The researchers from University College and the Institute of Psychiatry, at King's College, in London, wanted to learn more about the way the FTO gene on human chromosome 16, which has been linked to obesity, works and whether it had an impact on the ability to burn calories or appetite.
The FTO gene is the first common gene to be linked to obesity in Caucasian populations and the researchers found those with copies of the gene's risky variant were less likely to have their appetite "switched off" when they should be full.
Previous research has indicated that adults with two copies of the higher risk version of the gene are on average 3kg heavier, and those with a single copy are on average 1.5kg heavier, than those without the gene.
The researchers tested whether the children age 8 and 11 carrying the higher risk gene variation had an altered appetite through height, weight and waist circumference measurements, and gave parents a questionnaire which asked about their child's eating habits.
They found that such children tended to overeat and to struggle to recognise when they were full and the effect of the gene on appetite was the same regardless of age, sex, socio-economic background and body mass index.
Lead researcher Professor Jane Wardle says it is not simply the case that people who carry the risky variant of this gene automatically become overweight, but they are more susceptible to overeating, which makes them significantly more vulnerable to the modern environment which is confronting with large portion sizes and limitless opportunities to eat.
Professor Wardle says the effect of the gene in isolation was relatively small and it was likely that many genes contributed to obesity and appetite, each making a small contribution, but together creating a substantial effect.
The researchers believe that the results help to uncover how genes can make us fat.
The study is published in the Journal of Clinical Endocrinology & Metabolism.
Of 1,674 participants who were free of dementia at the start of the study, 27 percent, or 452 people, took statins at some point in the study. Over the five-year follow up period, 130 participants developed dementia or cognitive impairment. Researchers adjusted for factors such as education, smoking status, the presence of a particular gene thought to predict dementia, and history of stroke or diabetes.
"We aren't suggesting that people should take statins for purposes other than what they are indicated for, but hopefully this study and others will open the door to statin testing for dementia and other types of cognitive impairment," Haan said.
It's not clear exactly how statins work to decrease the development of dementia. An emerging risk factor for dementia is high insulin, Haan said, and one theory is that statins may work on those insulin pathways in a way that lowers the high insulin levels in the brain that can lead to the classic Alzheimer's pathology.
Statins lowered the risk of dementia in all participants, but the statins had more of an impact on the group at high risk due to metabolic syndrome. The next step, Haan said, is to determine exactly how the statins work on the biochemical pathways involved in dementia.
umich/