Paternal obesity could be a greater risk factor than maternal obesity in developmental disorders among offspring, according to a Norwegian study.
Pål Surén, MD, MPH, who was described as the first researcher to study the role of paternal obesity in autism, emphasized that the theory requires much more research before scientists can discuss possible causal relationships.
We have a long way to go, Surén said in a news release. We must study genetic factors in the relationship between obesity and autism, as well as environmental factors associated with switching the genes on or off so-called epigenetic factors.
For the study, published April 7 on the website of the journal Pediatrics, Surén and his fellow researchers used data from the Norwegian Mother and Child Cohort Study. The researchers studied questionnaire data about more than 90,000 Norwegian children at ages 3, 5 and 7, whose mothers had answered detailed questions about their own mental and physical health and about their children. The fathers completed a questionnaire about their mental and physical health while their partner was pregnant.
The researchers also collected data from the Norwegian Patient Registry and from studies of children who were referred for evaluation and treatment of possible autism or Aspergers syndrome. By the end of the follow-up period, the children were ages 4 to 13.
In all, 419 children, approximately 0.45% of the sample, had an autism spectrum diagnosis. That figure is slightly lower than in the general population (0.8%) because of the difficulty of diagnosing autism among the youngest children, the researchers noted.
In the sample, 22% of the mothers and 43% of the fathers were overweight, with a body mass index of between 25 and 30. Approximately 10% of mothers and fathers were obese, with a BMI of 30 or more.
The researchers found that maternal obesity had little association with the development of autism in the child. However, they found a doubled risk for development of autism and Aspergers syndrome in the child if the father was obese, compared with a normal-weight father.
We were very surprised by these findings because we expected that maternal obesity would be the main risk factor for the development of ASD, Surén said. 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 fetus in the womb, than both environmental and genetic factors before conception.
The researchers adjusted for variables that may also be associated with the development of autism in the child. In addition to adjusting for maternal obesity, they considered education, age, smoking, mental disorders, hormone therapy before pregnancy, use of folic acid, maternal diabetes, preeclampsia and the babys weight at birth.
Surén believes that the finding about paternal obesity is sound. The researchers found that the risk remained unchanged when adjusted for sociodemographic and lifestyle factors.
Our findings therefore suggest that there may be a genetic link between obesity in the father and the development of ASD in the child, Surén said.
He points out that genetic mutation may play a role in the development of both extreme obesity and autism. Researchers have shown, for example, that missing a section of chromosome 16 can lead to morbid obesity or developmental disorders in children. Mutations may be a basis for the development of a number of complex syndromes and diseases.
Another explanation may lie in epigenetics, the researchers noted. Epigenetic changes do not mean the gene is altered, but that the gene is activated or inactivated as a result of environmental conditions. Switching a gene on or off at the wrong time and place can lead to adverse consequences for the individual, and the epigenetic changes can be passed on to the next generation.
We still know very little about how epigenetic changes in germ cells are affected by obesity or other environmental factors, but animal experiments have shown that obese males have offspring with altered gene expression in early growth regulation, Surén said.