<img decoding="async" class="alignright size-full wp-image-7570" src="https://blog-api.23andme.com/wp-content/uploads/2010/10/apples-and-pears3.jpg" alt="" width="335" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/10/apples-and-pears3.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2010/10/apples-and-pears3-300x199.jpg 300w" sizes="(max-width: 425px) 100vw, 425px" />
You’ve probably heard about the fruit-based analogies to describe body shape. “Apples” tend to carry more weight around their waist whereas “pears” tend to be heavier around the hips and thighs. But the differences between apples and pears extend beyond simple appearance. Studies have shown that physical shape, primarily where you carry your excess weight, can have a profound impact on your overall health. Bad news for the apples &#8230; people who are rounder around the middle appear to be at greater risk for developing heart disease and type 2 diabetes than their pear-counterparts.
So, which fruit are you? One way to determine your body fat distribution pattern is to calculate your waist-hip ratio (WHR) by dividing the distance around your waist (measured just above the belly button) by the distance around your hips (measured at the widest part). A WHR over 0.8 for women or 0.95 for men is considered high and categorized as a risk factor for metabolic disease.
In a recent publication from <a title="Nature Genetics" href="https://dx.doi.org/10.1038/ng.685" target="_blank" rel="noopener">Nature Genetics</a>, a team of scientists from the Genetic Investigation of Anthropometric Traits (GIANT) report their findings from a two-phase study into how genetics influence waist and hip size. This investigation, including nearly 200,000 people of European descent drawn from more than 50 studies, is one of the largest genetic studies ever carried out for any trait. Following an impressive data analysis effort, authors announced the identification of 14 SNPs (13 new and one previously reported) associated with body fat distribution.
In addition to exciting new SNP discoveries, results from this study suggest that genetics play a more significant role in determining body fat distribution in women than in men. In women, not only do more of the SNPs associate with WHR (12 of 14 SNPs compared to three of 14 SNPs in men), but they also appear to have greater influence on waist and hip size.
The study authors also hint at potential associations between the 14 SNPs identified in their research and common risk factors for heart disease and type 2 diabetes. For example, the T version of showed strong associations with elevated triglycerides and insulin resistance. The risky versions of , ( in the 23andMe database*), and also demonstrate significant association with type 2 diabetes.
As with obesity and many other conditions with a strong environmental component, genes only account for a small piece of the puzzle underlying variability in body fat distribution.  Even so, this study establishes an important observation: the SNPs associated with body fat distribution (measured by WHR) appear to be mostly distinct from those SNPs associated with overall body fat content (measured by body mass index (BMI)). Since the location of body fat plays a pivotal role in disease risk, a better understanding of the genetic risk factors underlying increased waist and hip size may lead to improved therapies or lifestyle recommendations.

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Apple or Pear? How Genes Help Shape Your Shape

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In 2009, 27% of Americans met the clinical criteria for obesity–a body mass index (BMI) of 30 or greater–7 percentage points higher than a mere 9 years earlier. Even this staggering 27% estimate may be too low. A large National Health and Nutrition Examination Study (NHANES) study estimated the prevalence of obesity at 34%. No wonder losing weight is a national preoccupation.
But how much control do we really exert over our weight? We all know people who seemingly gorge themselves at every meal but never gain an ounce and others who all too easily pack on the pounds.
In a paper published in <a href="http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.1000332" target="_blank" rel="noopener noreferrer">PLoS Medicine</a>, Shengxu Li and colleagues tackled a piece of that puzzle. Using a sample of 20,000 Europeans, they compared the predictive power of 12 SNPs known to influence BMI in sedentary and physically active individuals. While carrying a greater number of risky versions of these SNPs was associated with higher BMI in both groups, the association was much weaker in the physically active.
In the sedentary group, each additional risky variant translated to a 0.21 increase in BMI, or an extra 1.3 lbs (592 g) for someone 5&#8217;7 (170 cm). By comparison, in the physically active people, each additional risky variant  translated to a 0.13 increase in BMI, or an extra 0.8 lbs (397 g) for someone 5&#8217;7 (170 cm). Leading a physically active lifestyle, they concluded, was associated with a 40% reduction in the genetic predisposition to obesity.
Although we only have 9 of the 12 SNPs covered in our database, a quick analysis using our customers&#8217; data replicated their findings. Carrying more risky variants was predictive of a higher BMI overall, but this effect was much more pronounced among our customers who reported low levels of physical activity.
Of course, the 12 SNPs under investigation do not represent the totality of genetic predisposition to obesity. In fact, the 12 SNPs combined accounted for only 1.2% of the variation in weight among the sedentary individuals, and even less, 0.6%, among the physically active. Other genetic factors not measured in this research, such as rare variants associated with BMI, likely play a role as well.

Jeans Too Tight? Don’t Just Blame Your Genes.

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We all know people struggling with weight issues. Maybe they’re overweight and can’t seem to lose the pounds no matter what new diet or exercise regime they try. Or, maybe they’re underweight and have a hard time bulking up no matter how many donuts they consume or weights they lift. Clearly, there’s more to your weight than what you eat.
Researchers have been hot on the trail of genetic factors influencing obesity ever since the <a href="http://www.hhmi.org/genesweshare/d130.html">discovery of the gene coding for leptin</a>, a protein responsible for telling the brain “I’m full.” But just having a genetic variant linked to obesity doesn’t mean stretchy waist pants are a certainty — many factors interact with diet to affect your health.
Several years ago, a team led by Dolores Corella and Jose Ordovas discovered that the variant in the APOA2 gene is <a href="http://www.clinchem.org/cgi/content/full/53/6/1144">associated with obesity</a> as well as general food measures like total calorie and protein intake. In a new study published last month in the <a href="http://archinte.ama-assn.org/cgi/content/abstract/169/20/1897">Archives of Internal Medicine</a>, Corella and Ordovas replicated the association with obesity in three independent populations  and determined that the association depends specifically on the amount of saturated fat in the diet. More than 3400 individuals across three population groups — 2532 people of European ancestry and 930 Hispanics from Puerto Rico — participated in the study, providing data on dietary intake, physical activity, body mass index (BMI) and other variables.
In the two European populations, individuals with two copies of the C version of had significantly higher calorie intake than individuals with at least one copy of the T version  — a finding that echoed their previous work. When Corella and her colleagues looked at BMI, however, they found that was significantly associated with higher BMI, but only in individuals who consumed high amounts of saturated fat, irrespective of total calorie intake.
In all three populations, there was no association between genotype and BMI in individuals who consumed diets low in saturated fat. Furthermore, there was no significant difference in BMI for individuals who had low intake and individuals who had high intake if they had at least one copy of the T version. But people with the CC genotype who consumed diets high in saturated fat had significantly higher BMI than people with either the TC or TT genotype who also consumed high saturated fat diets. After combining data from the three groups, Corella’s team determined that individuals with the CC genotype who had high saturated fat intake also had about 1.8 times higher odds of obesity than individuals with the T version  who consumed similar amounts of saturated fat, total calorie intake being equal.
Although earlier research in animals has implicated APOA2 in obesity, its role in human health has been controversial. In this study, Corella and her team show that saturated fat intake can interact with a genetic variant in APOA2 to increase obesity risk. In fact, the variant makes more of a difference the more saturated fat one consumes. While minimizing saturated fat intake continues to be common sense, in a society characterized by rich diets and increasingly sedentary lifestyles, discoveries like this drive home the fact that genetics and environment together form an intricately interwoven picture of our health.
(Many thanks to TRK for bringing this study to our attention!)

Do These Genes Make Me Look Fat? It Depends on What You Eat

<img decoding="async" class="right alignright" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/feetscale.jpg" alt="feetscale.jpg" />The Atkins diet, the South Beach diet, the Grapefruit diet, the Cabbage Soup diet — we know all these fad diets have their limits, because ultimately, the only way to lose weight is to eat fewer calories and burn more.
But have you ever thought about what controls your appetite? What if your body didn’t tell you to stop eating when you’d consumed enough calories?
You&#8217;d gain weight, that&#8217;s what. It&#8217;s long been known that mutations in a gene called MC4R cause mice to become bigger and fatter than their regular counterparts.
It&#8217;s thought that eating a lot causes the body to turn on MC4R, which in turn tells the mice to stop eating by making them feel full. There are also rare variations that disrupt the human MC4R protein and cause children to eat too much, leading to severe childhood obesity.
Interesting, you say, but does this apply to the general population too? Research published online Sunday in the journal <a href="https://www.nature.com/ng/index.html" target="_blank" rel="noopener noreferrer">Nature Genetics</a> suggests that the answer is yes.

A large study of over 77,000 Europeans by <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.140.html" target="_blank" rel="noopener noreferrer">Loos et al.</a> found a SNP near the MC4R gene, rs17782313, that was strongly associated with body mass index (BMI), a measure of obesity. (To calculate your own BMI, go to: http://www.nhlbisupport.com/bmi/bmicalc.htm) They found that each copy of the C version of rs17782313 was associated with an increase of 0.22 BMI units in adults (for a person of my height, 5 ft 3 in, that’s a little over a pound). In children, they found that this SNP had an even larger effect. Unlike the rare changes in MC4R that cause severe childhood obesity, 30 to 50% of the population has at least one copy of the C allele of rs17782313.
A second paper by <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.156.html" target="_blank" rel="noopener noreferrer">Chambers et al.</a>, also published online Sunday in Nature Genetics, studied more than 14,000 Indian Asians and Europeans and found that a different SNP near MC4R, rs12970134, is associated with waist circumference. Each copy of the A version is associated with a 0.88 cm (0.3 in) increase in waist circumference. That means that on average, the waists of people with two copies of the A version of rs12970134 are 0.6 inches larger than the waists of people with two copies of the other version of the SNP. Talk about pinching an inch!
Fortunately for most of us, genes are only one player in our risk for obesity, as our behavior and environment can still play a large role in maintaining a healthy weight.
Calculating your BMI: You can calculate your own BMI using the following formula: multiply your weight in pounds by 0.454 to get your weight in kilograms. Then multiply your height in inches by .0254 to get your height in meters and square the result. Divide your weight in kilograms by your height in meters squared to get your BMI. A BMI less than 18.5 is considered underweight, between 18.5 and 24.9 normal, between 25 and 29.9 overweight, and above 30, obese.

BMI — Page 3

Apple or Pear? How Genes Help Shape Your Shape

Jeans Too Tight? Don’t Just Blame Your Genes.

Do These Genes Make Me Look Fat? It Depends on What You Eat

MC4R Gene Associated with Body Mass

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