domingo, 12 de octubre de 2014

European Journal of Human Genetics - Do early paternal exposures to lifestyle factors such as smoking increase the risk of chronic diseases in the offspring[quest]

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European Journal of Human Genetics - Do early paternal exposures to lifestyle factors such as smoking increase the risk of chronic diseases in the offspring[quest]







European Journal of Human Genetics advance online publication 8 October 2014; doi: 10.1038/ejhg.2014.206

The legacy of paternal smoking

Do early paternal exposures to lifestyle factors such as smoking increase the risk of chronic diseases in the offspring?

Adelheid Soubry1, Geert Verbeke2 and Cathrine Hoyo3,4
  1. 1Epidemiology Research Group, KU Leuven, Leuven, Belgium
  2. 2I-Biostat, KU Leuven, Leuven, Belgium
  3. 3Department of Biological Sciences, NC State University, Raleigh, NC, USA
  4. 4Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC, USA
Correspondence: , E-mail: adelheid.soubry@hotmail.com
The results of a recent epidemiological study on the effects of paternal smoking on children's body composition published in EJHG1 contribute to the limited research in humans on environmentally induced risk for chronic diseases in the next generation(s) through the father. Inherited non-genetic changes may be an evolutionary response to adapt relatively quickly to environmental variations. However, if an individual is exposed to an adverse environmental exposure, such as a new pollutant, chemical, or pathogen, during a critical developmental stage in life, the risk of developing an endocrine, metabolic, or mental disorder or even cancer in the offspring may increase. Thus far, most research in this area focuses on maternal contributions, while a potential transgenerational epigenetic effect through the father has generally been underexplored. The Avon Longitudinal Study of Parents and Children (ALSPAC), led by Pembrey, showed that adolescent sons of fathers who started smoking before puberty are at high risk of being obese.1Although no underlying biological mechanism has been shown yet, this fascinating finding suggests that cigarette smoke metabolites may induce epigenetic changes during prepubertal production of spermatogonia in the testes. Remarkably, in order to persist until the offspring’s early adulthood, this epigenetic information needs to be carried on through all developmental processes, including spermatogenesis, conception, and embryonic growth. An earlier historical Swedish study by the same authors showed a similar transgenerational response to food availability. The longevity of men was decreased if their paternal grandfathers had been exposed to an excess of food during the slow growth period, before the prepubertal growth peak.2 These gender- and time-specific associations suggest that the epigenome of the male germ line is malleable by environmental factors at specific timepoints in life. An epigenetic link in humans was shown for the first time in the Newborn Epigenetic Study (NEST); this NC-based birth cohort showed that imprint-regulatory regions of newborns are differentially methylated in response to paternal obesity.3,4

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