OBESITY: last news
25.03.2014 16:13
One-third of kids with obesity 'metabolically healthy,' study shows
Geoff Ball is an associate professor of pediatrics at UAlberta and clinical director of the Stollery Children's Hospital's Pediatric Centre for Weight and Health.
Digits on a scale can help determine a child's weight, but their overall health status can be influenced by other factors such as physical activity, diet and screen time, according to new research from the University of Alberta and Alberta Health Services.
A study of 181 children with obesity aged eight to 17 years old showed that up to a third could be classified as "metabolically healthy," meaning they're not imminently at risk of developing insulin resistance—a precursor to Type 2 diabetes—high blood pressure, high cholesterol or other obesity-related diseases.
"It's not all about fat, even for kids who meet the definition of obesity," explained Geoff Ball, senior author and associate professor of pediatrics in the U of A's Faculty of Medicine & Dentistry, and clinical director of Stollery Children's Hospital's Pediatric Centre for Weight and Health, a weight management clinic for children with obesity. "Lifestyle behaviours—how physically active they are and what they eat—those things have an effect on their health, independent of fatness."
A PhD in nutrition and metabolism, Ball and his team studied five years' worth of clinical data, tracking the age and body composition of obese children, lifestyle behaviours such as physical activity and diet, along with clinical indicators associated with obesity such as insulin resistance, blood pressure, and fat and glucose levels in the blood.
Fewer calories consumed, less screen time
Though numerous studies have explored whether patients with obesity can be metabolically healthy, few have focused on children. In addition to being more physically active, metabolically healthier children were younger, shorter, lighter and less overweight than their metabolically unhealthy peers. They also spent less time in front of the TV, computer or video game console and ate fewer overall calories, including less fat and fewer servings of meat.
The study included traditional measures of obesity such as body mass index, which factors in an individual's height and weight but doesn't tell the whole story, Ball said.
"Obesity is often described as a complex disease with lots of causes and lots of consequences. Not everyone has the same consequences," he said. "Someone with Type 2 diabetes could have less body fat than somebody who has quite a bit more body fat and doesn't have Type 2 diabetes. There is considerable variability between individuals."
Ball said the findings should help physicians and other health professionals understand the complexity of obesity for treating patients and prioritizing referral to specialized weight-management care. Roughly two million young, obese Canadians meet eligibility criteria for such treatment—far more than the two dozen or so clinics across the country can accommodate, he added.
For Edmonton-area patients, having access to the comprehensive management approach at the Stollery's Pediatric Centre for Weight and Health means families receive the most appropriate intervention based on their health status and individual needs. The multidisciplinary team, including a physician, registered nurse, registered dietitian, exercise specialist, and psychologist provide healthy lifestyle messages to children and families that assist them on their journey towards greater health and well-being.
National study recruiting 1,600 children
Ball's team is now focusing on a larger national study, including what happens to children with obesity—metabolically healthy or otherwise—over time and whether risks of obesity-related illness eventually catch up. That work will see the researchers recruit 1,600 Canadian children currently receiving weight-management care and follow them over several years through lifestyle interventions that focus on improving health and well-being.
Ball said these kids and their families are accessing health services that hopefully have a positive effect on their health and well-being. Health professionals need to know whether children who are metabolically healthy stay that way over time as they mature and if there are conditions in the health system and beyond that help make it possible.
"Since most children with obesity find it challenging to lose and maintain weight loss over time, improving metabolic health by being physically active and eating healthfully is an important result in and of itself."
Ball's research was published in the journal Diabetes Care and funded by Alberta Innovates – Health Solutions and the Canadian Institutes of Health Research.
Salt, Obesity May Prematurely Age Young Cells
Published: Mar 20, 2014
By Salynn Boyles, Contributing Writer, MedPage Today
High sodium intake and obesity may act synergistically to accelerate cellular aging in adolescents, according to new research presented Thursday afternoon at the American Heart Association's EPI/NPAM Scientific Sessions 2014.
The study examined the effect of a high salt diet on telomere length in normal weight and overweight/obese teens.
After controlling for factors known to shorten telomeres, researchers observed a statistically significant interaction between weight and sodium intake. Telomere length was significantly shorter in overweight or obese adolescents who had a high sodium intake than in those with low sodium intake (telomere to single gene (TS) ratio, 1.24 ±0.22 versus 1.32 ± 0.21; P=0.02). The same was not true among the normal-weight teens (TS, 1.29 ± 0.24 versus 1.30 ± 0.24; P=0.69).
Telomeres are the protective end-caps on chromosomes that shorten with each round of cell division. When they reach a certain critical length they signal the cell to stop dividing.
Previous studies have suggested that telomere shortening influences cellular aging, and smoking, emotional stress, advancing age, and lack of physical exercise have all been shown to reduce telomere size.
Researcher Haidong Zhu, MD, an assistant professor of pediatrics at the Medical College of Georgia in Augusta, said the new study is among the first to suggest that increased salt intake may also shorten telomere size.
"It is well known that a high salt diet is an important risk factor for hypertension and cardiovascular disease, but the impact of a high salt diet on cardiovascular aging has not been well understood," she told MedPage Today. "This is early research, and it needs to be replicated. But it does suggest that high sodium intake impacts the telomere shortening process."
The study included 766 adolescents between the ages of 14 and 18 who were divided into two salt-intake groups based on self-reported 7-day, 24-hour food-frequency questionnaires. From these assessments it was determined that the low-intake teens consumed, on average, 2,388 mg/day of sodium, while high-intake teens consumed 4,142 mg/day of sodium.
The American Heart Association recommends consuming no more than 1,500 mg of sodium a day -- or about 2/3 of a teaspoon.
After adjusting for age, sex, race, energy intake, Tanner stage, and vigorous physical activity, multiple linear regression analysis revealed that higher dietary sodium intake was associated with shorter leukocyte telomere length in the overweight and obese teens, (beta=-0.37, P=0.045), but not in the teens whose weight was normal.
Zhu said lowering sodium intake in the diets of overweight and obese adolescents by encouraging them to limit processed foods and eat more meals cooked at home may be a more effective strategy for lowering their future heart disease risk than simply telling them to lose weight.
Primary source: American Heart Association Epidemiology & Prevention/Nutrition, Physical Activity & Metabolism Scientific Sessions 2014
Source reference: Zhu H, et al "High sodium intake is associated with short leukocyte telomere length in overweight and obese adolescents" AHA EPI/NPAM 2014; Abstract #MP64.
Increased adiposity and reduced physical activity in children: Cause or effect?
Friday 21 March 2014 - 12am PST
Increased adiposity is likely to cause reduced physical activity in children, according to research published in this week's PLOS Medicine. The results of the study, conducted by Rebecca Richmond and colleagues from the MRC Integrative Epidemiology Unit at the University of Bristol, UK, suggest that promoting weight loss in overweight and obese children might also increase childhood activity levels.
Previous studies have shown an association between low physical activity and higher body mass index (BMI) in children but were not able to determine whether childhood adiposity influences physical activity levels. To address this question, the authors analyzed a panel of genes reliably associated with adiposity to examine whether children with a genetic predisposition for increased BMI were more likely to have lower rates of physical activity, which would imply a causal effect.
Because there are no common genetic variants known to be linked to reduced physical activity, the researchers could not investigate whether the reverse is also true, namely that genetic predisposition to lower physical activity might also cause higher BMI.
They studied a group of children from the Avon Longitudinal Study of Parents and Children (Children of the 90s/ALSPAC) and measured their BMI and total body fat. A small movement-counting device also recorded the total daily activity of 5,595 of the children. In addition, the researchers examined the children's genetic make-up for the presence of variants known to be linked to obesity. By applying Mendelian randomization, a method of using measured variation in genes of known function to assess the causal effect of a modifiable exposure on disease, the authors showed that greater BMI is likely to be causally associated with lower daily activity. Specifically, the analysis demonstrated that for every 3.3 kg/m2 increase in BMI, the children recorded ~2.8 less minutes per day of moderate-to-vigorous-intensity activity.
The findings show that obese children have a propensity to reduced levels of physical activity, which may in turn lead to further weight gain, and support targeting weight reduction in efforts to increase childhood activity levels. According to the authors,
"The study illustrates how genetics can be used to help find causal relationships in complex networks of observational measurements. It is intuitive to think of and observe relationships between factors such as obesity and activity in the population, however it is less clear in which direction these associations lie, whether they are causal or whether it is worth allocating considerable resources to assessing the impact of potential interventions."
Citation: Richmond RC, Smith GD, Ness AR, Hoed Md, McMahon G, et al. (2014) Assessing Causality in the Association between Child Adiposity and Physical Activity Levels: A Mendelian Randomization Analysis. PLoS Med 11(3): e1001618. doi:10.1371/journal.pmed.1001618
Rigid Parenting Style Linked to Obese Kids
Demanding, inflexible approach might foster negative response, study suggests
Rigid Parenting Style Linked to Obese Kids
By Maureen Salamon
WEDNESDAY, March 19, 2014 (HealthDay News) -- Kids with demanding parents who are rigid about rules, stingy with affection and won't discuss limits are far more likely to be obese than children whose parents practice a more balanced parenting style, new research suggests.
Canadian scientists found that obesity rates were about one-third higher in children up to age 11 whose parents used a so-called "authoritarian" parenting style, marked by inflexibility over rules and a lack of emotional responsiveness. In a group of more than 37,000 children, these kids were significantly heavier compared to those whose "authoritative" parents were generally affectionate, willing to discuss behavior limits and set healthy boundaries.
"These findings are consistent with what's been found for other dimensions of children's health -- that an authoritative parenting style [compared to an "authoritarian" approach] is the best one for children's health," said study author Lisa Kakinami, a postdoctoral epidemiologist at McGill University in Montreal.
"Parents with that style are also less likely to have children engaging in risky behaviors," Kakinami said. "The results are what we expected, but it's nice to see it show up in this way."
Although the study, scheduled for presentation Wednesday at an American Heart Association meeting in San Francisco, showed an association between parenting style and obesity rates, it did not prove a cause-and-effect relationship.
Obesity rates in the United States have more than doubled in children (to nearly 18 percent) and have quadrupled in adolescents (to almost 21 percent) in the past 30 years, according to the U.S. Centers for Disease Control and Prevention. In Canada, obesity rates among children and teens have nearly tripled in the past three decades, government officials said.
For this study, children whose weight approached the 98th percentile among others their age and gender were considered obese.
In the nationally representative analysis of Canadian children, Kakinami and her colleagues found that youngsters aged 2 to 5 with authoritarian parents were 30 percent more likely to be obese than those with authoritative parents. Among kids from 6 to 11 years old, the obesity rate was 37 percent higher in the authoritarian group.
The analysis also included two other parenting styles: permissive, defined as responsive but not demanding, and negligent, defined as not demanding and not responsive. Overall, parents in both age groups of children were primarily found to be authoritative.
Dr. Stephen Daniels, pediatrician-in-chief and chairman of pediatrics at Children's Hospital Colorado, said pediatricians and other clinicians have long been curious about the impact of different parenting styles on children's obesity risk and health behaviors.
"What this study does is pin down some specific styles of parenting that seem to have the biggest influence," said Daniels, who wasn't involved in the research. "That's the part that's new and interesting and useful."
Kakinami and Daniels agreed that the study wasn't able to directly identify the reason children with authoritarian parents appeared so much more likely to become obese, but they said many theories make sense.
"It appears that parents who are more engaged in discussing eating and physical activity behaviors with children -- where the child has the ability to participate in making decisions for the family as well as themselves -- seems to be the style that has the best impact," said Daniels, who also is professor and chairman of pediatrics at the University of Colorado School of Medicine.
The higher obesity risk among kids with authoritarian parents "may in part be kids responding negatively to not being able to question things or discuss things," he added.
Kakinami said future research on the topic is needed and should look at the long-term impact of parenting styles on children's weight.
"This study looked at only one point in time, not over the course of childhood," she said.
Data and conclusions presented at meetings typically are considered preliminary until published in a peer-reviewed medical journal.
SOURCES: Lisa Kakinami, Ph.D., postdoctoral epidemiologist, McGill University, Montreal; Stephen Daniels, M.D., Ph.D., pediatrician-in-chief and chairman of pediatrics, Children's Hospital Colorado, and professor and chairman, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colo.; March 19, 2014, presentation, American Heart Association meeting, San Francisco
Last Updated: Mar 19, 2014
Weight-regulating hormones may be impaired by childhood abuse
Monday 24 March 2014 - 12am PST
Childhood abuse or neglect can lead to long-term hormone impairment that raises the risk of developing obesity, diabetes or other metabolic disorders in adulthood, according to a new study published in the Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM).
The study examined levels of the weight-regulating hormones leptin, adiponectin and irisin in the blood of adults who endured physical, emotional or sexual abuse or neglect as children. Leptin is involved in regulating appetite and is linked to body-mass index (BMI) and fat mass. The hormone irisin is involved in energy metabolism. Adiponectin reduces inflammation in the body, and obese people tend to have lower levels of the hormone. The study found dysregulation of these hormones in people who had been abused or neglected as children.
"This study helps illuminate why people who have dealt with childhood adversity face a higher risk of developing excess belly fat and related health conditions," said one of the study's authors, Christos S. Mantzoros, MD, DSc, PhD, of Beth Israel Deaconess Medical Center and the VA Boston Healthcare System, both affiliated with Harvard Medical School in Boston, MA. "The data suggest that childhood adversity places stress on the endocrine system, leading to impairment of important hormones that can contribute to abdominal obesity well into adulthood."
The cross-sectional study examined hormone levels in the blood of 95 adults ages 35 to 65. Using questionnaires and interviews, each participant was assigned a score based on the severity of the abuse or neglect experienced during childhood. Researchers divided the participants into three groups and compared hormone levels in people with the highest adversity scores to the other two-thirds of the participants.
Participants with the highest adversity scores tended to have higher levels of leptin, irisin and the inflammatory marker C-reactive protein in their blood. All of these markers are linked to obesity. In addition, the group of people who suffered the most adversity tended to have lower levels of adiponectin, another risk factor for obesity. Even after researchers adjusted for differences in diet, exercise and demographic variables among the participants, high levels of leptin and irisin continued to be associated with childhood adversity.
"What we are seeing is a direct correlation between childhood adversity and hormone impairment, over and above the impact abuse or neglect may have on lifestyle factors such as diet and education," Mantzoros said. "Understanding these mechanisms could help health care providers develop new and better interventions to address this population's elevated risk of abdominal obesity and cardiometabolic risk later in life."
The study, "Early Life Adversity is Associated with Elevated Levels of Circulating Leptin, Irisin, and Decreased Levels of Adiponectin in Midlife Adults," will appear in the June issue of JCEM.
Kids of authoritarian parents 'more likely to be obese'
Thursday 20 March 2014 - 12am PST
Every parent has their own sense of what is best for raising their child. But a new study, presented at the American Heart Association's Scientific Sessions 2014 meeting, suggests that kids whose parents are strict but not emotionally receptive are more likely to be obese, compared with kids whose parents set boundaries but are affectionate.
According to the American Heart Association (AHA), over one third of children in the US are overweight or obese. Researchers from the latest study say exploring factors at home that may contribute to this public health issue could potentially lead to better interventions.
"Parents should at least be aware of their parenting style," says Lisa Kakinami, PhD, study author from McGill University in Montreal, Canada. "If you're treating your child with a balance of affection and limits - these are the kids who are least likely to be obese."
The research team followed a nationally representative group of Canadian children up to the age of 11 years old. In total, there were 37,577 children who were part of the study.
The team identified four styles of parenting, based on previous parenting theories:
Authoritative: parents are demanding but responsive to child's emotions/issues
Authoritarian: parents are demanding but not responsive
Permissive: parents are responsive but not demanding
Negligent: parents are neither demanding nor responsive.
While the most problematic parenting styles were authoritarian and negligent, the researchers compared kids whose parents were affectionate, had discussions about behavior with their child and who set healthy boundaries (authoritative) with kids whose parents were strict but who did not have much dialogue or show affection (authoritarian).
'Some parenting styles are better than others'
After comparing parents' answers to a cross-sectional survey, the researchers then categorized the parenting styles and studied them in light of children's body mass index (BMI) percentile.
Results showed that kids whose parents were authoritarian had a 30% higher likelihood of being obese in kids between 2 and 5 years old, while kids between 6 and 11 years old had a 37% higher chance. This is compared with children whose parents were authoritative.
Another finding from the study showed that poverty was also associated with childhood obesity, but the researchers say parenting style affected obesity regardless of socioeconomic status.
Dr. Stephen R. Daniels, AHA spokesperson from the University of Colorado School of Medicine, says the study has some important messages for parents:
"It focuses on different styles of parenting and it makes it clear that some styles are better than others in terms of helping their children avoid becoming overweight and obese."
Though the study took place in Canada, Dr. Daniels says he believes the findings will apply to individuals in the US.
He adds that the study gives clinicians something to consider in terms of how they could help parents change their parenting style or, for new parents, to teach them how to adopt a parenting style that is best for the child.
"Ignoring bad behavior but rewarding good behavior is the best way to think about this," he adds. "Punishing bad behavior and ignoring good behavior doesn't work from a psychological standpoint."
Medical News Today recently reported on a study that suggested watching television, using computers and playing video games is linked to poorer well-being for children.
Written by Marie Ellis
Obesity prevention programs might help lower kids' blood pressure
BY SHEREEN JEGTVIG
(Reuters Health) - Programs designed to prevent obesity in children may help lower kids' blood pressure, according to a new review of past studies.
Researchers found that programs targeting both diet and physical activity were more effective than programs that focused on one or the other.
Although it's generally thought of as a disease of middle-aged and elderly people, children can also develop high blood pressure, or hypertension. The American Heart Association recommends that children have yearly blood pressure checks, saying that detecting high blood pressure early will improve a child's health.
Dr. Bonita Falkner told Reuters Health that in the U.S., at least 3.5 percent of children and adolescents have hypertension and another 3.5 percent are at risk because of slightly elevated blood pressure.
Falkner studies hypertension at Jefferson Medical College at Thomas Jefferson University in Philadelphia and was not involved in the new review.
High blood pressure is more common among children who are overweight and obese, so the authors of the review wanted to see if obesity-prevention programs also improved blood pressure in kids.
"Blood pressure during childhood can track into adulthood, and when kids have elevated blood pressure they are more likely to have hypertension when they become adults," coauthor Dr. Youfa Wang told Reuters Health in an email.
Wang, from the University at Buffalo, State University of New York, said the new review is part of a larger comprehensive study on childhood obesity funded by the Agency for Healthcare Research and Quality (AHRQ). The project also includes researchers from the Johns Hopkins Bloomberg School of Public Health in Baltimore.
Wang and his colleagues analyzed data from 23 studies of obesity interventions, including almost 19,000 kids in total. The interventions targeted diet, physical activity or both and lasted at least one year, or six months for school-based programs.
Studies compared children who received a particular intervention with those who did not. In the majority of studies, children were randomly assigned to go through the obesity-prevention program or to be in a comparison group.
The 23 studies tested a total of 28 different interventions. Most of them were done in schools or in combined school and home settings.
Four of the interventions showed positive effects on both body fat and blood pressure. Eleven suggested a beneficial effect on blood pressure, but no effect on body fat.
Wang and his colleagues then combined the findings of 19 studies that reported on systolic blood pressure (the top number in a blood pressure reading) and 18 that reported on diastolic blood pressure (the bottom number).
They found that obesity prevention programs reduced blood pressure among children, by an average of 1.64 millimeters of mercury (mm Hg) in systolic blood pressure and 1.44 mm Hg in diastolic blood pressure.
The reduction was more pronounced in the studies that used a combined approach with both diet and physical activity interventions, the authors wrote in Circulation.
"It's not a huge impact, but the totality of the data that they looked at with the analysis of multiple projects seemed to be optimistic," Falkner said.
"So it's hopeful that some impact can be achieved," she said. "No one really lost a lot of weight but at least with the efforts there was some decrease in blood pressure."
Falkner said measuring blood pressure has become a standard part of children's medical care, just like measuring height and weight. But deciding what's normal and what's high blood pressure is more complicated than it is in adults.
"In adults, generally, there is an accepted standard of 140/90 (mm Hg), which is the cut-off point," she said. "If blood pressure goes beyond that it becomes a risk factor for cardiovascular diseases."
For kids, on the other hand, assessments are based on how their blood pressure compares to other children of their age, height and gender.
Treatment depends on how high the blood pressure is, Falkner said.
"If it's markedly elevated then the doctors generally do some testing to see if there's some underlying cause for the high blood pressure," she said.
She said there are things parents can do that are beneficial for kids' blood pressure, such as helping them lose weight if they're overweight or obese.
Dietary changes such as reducing sodium or following the DASH diet could help, she added. DASH stands for Dietary Approaches to Stop Hypertension.
"The DASH diet is kind of like the Mediterranean diet," Falkner said. "It's rich in fruits and vegetables, fiber and low-fat dairy."
"The idea behind this is that there are multiple nutrients that are beneficial for the cardiovascular system," she said.
SOURCE: bit.ly/1j1j3Gy Circulation, online February 19, 2014.
Obesity, genetic risk, and environment
BMJ 2014; 348 doi: https://dx.doi.org/10.1136/bmj.g1900 (Published 19 March 2014)
Cite this as: BMJ 2014;348:g1900
Alexandra I F Blakemore, professor of human molecular genetics, Jessica L Buxton, research associate
Genetic makeup can inflate effects of bad diet
The alarming global rise in prevalence of obesity is caused by unhealthy obesogenic environments. In westernised societies we are all exposed to calorie dense food, sedentary lives, stress, and sleep deficit. Some people seem relatively insensitive to these environmental pressures, while others are severely affected and become obese.
In a linked paper, Qi and colleagues (doi:10.1136/bmj.g1610) examined the interaction between common genetic variants associated with body mass index (BMI) and frequency of fried food consumption in over 37?000 people.1 The large study size was necessary to obtain adequate statistical power because the individual effects of these variants (single nucleotide polymorphisms, SNPs) on BMI are relatively subtle.2 The authors combined the weighted individual effects of 32 SNPs into a single “genetic risk score” for each participant.
As expected, participants who ate fried food more often tended to have higher BMI, and, independently, those with the highest genetic risk score also had higher BMI. The novel finding in this study is the observed interaction between genetic risk and fried food consumption: people in the highest risk groups for both had the highest BMI overall. Eating fried food more than four times a week had twice the effect on BMI for those in the highest third of genetic risk score as those in the lowest third.
This work provides formal proof of interaction between a combined genetic risk score and environment in obesity. Similar studies have already shown interaction between genetic risk scores for obesity and physical activity3 and dietary calcium.4 These results are unlikely to have a direct impact on personal healthcare because, though such genetic risk scores are statistically robust at the population level, they have poor predictive power for any given individual. Similarly, the results of the latest study are unlikely to influence public health advice, as most of us should be eating less fried food.
It would be a great shame, however, to assume that genetics can be ignored in the management of obesity. This widespread misconception arises from confusion of the common SNPs that have relatively subtle effects on BMI (the strongest of which, close to the FTO gene, raises body weight by only a mean of 3 kg even in those who inherit a double dose of the variant) with more dramatic genetic alterations that cause “Mendelian” forms of obesity.
There are, in fact, at least 15 single gene forms of obesity, with new ones reported almost monthly with advances in DNA sequencing technology.5 6 7 8 There are also chromosome microdeletions that cause Mendelian obesity.9 10 These forms of obesity are inherited in the same way as other genetic conditions such as cystic fibrosis or Huntington’s disease. Mutations in just one of the obesity genes (MC4R) cause around one in 20 cases of severe childhood obesity,11 and the total number of obese adults with Mendelian obesity is likely to be substantial.
Where molecular mechanisms are understood, obesity-causing genetic mutations disrupt appetite control systems in the brain, so affected people are unlikely to be able to maintain long term dietary restraint. It might also be unwise to offer them some types of weight loss surgery, such as adjustable gastric banding.
Why is this important? Our current options for management of morbidly obese people are limited, though several new therapeutic approaches are in development. Different types of obesity might require different management. For example, lifestyle interventions are likely to be much more successful in people whose BMI is not too far from the desirable range. The UK’s National Institute for Health and Care Excellence (NICE) already implicitly recognises that lifestyle and medical approaches are unlikely to help those with the most severe forms of obesity. Weight loss surgery is recommended as the first line treatment in people with BMI >50.
As researchers, policy makers, and healthcare professionals, we should adopt an evidence based approach. Unfortunately, clinical logic is not always applied in the consideration of obesity—health professionals commonly recommend the same lifestyle based interventions to those with overweight or mild obesity as to those with more severe problems. We would not adopt this approach with hypertension or type 2 diabetes, where it is well recognised that diet and appropriate physical exercise might be sufficient for mild cases, but more severely affected people need drugs (or even surgery) and a lifelong care plan. There is a danger that issues surrounding blame and “personal responsibility” in obesity might lead to lack of appropriate support for extremely obese people, who often have complex care needs. This can be the case in families with undiagnosed inherited obesity: genetic screening and counselling is rarely offered in those with morbid obesity.
In summary, use of combined genetic risk scores in gene-environment interaction studies allows joint analysis of factors influencing obesity. Inclusion of multiple genetic variants into a single risk score is helpful in terms of power for such investigations. It would be useful if similar studies could be carried out in individuals with Mendelian forms of obesity, who might show even more striking gene-environment interactions. Complex analyses integrating thousands of common variants have the potential to explain yet more of the genetic contribution to traits such as BMI.12 Predictive power at the individual level, however, remains low when only common genetic variants are considered. Integration of rare genetic alterations that cause Mendelian forms of obesity mighty improve this, providing clinically useful predictions for individuals and enabling stratification of patients for appropriate care and treatment.
References
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?Speliotes EK, Willer CJ, Berndt SI, Monda KL, Thorleifsson G, Jackson AU, et al. Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index. Nat Genet2010;42:937-48.CrossRefMedlineWeb of Science
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?Shalata A, Ramirez MC, Desnick RJ, Priedigkeit N, Buettner C, Lindtner C, et al. Morbid obesity resulting from inactivation of the ciliary protein CEP19 in humans and mice. Am J Hum Genet2013;93:1061-71.CrossRef
?Asai M, Ramachandrappa S, Joachim M, Shen Y, Zhang R, Nuthalapati N, et al. Loss of function of the melanocortin 2 receptor accessory protein 2 is associated with mammalian obesity. Science2013;341:275-8.Abstract/FREE Full Text
?Pearce LR, Atanassova N, Banton MC, Bottomley B, van der Klaauw AA, Revelli JP, et al. KSR2 mutations are associated with obesity, insulin resistance, and impaired cellular fuel oxidation. Cell2013;155:765-77.CrossRefWeb of Science
?Walters RG, Coin LJ, Ruokonen A, de Smith AJ, El-Sayed Moustafa JS, Jacquemont S, et al. Rare genomic structural variants in complex disease: lessons from the replication of associations with obesity. PLoS ONE2013;8:e58048.CrossRefMedline
?Walters RG, Jacquemont S, Valsesia A, de Smith AJ, Martinet D, Andersson J, et al. A new highly penetrant form of obesity due to deletions on chromosome 16p11.2. Nature2010;463:671-5.CrossRefMedlineWeb of Science
?Farooqi IS, Keogh JM, Yeo GS, Lank EJ, Cheetham T, O’Rahilly S. Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. N Engl J Med2003;348:1085-95.CrossRefMedlineWeb of Science
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Assessing Causality in the Association between Child Adiposity and Physical Activity Levels: A Mendelian Randomization Analysis
Rebecca C. Richmond,
George Davey Smith,
Andy R. Ness,
Marcel den Hoed,
George McMahon,
Nicholas J. Timpson
https://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.1001618
Background
Cross-sectional studies have shown that objectively measured physical activity is associated with childhood adiposity, and a strong inverse dose–response association with body mass index (BMI) has been found. However, few studies have explored the extent to which this association reflects reverse causation. We aimed to determine whether childhood adiposity causally influences levels of physical activity using genetic variants reliably associated with adiposity to estimate causal effects.
Methods and Findings
The Avon Longitudinal Study of Parents and Children collected data on objectively assessed activity levels of 4,296 children at age 11 y with recorded BMI and genotypic data. We used 32 established genetic correlates of BMI combined in a weighted allelic score as an instrumental variable for adiposity to estimate the causal effect of adiposity on activity.
In observational analysis, a 3.3 kg/m2 (one standard deviation) higher BMI was associated with 22.3 (95% CI, 17.0, 27.6) movement counts/min less total physical activity (p = 1.6×10-16), 2.6 (2.1, 3.1) min/d less moderate-to-vigorous-intensity activity (p = 3.7×10-29), and 3.5 (1.5, 5.5) min/d more sedentary time (p = 5.0×10-4). In Mendelian randomization analyses, the same difference in BMI was associated with 32.4 (0.9, 63.9) movement counts/min less total physical activity (p = 0.04) (~5.3% of the mean counts/minute), 2.8 (0.1, 5.5) min/d less moderate-to-vigorous-intensity activity (p = 0.04), and 13.2 (1.3, 25.2) min/d more sedentary time (p = 0.03). There was no strong evidence for a difference between variable estimates from observational estimates. Similar results were obtained using fat mass index. Low power and poor instrumentation of activity limited causal analysis of the influence of physical activity on BMI.
Conclusions
Our results suggest that increased adiposity causes a reduction in physical activity in children and support research into the targeting of BMI in efforts to increase childhood activity levels. Importantly, this does not exclude lower physical activity also leading to increased adiposity, i.e., bidirectional causation.
Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies
BMJ 2014; 348 doi: https://dx.doi.org/10.1136/bmj.g1610 (Published 19 March 2014)
Qibin Qi, assistant professor12, Audrey Y Chu, research fellow3, Jae H Kang, assistant professor4, Jinyan Huang, research fellow5, Lynda M Rose, statistician3, Majken K Jensen, assistant professor1, Liming Liang, assistant professor5, Gary C Curhan, professor45, Louis R Pasquale, associate professor46, Janey L Wiggs, associate professor6, Immaculata De Vivo, associate professor45, Andrew T Chan, associate professor47, Hyon K Choi, professor48, Rulla M Tamimi, associate professor45, Paul M Ridker, professor3910, David J Hunter, professor145, Walter C Willett, professor145, Eric B Rimm, associate professor145, Daniel I Chasman, associate professor310, Frank B Hu, professor145, Lu Qi, assistant professor14
Author Affiliations
Objective To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity.
Design Prospective cohort study.
Setting Health professionals in the United States.
Participants 9623 women from the Nurses’ Health Study, 6379 men from the Health Professionals Follow-up Study, and a replication cohort of 21?421 women from the Women’s Genome Health Study.
Main outcome measure Repeated measurement of BMI over follow-up.
Results There was an interaction between fried food consumption and a genetic risk score based on 32 BMI-associated variants on BMI in both the Nurses’ Health Study and Health Professionals Follow-up Study (P=0.001 for interaction). Among participants in the highest third of the genetic risk score, the differences in BMI between individuals who consumed fried foods four or more times a week and those who consumed fried foods less than once a week amounted to 1.0 (SE 0.2) in women and 0.7 (SE 0.2) in men, whereas the corresponding differences were 0.5 (SE 0.2) and 0.4 (SE 0.2) in the lowest third of the genetic risk score. The gene-diet interaction was replicated in the Women’s Genome Health Study (P<0.001 for interaction). Viewed differently, the genetic association with adiposity was strengthened with higher consumption of fried foods. In the combined three cohorts, the differences in BMI per 10 risk alleles were 1.1 (SE 0.2), 1.6 (SE 0.3), and 2.2 (SE 0.6) for fried food consumption less than once, one to three times, and four or more times a week (P<0.001 for interaction); and the odds ratios (95% confidence intervals) for obesity per 10 risk alleles were 1.61 (1.40 to 1.87), 2.12 (1.73 to 2.59), and 2.72 (2.12 to 3.48) across the three categories of consumption (P=0.002 for interaction). In addition, the variants in or near genes highly expressed or known to act in the central nervous system showed significant interactions with fried food consumption, with the FTO (fat mass and obesity associated) variant showing the strongest result (P<0.001 for interaction).
Conclusion Our findings suggest that consumption of fried food could interact with genetic background in relation to obesity, highlighting the particular importance of reducing fried food consumption in individuals genetically predisposed to obesity.
Eat more, die young: Why eating a diet very low in nutrients can extend lifespan
Date:March 17, 2014
Source:Wiley
Summary:
A new evolutionary theory claims that consuming a diet very low in nutrients can extend lifespan in laboratory animals, a finding which could hold clues to promoting healthier aging in humans. Scientists have known for decades that severely restricted food intake reduces the incidence of diseases of old age, such as cancer, and increases lifespan. The most widely accepted theory is that this effect evolved to improve survival during times of famine.
Hamster (stock image). Dietary restriction leads to increased rates of cellular recycling and repair mechanisms in the body. The UNSW researchers' new theory is that this effect evolved to help animals continue to reproduce when food is scarce; they require less food to survive because stored nutrients in the cells can be recycled and reused.
A new evolutionary theory in BioEssays claims that consuming a diet very low in nutrients can extend lifespan in laboratory animals, a finding which could hold clues to promoting healthier ageing in humans.
Scientists have known for decades that severely restricted food intake reduces the incidence of diseases of old age, such as cancer, and increases lifespan.
"This effect has been demonstrated in laboratories around the world, in species ranging from yeast to flies to mice. There is also some evidence that it occurs in primates," says lead author, Dr Margo Adler, an evolutionary biologist at UNSW Australia.
The most widely accepted theory is that this effect evolved to improve survival during times of famine. "But we think that lifespan extension from dietary restriction is more likely to be a laboratory artefact," says Dr Adler.
Lifespan extension is unlikely to occur in the wild, because dietary restriction compromises the immune system's ability to fight off disease and reduces the muscle strength necessary to flee a predator.
"Unlike in the benign conditions of the lab, most animals in the wild are killed young by parasites or predators," says Dr Adler.
"Since dietary restriction appears to extend lifespan in the lab by reducing old-age diseases, it is unlikely to have the same effect on wild animals, which generally don't live long enough to be affected by cancer and other late-life pathologies."
Dietary restriction, however, also leads to increased rates of cellular recycling and repair mechanisms in the body.
The UNSW researchers' new theory is that this effect evolved to help animals continue to reproduce when food is scarce; they require less food to survive because stored nutrients in the cells can be recycled and reused.
It is this effect that could account for the increased lifespan of laboratory animals on very low-nutrient diets, because increased cellular recycling reduces deterioration and the risk of cancer.
"This is the most intriguing aspect, from a human health stand point. Although extended lifespan may simply be a side effect of dietary restriction, a better understanding of these cellular recycling mechanisms that drive the effect may hold the promise of longer, healthier lives for humans," she says.
It may be possible in future, for example, to develop drugs that mimic this effect.
Watch the video abstract: https://www.youtube.com/watch?v=KG2Etkr8Hek&feature=youtu.be
Story Source:
The above story is based on materials provided by Wiley. Note: Materials may be edited for content and length.
Journal Reference:
Margo I. Adler, Russell Bonduriansky. Why do the well-fed appear to die young? BioEssays, 2014; DOI: 10.1002/bies.201300165
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Parents 'increase infant's obesity risk through feeding and activity practices'
Monday 17 March 2014 - 12am PST
In 2012, more than one third of children and adolescents were overweight or obese. Now, new research suggests parents may need to shoulder some of the blame. A study found that many parents adopt infant feeding and activity practices that may increase a child's risk of obesity later in life.
The research team, led by Dr. Eliana M. Perrin of the University of North Carolina School of Medicine, recently published their findings in the journal Pediatrics.
For their study, the researchers analyzed 863 low-income parents and their infants who were a part of an obesity prevention trial called Greenlight.
Results of the study revealed that all parents adopted some infant feeding and activity behaviors that have been linked to the development of obesity later in life.
On assessing feeding behaviors, the researchers found that 45% of parents exclusively formula fed their infants, while only 19% exclusively breastfed.
Solid food had been introduced to infants early by 12% of parents - a feeding behavior that has been linked to obesity in the past. In 2011, Medical News Today reported on a study suggesting that babies who are fed solid foods before 4 months of age are more likely to be obese by the age of 3 years.
Infants were put to bed with their bottles by 43% of parents, while 23% of parents propped bottles up instead of holding them by hand - a process that can lead to excessive feeding.
Around 20% of parents fed their infants when they cried, while 38% always tried to get their babies to finish their milk.
When it came to other activities linked to obesity, the researchers found that 90% of infants were exposed to television, and 50% actively watched TV - meaning parents intentionally put their children in front of the television so they could watch it.
Watching television is a factor that past research has associated with childhood obesity. Medical News Today recently reported on a study suggesting that children who have televisions in their bedroom are at higher risk of weight gain.
Parents 'need to do more to prevent their children from developing obesity'
Childhood obesity has both immediate and long-term impacts on health.
Research has shown that obese children and adolescents are more likely to be obese as adults. This means they are at higher risk of obesity-related health problems, such as heart disease, type 2 diabetes, stroke, osteoarthritis and even some types of cancer.
And it is not only health that can be affected by obesity. We recently reported on a study revealing that obese teenage girls may have lower academic performance, compared with those of a healthy weight.
Dr. Perrin says the team's findings show that parents need to do more to reduce "obesogenic" behaviors and ensure their child does not develop obesity later in life.
She adds:
"These results from a large population of infants - especially the high rates of television watching - teach us that we must begin obesity prevention even earlier."
She believes that families could benefit from early "culturally-tailored" counseling on how to lead healthier lives. "We are hoping our research sheds light on the best ways to do that," she concludes.
Written by Honor Whiteman
Rethinking genetic links to obesity: IRX3 is likely the 'fat gene'
Mutations within the gene FTO have been implicated as the strongest genetic determinant of obesity risk in humans, but the mechanism behind this link remained unknown. Now, an international team of scientists has discovered that the obesity-associated elements within FTO interact with IRX3, a distant gene on the genome that appears to be the functional obesity gene. The FTO gene itself appears to have only a peripheral effect on obesity. The study appears online March 12 in Nature.
"Our data strongly suggest that IRX3 controls body mass and regulates body composition," said senior study author Marcelo Nobrega, PhD, associate professor of human genetics at the University of Chicago. "Any association between FTO and obesity appears due to the influence of IRX3."
Mutations to introns (noncoding portions) of the gene FTO have been widely investigated after genome-wide association studies revealed a strong link between FTO and obesity and diabetes. Yet overexpressing or deleting FTO in animal models affects whole body mass and composition, not just fat, and experiments have failed to show that these obesity-linked introns affect the function of the FTO gene itself.
Hoping to explain these observations, Nobrega and his team mapped the behavior of promoters—regions of DNA that activate gene expression—located within one million base pairs on either side of the FTO gene. In adult mice brains, where FTO was thought to affect metabolic function, they discovered that the promoter that turns on FTO did not interact with obesity-associated FTO introns.
"Instead, we found that the promoter for IRX3, a gene several hundred thousand base pairs away, did interact with these introns, as well as a large number of other elements across the vast genetic distance we studied," said co-author Jose Luis Gomez-Skarmeta, PhD, a geneticist at the Andalusian Center of Developmental Biology in Sevilla, Spain. The researchers found a similar pattern of interactions in humans after analyzing data from the ENCODE project, which they confirmed with experiments on human cells.
Using data from 153 brain samples from individuals of European ancestry, they discovered that the mutations to FTO introns that affected body weight are associated with IRX3 expression, but not FTO. Obesity-related FTO introns enhanced the expression of IRX3, functioning as regulatory elements. The FTO gene itself did not appear to play a role in this interaction.
"Regulatory elements are switches that turn genes on and off. What we've found is that the switches that control IRX3 are far away from the gene and actually inside the FTO gene", says Nobrega.
To verify the role of IRX3, the researchers engineered mice without the IRX3 gene. These mice were significantly leaner than their normal counterparts. They weighed about 30 percent less, primarily through reduced fat.
The decrease in weight gain occurred despite normal levels of food consumption and physical activity. When fed a high-fat diet, mice without IRX3 retained the same weight and fat levels as on normal diets. Normal mice fed a high-fat diet gained almost twice as much weight. Fat cells in IRX3-deficient mice were smaller, and increased levels of brown fat were observed. In addition, these mice were better able to process glucose.
"These mice are thin. They lose weight primarily through the loss of fat. But they are not runts," said co-author Chin-Chung Hui, PhD, professor of molecular genetics at the University of Toronto. "They are also completely resistant to high-fat diet-induced obesity. They have much better ability to handle glucose, and seem protected against diabetes."
The researchers also discovered that mice with altered IRX3 function in the hypothalamus, the portion of the brain known to regulate feeding behavior and energy expenditure, showed an identical pattern of leanness as mice which completely lacked IRX3. Hypothalamic function of IRX3, therefore, appears to control body mass and composition in these animals, indicating that the genetic predisposition to obesity is wired in the brain.
IRX3 codes for a protein that regulates other genes, and is present both in and outside the brain, in organs and cells such as fat cells. Nobrega and his team are currently investigating how IRX3 interacts with genes and molecules that it regulates, and hope to identify targets for the development of novel therapies against obesity and diabetes.
"IRX3 is probably a master regulator of genetic programs in the cells where it is expressed," Nobrega said. "We're interested in what its targets are and what they alter. The goal is to identify downstream targets of IRX3 that become models for drug targeting."
Explore further: Fat and obesity gene also affects hip fracture
More information: "Obesity-associated variants within FTO form long-range functional connections with IRX3," Nature, dx.doi.org/10.1038/nature13138
Journal reference: Nature
Bread, cereal drive UK children's high salt diet
Children in London eat an unhealthy amount of salt on a daily basis—with much of it coming from breads and cereals, according to new research in the American Heart Association journal Hypertension.
In this London study—so far the largest to measure salt intake in U.K. youth—teens in particular ate more salt each day than is recommended for adults. Cereal- and bread-based products accounted for more than a third, 36 percent, of the salt in children's diets.
"We know that salt starts increasing the risk of high blood pressure in children starting at age one," said Graham MacGregor, M.D., study author and professor of Cardiovascular Medicine at Wolfson Institute of Preventive Medicine, Barts and The London School of Medicine & Dentistry, Queen Mary University of London. "There needs to be a much greater effort to reduce salt in foods."
Researchers analyzed 24-hour urine samples of 340 children. This is considered the gold standard of measuring salt consumption. Participants or their parents also kept a detailed food diary and snapped photos of all foods and beverages consumed before they started eating as well as the leftovers when they finished. The study found:
5 and 6 year olds consumed 3.75 grams of salt daily.
8 and 9 year olds consumed 4.72 grams of salt daily.
13 to 17 year olds consumed 7.55 grams of salt daily.
Boys tended to have higher salt intake than girls, particularly in the older and younger groups – about 1 gram higher per day in 5-6 yr olds, and 2 ½ grams per day higher in 13-17 year olds.
In addition to the 36 percent of salt from breads and cereals, meat products provided 19 percent while dairy products accounted for 11 percent.
In the U.K., adults are advised to eat no more than 6 grams of salt daily. In the U.S. the American Heart Association recommends adults and children eat less than 1,500 mg of sodium, which is equal to 3.7 grams (a little less than a teaspoon) of salt.
The U.S. Centers for Disease Control and Prevention estimates that 73 percent to 93 percent of U.S. children ages 1 to 18 consume too much sodium.
The large amount of salt the children ate was seen despite a nationwide salt reduction program in the U.K., which is cutting the amount of salt major food companies include in supermarket and restaurant foods.
"While salt intake in children wasn't measured prior to the U.K.'s salt-reduction campaign, the salt intake in adults has fallen 15 percent in six years," he said. "So, that policy is working, but it's not working fast enough. We need to do more and the U.S. needs a similar program," as children eat the same brands of processed foods and fast foods in both countries, MacGregor said.
Excessive salt consumption is one of the major factors contributing to high blood pressure which can lead to heart disease and stroke. Earlier studies have shown that kids with high sodium diets are about 40 percent more likely to have elevated blood pressure than kids who have lower sodium diets.
MacGregor said the study was conducted because there is very little information on exactly how much salt kids eat and what salty foods they are eating, information he said is necessary before designing an effective salt-reduction plan for kids.
"It is very difficult for parents to reduce children's salt intake unless they avoid packaged and restaurant foods and prepare each meal from scratch using fresh, natural ingredients," MacGregor said.
Explore further: Americans still eat too much salt, CDC says
Journal reference: Hypertension
Too Little Sleep Increases Heart Disease Risk in Obese Adolescents
By Agata Blaszczak-Boxe, Staff Writer | March 07, 2014 04:44pm ET
Obese adolescents who do not get enough sleep may be at an increased risk of heart disease and other health issues, compared with other obese teens who get more sleep, a new study suggests.
Researchers looked at the teens' risk factors for developing heart disease, diabetes and stroke, and found that the less sleep the adolescents got, the higher their "cardiometabolic risk score," which is a measure that combines the risk of developing these conditions into a single number.
"More sleep means less risk," said study author Heidi IglayReger, supervisor of the Physical Activity Laboratory at the Michigan Metabolomics and Obesity Center.
In the study, the researchers examined 37 obese teenagers, ages 11 to 17. The research team measured the participants' body mass index, waist circumference, blood pressure and blood sugar. They also gave each participant an accelerometer — a device used to measure people's physical activity and sleep patterns.
It turned out that only five of the teenagers in the study slept for at least 8.5 hours per night, which is the recommended minimum for this age group. The remaining kids slept about 7 hours per night.
"We know that obese adolescents, just because of the fact that they are obese, they are already at a higher risk for developing cardiovascular disease," IglayReger said.[10 Ways to Promote Kids' Healthy Eating Habits]
"We found that, even in a high-risk population [such as obese adolescents], the amount of sleep does seem to matter," she told Live Science.
The results of the study do not mean that insufficient sleep directly causes obesity, heart disease or diabetes, the researchers said.
"However, the strong association between sleep duration and cardiometabolic risk score independent of the effects of body composition and physical activity suggest a potential influence of sleep duration on cardiometabolic health in obese adolescents," IglayReger said in a statement.
In general, sleep issues appear to be a common problem among adolescents, the researchers said.
"Teenagers are notorious for not sleeping enough," because they often want to stay up later and sleep in later during the day, which is hardly possible due to their school schedules, IglayReger said.
Previous research has found an association between an insufficient amount of sleep and a higher risk of dying of heart disease in adults. Studies have also shown a link between an insufficient amount of sleep and an increased likelihood of obesity in teenage boys.
Follow Agata Blaszczak-Boxe on Twitter. Follow us @livescience, Facebook & Google+. Original article on Live Science.
Role of Dietary Factors and Food Habits in the Development of Childhood Obesity: A Commentary by the ESPGHAN Committee on Nutrition
Agostoni, Carlo; Braegger, Christian; Decsi, Tamas; Kolacek, Sanja; Koletzko, Berthold; Mihatsch, Walter; Moreno, Luis A; Puntis, John; Shamir, Raanan; Szajewska, Hania; Turck, Dominique; van Goudoever, Johannes; ESPGHAN Committee on Nutrition
Journal of Pediatric Gastroenterology and Nutrition
June 2011
Vol. 52 - Issue 6: p 662–669
Obesity is the most prevalent nutritional disorder among children and adolescents throughout the world (1,2). Notwithstanding recent reports suggesting a levelling off of the prevalence of obesity in some countries (3–5), the burden of paediatric obesity for society is still high (6–8). In addition to short-term complications such as psychosocial disturbances or orthopaedic problems, the origins of potential long-term metabolic consequences are also identifiable in many obese children (9). It is well established that obesity is a multifactorial disease in which genetic as well as psychological and environmental causative factors are implicated, with diet and physical inactivity looming large.
The focus of this comment is to assess the role of dietary factors and food habits in the prevention of obesity in childhood. For the roles of physical activity and sedentary behaviour, we refer readers to available reviews and position papers (10–13). The treatment of obesity is also beyond the scope of this Comment. For the role of dietary interventions in the treatment of obese children, we refer readers to a recent Cochrane review (14). Finally, the role of early nutrition in obesity development is not covered because nutrition during the first year of life has been extensively discussed in 2 recent comments published by the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition Committee on Nutrition (15,16). In summary, it was stated that the potential for breast-feeding to contribute to reduction of later obesity should be explored in more detail, and that the available evidence on how complementary feeding influences later obesity risk is not conclusive.
This Comment aims to provide a state-of-the-art summary on the role of nutrition-related factors that may contribute to the development of obesity in children ages 2 to 18 years. This Comment also provides recommendations on healthy nutrition patterns with the potential to decrease obesity risk to be promoted by paediatricians and other health care professionals.
Study finds genetic link between height and IQ
by Bob Yirka report
A team of researchers at Edinburgh University in Scotland has found a correlation between genes associated with height and those associated with intelligence. In their paper published in the journal Behavior Genetics, the group describes how they studied the DNA of 6,815 unrelated people and discovered what they describe as a direct correlation between height and intelligence—taller people are smarter, they say.
While the team's study results are likely to cause quite a stir, particularly among those lower in physical stature, it does add to a growing body of research that suggests there are physical, mental and in some cases emotional differences between people related to body size (both height and girth). In this effort, the team used data obtained from Generation Scotland: Scottish Family Health Study—where both medical tests and mental aptitude were tested—intelligence was measured via four basic metrics: mental reaction times, linguistic ability, processing speed and powers of recall.
In analyzing data from the study, the team found what they describe as a "significant genetic correlation" between IQ and height—between taller and shorter people. Those that were shorter were on average, found to be slightly less intelligent than their taller counterparts. It's important to note that the researchers are not suggesting that all short people are less intelligent, or that all tall people are more intelligent. Instead they are pointing out averages across a population. Also important to note is that the Family Health Study did not use standard IQ tests to measure intelligence.
The research team also claim that 70 percent of the genetic differences they found regarding IQ and height could be attributed to genetic factors—the rest could be chalked up to environment.
Other studies have found that there exists different health risks for people of different heights—some have found that shorter people, for example, are more likely to suffer from cardiovascular disease, while taller people tend to die younger than shorter people. Studies that have looked for intelligence differences based on height, however, have been few and far between. The researchers in Scotland point out that prior studies have relied mainly on testing people related to one another—theirs, they claim, is the first study to measure people who are completely unrelated.
Explore further: Study relies on twins and their parents to understand height-IQ connection
More information: Behavior Genetics March 2014, Volume 44, Issue 2, pp 91-96. DOI: 10.1007/s10519-014-9644-z
TV in child's bedroom tied to weight gain
by Steven Reinberg, Healthday Reporter
But 'active' video games might help youngsters stay slim, researchers say.
(HealthDay)—Children who have a TV in their bedroom are likely to gain weight. But kids who play active video games might lose unwanted pounds, according to two new studies.
"In an age of widespread childhood and adolescent obesity, technology is clearly the proverbial double-edged sword," said Dr. David Katz, director of the Yale University Prevention Research Center.
"On the one edge, technological innovation and screen time, in particular, is associated with sedentariness and weight gain," said Katz, who had no part in either study. "But then there is the other edge: Technology can be used to encourage activity."
In other words, not all video games are bad, said Stewart Trost, a professor of physical activity and health at the University of Queensland in Australia. Trost was the lead author of the video game study published online March 3 in the journal JAMA Pediatrics.
"The latest and greatest active video games that require players to move their whole body are an appealing way to promote exercise among overweight and obese children," Trost said.
His study of 75 overweight or obese children—their average age was 10—found that those assigned to active gaming plus family-based weight management increased their moderate-to-vigorous activity an average of 7.4 minutes per day and vigorous physical activity by nearly three minutes per day.
The active gamers lost about twice as much weight over four months as those assigned to a weight-management program alone—10.9 percent of body weight versus 5.5 percent, the researchers found.
Children in the weight-management-only group saw no change in calorie-burning activity, said the researchers, who received no funding from the video game industry.
More than one-third of children and adolescents in the United States are overweight or obese, putting them at risk of serious health problems as they grow older, the researchers said.
Anything that gets children moving is a good thing, said Dr. William Muinos, co-director of the division of gastroenterology at Miami Children's Hospital in Florida. "Having these active games gives obese kids another avenue of activity," said Muinos, who was not involved in either study.
Moreover, active video games can help obese kids get past the stigma they encounter trying to play team sports, said Muinos, who runs an obesity clinic.
But bedroom TVs are another matter entirely, he and other experts say.
A study of more than 6,500 middle-school-age kids, published in the same journal issue, found that those with a TV in their bedroom "gained about one extra pound a year," said lead author Diane Gilbert-Diamond, an assistant professor of community and family medicine at Dartmouth Medical School. This held true whether or not the kids watched a lot of TV.
"Removing a TV from a child's bedroom is a single concrete action that a parent can take to help reduce their child's risk of excessive weight gain," Gilbert-Diamond said.
The researchers said they don't know the exact reasons for the weight gain but they offered two possibilities: greater exposure to food advertising and disrupted sleep patterns, including later bedtimes and poorer sleep quality.
Muinos, who runs an obesity clinic, supported the disrupted-sleep theory. "It's well known that kids who continue to watch TV while the parents are already in bed will have disrupted sleep patterns," he said. "We know that increases weight."
"When kids have TV in the bedroom, they isolate themselves from the family," he added. "They tend to go to bed later. They tend to be less active. They tend to snack on junk food. All of this will increase weight."
Gilbert-Diamond's survey asked more than 6,500 boys and girls aged 10 to 14 if they had a television in their bedroom. Two to four years later, their parents were asked about their kids' height and weight.
Fifty-nine percent of the children had a bedroom TV, and they were more likely to be boys, poor and black or Hispanic, the study found.
At both two years and four years after the survey, having a bedroom TV was associated with an increase in body-mass index (BMI) of nearly one point. BMI is a measurement of body fat based on height and weight.
Explore further: Many parents of obese children underestimate their weight
More information: For more information on childhood obesity, visit the U.S. National Library of Medicine.
Journal reference: JAMA Pediatrics