BACKGROUND: Paternal aging is associated with premeiotic damage to spermatogonia, a mechanism by which new point mutations are introduced into the gene pool. We hypothesized that paternal age might contribute to preeclampsia. METHODS: We studied the incidence of preeclampsia in 81,213 deliveries surveyed in 1964-1976 in the Jerusalem Perinatal Study. We controlled for maternal age, parity and other risk factors using logistic regression. RESULTS: Preeclampsia was reported in 1303 deliveries (1.6%). Compared with fathers age 25-34 years, the odds ratios (ORs) for preeclampsia were 1.24 (95% confidence interval = 1.05-1.46) for age 35-44 and 1.80 (1.40-2.31) for age 45+. For fathers age <25, the OR was 1.25 (1.04-1.51). Although weaker than maternal age effects, paternal effects were consistent within subgroups of other variables. CONCLUSIONS: These findings support the hypothesis that a modest proportion of preeclampsia might be explained by new mutations acquired from fathers and add to a growing body of evidence for paternal age effects in birth defects, neuropsychiatric disease and neoplasia.
BACKGROUND: Paternal aging is associated with premeiotic damage to spermatogonia, a mechanism by which new point mutations are introduced into the gene pool. We hypothesized that paternal age might contribute to preeclampsia. METHODS: We studied the incidence of preeclampsia in 81,213 deliveries surveyed in 1964-1976 in the Jerusalem Perinatal Study. We controlled for maternal age, parity and other risk factors using logistic regression. RESULTS: Preeclampsia was reported in 1303 deliveries (1.6%). Compared with fathers age 25-34 years, the odds ratios (ORs) for preeclampsia were 1.24 (95% confidence interval = 1.05-1.46) for age 35-44 and 1.80 (1.40-2.31) for age 45+. For fathers age <25, the OR was 1.25 (1.04-1.51). Although weaker than maternal age effects, paternal effects were consistent within subgroups of other variables. CONCLUSIONS: These findings support the hypothesis that a modest proportion of preeclampsia might be explained by new mutations acquired from fathers and add to a growing body of evidence for paternal age effects in birth defects, neuropsychiatric disease and neoplasia.
Authors: Susan Harlap; A Michael Davies; Lisa Deutsch; Ronit Calderon-Margalit; Orly Manor; Ora Paltiel; Efrat Tiram; Rivka Yanetz; Mary C Perrin; Mary B Terry; Dolores Malaspina; Yechiel Friedlander Journal: Paediatr Perinat Epidemiol Date: 2007-05 Impact factor: 3.980
Authors: V Katsi; I Felekos; C Siristatidis; S Kasioni; A Drakontaidis; G Farmakides; T Makris; C Aggeli; P Nihoyannopoulos; D Tousoulis; I Kallikazaros Journal: Curr Hypertens Rep Date: 2015-08 Impact factor: 5.369
Authors: Mark G A Opler; Susan Harlap; Katherine Ornstein; Karine Kleinhaus; Mary Perrin; James E Gangwisch; Pesach Lichtenberg; Benjamin Draiman; Dolores Malaspina Journal: Schizophr Res Date: 2010-02-13 Impact factor: 4.939
Authors: K Kleinhaus; M C Perrin; O Manor; Y Friedlander; R Calderon-Margalit; S Harlap; D Malaspina Journal: Eur J Obstet Gynecol Reprod Biol Date: 2008-09-03 Impact factor: 2.435
Authors: K Kleinhaus; S Harlap; M C Perrin; O Manor; R Calderon-Margalit; Y Friedlander; D Malaspina Journal: Schizophr Res Date: 2008-08-23 Impact factor: 4.939