Princess Health and Princess Health andPeople with a genetic risk of obesity should avoid saturated fat, national study of 2,800 people suggests.Princessiccia

Princess Health and Princess Health andPeople with a genetic risk of obesity should avoid saturated fat, national study of 2,800 people suggests.Princessiccia

diet genetics nutrition obesity research

Gusty 21:20 Add Comment

A new study shows that avoiding saturated fat may be advantageous for those whose genetic makeup predisposes them to obesity. Researchers from the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University used 63 gene variants associated with obesity to determine a genetic risk score for obesity for more than 2,800 white, American adults participating in two studies about heart disease prevention.

"People with a higher genetic risk score, who also consumed more of their calories as saturated fat, were more likely to have a higher body mass index, the ratio of body weight to height," Newswise reports.

"We already know there are certain genes that interact with dietary fat and affect BMI," said senior author Jose M. Ordovas, Ph.D., director of the Nutrition and Genomics Laboratory at the USDA center and a professor at the Friedman School of Nutrition Science and Policy at Tufts. We "saw that while total fat intake was related to higher BMI, people who were genetically predisposed to obesity and ate the most saturated fat had the highest BMIs."

The study is published in the Journal of the Academy of Nutrition and Dietetics. The findings also take into consideration factors like age, sex and physical activity levels. Ordovas and the other researchers believe that those who have genetic makeups predisposing them to obesity might be more easily affected by saturated fat, which is often found in fatty cuts of meats, butter, cheese and other high-fat dairy products.

Ordovas said that although they cannot yet explain with confidence the "role of saturated fat intake in obesity . . . Some clinical models suggest that saturated fat might interfere with activity in the part of the brain that lets us know we're full, in addition to a few studies in people that suggest a diet high in saturated fat interferes with satiety." Ordovas also said that if additional research could explain the connection between obesity-related genes and saturated fat, people would have even more convincing reasons to eat less saturated fat. (Read more)

Princess Health and A New Understanding of an Old "Obesity Gene". Princessiccia

Princess Health and A New Understanding of an Old "Obesity Gene". Princessiccia

genetics overweight

Gusty 17:13 Add Comment

As you know if you've been following this blog for a while, obesity risk has a strong genetic component. Genome-wide association studies (GWAS) attempt to identify the specific locations of genetic differences (single-nucleotide polymorphisms or SNPs) that are associated with a particular trait. In the case of obesity, GWAS studies have had limited success in identifying obesity-associated genes. However, one cluster of SNPs consistently show up at the top of the list in these studies: those that are near the gene FTO.

As with many of the genes in our genome, different people carry different versions of FTO. People with two copies of the "fat" version of the FTO SNPs average about 7 pounds (3 kg) heavier than people with two copies of the "thin" version, and they also tend to eat more calories (1, 2).

Despite being the most consistent hit in these genetic studies, FTO has remained a mystery. As with most obesity-associated genes, it's expressed in the brain and it seems to respond somewhat to nutritional status. Yet its function is difficult to reconcile with a role in weight regulation:

• It's an enzyme that removes methyl groups from RNA, which doesn't immediately suggest a weight-specific function.
• It's not primarily expressed in the brain or in body fat, but in all tissues.
• Most importantly, as far as we know, the different versions of the gene do not result in different tissue levels of FTO, or different activity of the FTO enzyme, so it's hard to understand how they would impact anything at all.

An important thing to keep in mind is that GWAS studies don't usually pinpoint specific genes. Typically, they tell us that obesity risk is associated with variability in a particular region of the genome. If the region corresponds to the location of a single gene, it's a pretty good guess that the gene is the culprit. However, that's not always the case...

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Princess Health and The Genetics of Obesity, Part III. Princessiccia

Princess Health and The Genetics of Obesity, Part III. Princessiccia

genetics overweight

Gusty 03:00 Add Comment

Genetics Loads the Gun, Environment Pulls the Trigger

Thanks to a WHS reader* for reminding me of the above quote by Dr. Francis Collins, director of the US National Institutes of Health**. This is a concept that helps reconcile the following two seemingly contradictory observations:

1. Roughly 70 percent of obesity risk is genetically inherited, leaving only 30 percent of risk to environmental factors such as diet and lifestyle.
2. Diet and lifestyle have a large impact on obesity risk. The prevalence of obesity has tripled in the last 30 years, and the prevalence of extreme obesity has increased by almost 10-fold. This is presumably not enough time for genetic changes to account for it.

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Princess Health and The Genetics of Obesity, Part II. Princessiccia

Princess Health and The Genetics of Obesity, Part II. Princessiccia

genetics overweight

Gusty 03:00 Add Comment

Rodents Lead the Way

The study of obesity genetics dates back more than half a century. In 1949, researchers at the Jackson Laboratories identified a remarkably fat mouse, which they determined carried a spontaneous mutation in an unidentified gene. They named this the "obese" (ob/ob) mouse. Over the next few decades, researchers identified several other genetically obese mice with spontaneous mutations, including diabetic (db/db) mice, "agouti" (Avy) mice, and "Zucker" (fa/fa) rats.

At the time of discovery, no one knew where the mutations resided in the genome. All they knew is that the mutations were in single genes, and they resulted in extreme obesity. Researchers recognized this as a huge opportunity to learn something important about the regulation of body fatness in an unbiased way. Unbiased because these mutations could be identified with no prior knowledge about their function, therefore the investigators' pre-existing beliefs about the mechanisms of body fat regulation could have no impact on what they learned. Many different research groups tried to pin down the underlying source of dysfunction: some thought it was elevated insulin and changes in adipose tissue metabolism, others thought it was elevated cortisol, and a variety of other hypotheses.

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Princess Health and The Genetics of Obesity, Part I. Princessiccia

Princess Health and The Genetics of Obesity, Part I. Princessiccia

genetics overweight

Gusty 04:00 Add Comment

Choosing the Right Parents: the Best Way to Stay Lean?

In 1990, Dr. Claude Bouchard and colleagues published a simple but fascinating study demonstrating the importance of genetics in body fatness (1). They took advantage of one of the most useful tools in human genetics: identical twins. This is what happens when a single fertilized egg generates two embryos in utero and two genetically identical humans are born from the same womb. By comparing identical twins to other people who are not genetically identical (e.g., non-identical twins), we can quantify the impact of genes vs. environment on individual characteristics (2).

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Princess Health and Two gene variants identified as risk factors for childhood obesity.Princessiccia

Princess Health and Two gene variants identified as risk factors for childhood obesity.Princessiccia

childhood obesity genetics research

Gusty 08:40 Add Comment

The largest ever genome-wide study has identified two new gene variants that increase the risk of common childhood obesity.

"We have definitively identified and characterized a genetic predisposition to common childhood obesity," said lead investigator Struan F.A. Grant, associate director of the Center for Applied Genomics at The Children's Hospital of Philadelphia.

The analysis included 14 previous studies "encompassing 5,530 cases of childhood obesity and 8,300 control subjects, all of European ancestry," reports research-reporting service Newswise.

The study team identified two novel loci, or specific locations of a gene or DNA sequence on a chromosome. One is near the OLFM4 gene on Chromosome 13, the other in the HOXB5 gene on Chromosome 17. There was a degree of evidence for two other gene variants as well. "The known biology of three of the genes hints at a role of the intestine, although their precise functional role in obesity if currently unknown," Newswise reports. (Read more)