerical data; D003865:Major Depressive Disorder / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D005602:France / Q000453:epidemiology; D005838:Genotype; D006801:Humans; D008016:Life Change Events; D008137:Longitudinal Studies; D008297:Male; D011110:Polymorphism, Genetic; D011569:Psychiatric Status Rating Scales / Q000706:statistics & numerical data; D012189:Retrospective Studies; D012307:Risk Factors; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics*; D012931:Social Environment; D013315:Stress, Psychological
C493230:SLC6A4 protein, human; D050486:Serotonin Plasma Membrane Transport Proteins