Parental Obesity Linked to Delays in Child Development, Study Suggests
Children of obese parents may be at risk for developmental delays, according to a study by researchers at NIH. The investigators found that children of obese mothers were more likely to fail tests of fine motor skill—the ability to control movement of small muscles, such as those in the fingers and hands. Children of obese fathers were more likely to fail measures of social competence and those born to extremely obese couples also were more likely to fail tests of problem-solving ability.
The study, which appeared in Pediatrics, was conducted by scientists at NICHD.
“The previous U.S. studies in this area have focused on the mothers’ pre- and post-pregnancy weight,” said the study’s first author, Dr. Edwina Yeung, an investigator in NICHD’s Division of Intramural Population Health Research. “Our study is one of the few that also includes information about fathers, and our results suggest that dad’s weight also has significant influence on child development.”
Yeung and her coauthors cited research indicating that about 1 in 5 pregnant women in the United States is overweight or obese.
More than 5,000 women enrolled in the study roughly 4 months after giving birth between 2008 and 2010.
Compared to children of normal weight mothers, children of obese mothers were nearly 70 percent more likely to have failed the test indicator on fine motor skill by age 3. Children of obese fathers were 75 percent more likely to fail the test’s personal-social domain—an indicator of how well they were able to relate to and interact with others by age 3. Children with two obese parents were nearly three times more likely to fail the test’s problem-solving section by age 3.
It is not known why parental obesity might increase children’s risk for developmental delay.
If the link between parental obesity and developmental delays is confirmed, the authors wrote, physicians may need to take parental weight into account when screening young children for delays and early interventional services.
TCGA Study Identifies Genomic Features of Cervical Cancer
Investigators with the Cancer Genome Atlas (TCGA) Research Network have identified novel genomic and molecular characteristics of cervical cancer that will aid in the sub-classification of the disease and may help target therapies that are most appropriate for each patient.
The new study, a comprehensive analysis of the genomes of 178 primary cervical cancers, found that over 70 percent of the tumors had genomic alterations in either one or both of two important cell signaling pathways. The researchers also found, unexpectedly, that a subset of tumors did not show evidence of human papillomavirus (HPV) infection. The study included authors from NCI and NHGRI and appeared Jan. 23 in Nature.
Cervical cancer accounts for more than 500,000 new cases of cancer and more than 250,000 deaths each year worldwide. “The vast majority of cases of cervical cancer are caused by persistent infection with oncogenic types of HPV,” said NCI acting director Dr. Douglas Lowy. “Effective preventive vaccines against the most oncogenic forms of HPV have been available for a number of years, with vaccination having the long-term potential to reduce the number of cases of cervical cancer. However, most women who will develop cervical cancer in the next couple of decades are already beyond the recommended age for vaccination and will not be protected by the vaccine. Therefore, cervical cancer is still a disease in need of effective therapies. This latest TCGA analysis could help advance efforts to find drugs that target important elements of cervical cancer genomes in addition to the HPV genes.”
An aspect of the study that is of particular interest was the identification of a unique set of eight cervical cancers that showed molecular similarities to endometrial cancers. These endometrial-like cancers were mainly HPV-negative.
“The identification of HPV-negative endometrial- like tumors confirms that not all cervical cancers are related to HPV infection and that a small percentage of cervical tumors may be due to strictly genetic or other factors,” said Dr. Jean- Claude Zenklusen, director of the TCGA program office. “This aspect of the research is one of the most intriguing findings to come out of the TCGA program, which has been looking at more than 30 tumor types over the past decade.”
Sex Hormone-Sensitive Gene Complex Linked to Premenstrual Mood Disorder
NIH researchers have discovered molecular mechanisms that may underlie a woman’s susceptibility to disabling irritability, sadness and anxiety in the days leading up to her menstrual period. Such premenstrual dysphoric disorder (PMDD) affects 2 to 5 percent of women of reproductive age, whereas less severe premenstrual syndrome (PMS) is much more common.
“We found dysregulated expression in a suspect gene complex which adds to evidence that PMDD is a disorder of cellular response to estrogen and progesterone,” said Dr. Peter Schmidt of NIMH’s Behavioral Endocrinology Branch. “Learning more about the role of this gene complex holds hope for improved treatment of such prevalent reproductive endocrine-related mood disorders.”
Schmidt, Dr. David Goldman of NIAAA and colleagues reported on their findings Jan. 3 in the journal Molecular Psychiatry.
“This is a big moment for women’s health, because it establishes that women with PMDD have an intrinsic difference in their molecular apparatus for response to sex hormones—not just emotional behaviors they should be able to voluntarily control,” said Goldman.
“For the first time, we now have cellular evidence of abnormal signaling in cells derived from women with PMDD and a plausible biological cause for their abnormal behavioral sensitivity to estrogen and progesterone,” said Schmidt.
Using cutting edge “disease in a dish” technologies, the researchers are now following up the leads discovered in blood cell lines in neurons induced from stem cells derived from the blood of PMDD patients. They hope to gain a more direct window into the gene complex’s role in the brain.