“Paternal obesity is an independent risk factor for ASDs [autism spectrum disorders] in children” according to new research from Pål Surén and colleagues based on their analysis of data from The Norwegian Mother and Child Cohort Study (MoBa).
Looking at the family records for over 90,000 women who were pregnant in Norway between 1999 and 2008, and analysing questionnaire responses completed by mothers and fathers on the state of their physical health during the pregnancy period, researchers linked data to offspring who were subsequently referred and diagnosed with an autism spectrum condition. They found only a weak connection between maternal reports of obesity, defined as having a body mass index (BMI) equal to or above 30, but a stronger correlation between obesity in fathers and subsequent risk of offspring autism. In the case of Asperger syndrome, there was double the risk of an offspring diagnosis when the father was categorised as obese.
“We were very surprised by these findings because we expected that maternal obesity would be the main risk factor for the development of ASD. It means that we have had too much focus on the mother and too little on the father. This probably reflects the fact that we have given greater focus to conditions in pregnancy, such as the growth environment for the foetus in the womb than both environmental and genetic factors before conception,”
says Surén commenting on their latest research.
Previous research had suggested that maternal obesity before and during pregnancy may have been a risk factor for autism although the current study seemed to downplay this risk. The reliance on retrospective data and the use of BMI as a marker for weight categorisation (for example, taking no account of muscle mass) might be considered weaknesses to the latest Surén research. That being said, the MoBa data represents a comprehensive resource for looking at various factors which may impact on offspring development.
Further research is required to evaluate the relationship between paternal obesity and offspring autism risk including the possibility of shared genetic issues to account for results. The authors also suggested further explanations may be found in the science of epigenetics, that is alterations to gene function not attributed to structural changes to the genome; potentially implicating more external factors to account for the relationship such as environmental exposures or nutritional variables.
* Surén P. et al. Parental Obesity and Risk of Autism Spectrum Disorder. Pediatrics. 2014. April 7.
Further commentary on this study can be found at: http://questioning-answers.blogspot.fr/2014/04/dads-obesity-and-risk-of-offspring-autism.html