Family, friends, social ties influence weight status in young adults

Family, Friends, Social Ties Influence Weight Status in Young Adults


ScienceDaily (Jan. 11, 2011) — Does obesity tend to "cluster" among young adults? And if so, what impact does it have on both their weight and weight-related behaviors? That's what researchers from The Miriam Hospital's Weight Control and Diabetes Research Center set out to answer to better understand how social influences affect both weight status and weight loss intentions in this difficult-to-reach age group.



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According to the study, published online by the journal Obesity, overweight and obese young adults between the ages of 18 and 25 were more likely to have overweight romantic partners and best friends and also had more overweight casual friends and family members compared to normal weight peers. Also, overweight and obese young adults who reported having social contacts trying to lose weight had greater weight loss intentions.
Why is this an important issue? Forty percent of young adults age 18-25 are considered overweight or obese, and young adults experience the highest rate of weight gain per year -- typically one to two pounds -- of any age group. While previous research has consistently demonstrated the powerful impact of social influence on health behaviors, especially for younger individuals, no previous study has examined whether social ties influence weight status and weight loss intentions among young adults.
Lead author Tricia Leahey, PhD, a researcher with The Miriam Hospital's Weight Control and Diabetes Research Center, also points out that young adults are less likely to participate in behavioral weight loss interventions, and when they do, they tend to lose less weight than older adults. "Identifying the factors that influence both weight status and weight control in this high-risk age group can help us develop appealing and effective obesity treatment and prevention programs for this population," she said.
The study included 288 young adults between the ages of 18 and 25; 151 individuals were of normal weight, while 137 were considered overweight or obese (BMI of 25 or greater). The majority of participants were female and Caucasian. All participants completed questionnaires to determine their weight and height, number of overweight social contacts (including best friends, romantic partners, casual friends, relatives and colleagues/classmates) and perceived social norms for obesity and obesity-related behaviors.
Overweight and obese study participants completed additional questionnaires to assess how many of their overweight social contacts were currently trying to lose weight, perceived social norms for weight loss (such as how frequently social contacts encouraged them to lose weight or whether the people closest to them would approve if they were to lose weight), and intentions to lose weight within the next three months.
Compared to normal weight young adults, those who were overweight or obese were more likely to have an overweight romantic partner (25 percent vs. 14 percent) and an overweight best friend (24 percent vs. 14 percent). "Our data suggests that obesity 'clusters' in this population. But interestingly, social norms for obesity did not differ between the two groups and did not account for the clustering," said Leahey. "Both groups reported similarly low levels of social acceptability for being overweight, eating unhealthy foods and being inactive."
The study also showed overweight and obese young adults who had more social contacts trying to lose weight were more likely to want to lose weight themselves. Social norms for weight loss, such as encouragement and approval from social contacts, account for this association, researchers say.
Leahey is also assistant professor of psychiatry/human behavior at The Warren Alpert Medical School of Brown University. The study was funded by grants from the National Institute of Diabetes and Digestive and Kidney Diseases. Co-authors included Rena Wing, PhD, Jessica LaRose, PhD, and Joseph Fava, PhD, all of the Weight Control and Diabetes Research Center at The Miriam Hospital and Alpert Medical School.

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Feast or famine: Researchers identify leptin receptor's sidekick as a target for appetite regulation

Feast or Famine: Researchers Identify Leptin Receptor's Sidekick as a Target for Appetite Regulation


ScienceDaily (Jan. 11, 2011) — A study by researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine adds a new twist to the body of evidence suggesting human obesity is due in part to genetic factors. While studying hormone receptors in laboratory mice, neuroscientists identified a new molecular player responsible for the regulation of appetite and metabolism.



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In the Jan. 11 online issue of PLoS Biology, the authors report that mice engineered not to express the lipoprotein receptor LRP1, in the brain's hypothalamus, began to eat uncontrollably, growing obese as well as lethargic. They found that LRP1, a major transporter of lipids and proteins into brain cells, is a "co-receptor" with the leptin receptor -- meaning that both the leptin and LRP1 receptors need to work together to transmit leptin signals.
Leptin decides whether fat should be stored or used, resulting in lethargy or energy. When working properly, the hormone, which is made when body cells take in fat from food, travels to the brain to tamp down appetite.
"If a person is born with too little gene expression in the leptin pathway, which includes its receptors, or the circuitry is not functioning well, then leptin will not work as well as it should," says the study's lead investigator, neuroscientist Guojun Bu, Ph.D., of Mayo Clinic. "Appetite will increase, and body fat will be stored."
Given these results, Dr. Bu says it may be possible to develop a treatment that increases gene expression in one or both of the protein receptors, which then increases the messages meant to decrease appetite sent to the brain.
The serendipitous findings were born out of Dr. Bu's primary research focus, Alzheimer's disease. He has been studying how cholesterol, essential to the smooth functioning of neurons, is carried from star-shaped astrocytes to the surface of neurons by apolipoprotein E (APOE). There are two major receptors for APOE on brain neurons, and LRP1 is one of them.
Inheriting one version of APOE -- APOE4 -- is a known risk factor for development of Alzheimer's disease, and Dr. Bu has found that APOE4 is less effective at transporting cholesterol. To understand what role LRP1 plays in bringing APOE4 into neurons, he created a knockout mouse model with no expression of LRP1 in its forebrain neurons; the rest of its body expressed the receptor normally.
He found neurons lacking LRP1 had even less ability to absorb cholesterol, and that they lost synaptic contact with other neurons, impairing their ability to retain memory.
But Dr. Bu was surprised to find the mice suddenly gained weight. "This is the opposite of what had been observed in mice who did not have the receptor in their body fat cells," he says. "Those animals became skinny because they couldn't absorb enough lipoproteins."
The knockout mice were indistinguishable from control mice for the first six months of life but then gained weight rapidly, a phenomenon that correlated with a decrease in LPR1 expression in the central nervous system. At 12 months old, the genetically engineered mice had twice as much body fat as control mice, lacked energy, and were insulin resistant. "Together, these results indicate that LRP1, which is critical in lipid metabolism, also regulates food intake and energy balance in the adult central nervous system," Dr. Bu says.
The study was funded by the National Institutes of Health and the Alzheimer's Association.

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Qiang Liu, Juan Zhang, Celina Zerbinatti, Yan Zhan, Benedict J. Kolber, Joachim Herz, Louis J. Muglia, Guojun Bu. Lipoprotein Receptor LRP1 Regulates Leptin Signaling and Energy Homeostasis in the Adult Central Nervous System. PLoS Biology, 2011; 9 (1): e1000575 DOI: 10.1371/journal.pbio.1000575

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Eating vegetables gives skin a more healthy glow than the sun, study shows

Eating Vegetables Gives Skin a More Healthy Glow Than the Sun, Study Shows


ScienceDaily (Jan. 12, 2011) — New research suggests eating vegetables gives you a healthy tan. The study, led by Dr Ian Stephen at The University of Nottingham, showed that eating a healthy diet rich in fruit and vegetables gives you a more healthy golden glow than the sun.



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The research, which showed that instead of heading for the sun the best way to look good is to munch on carrots and tomatoes, has been published in the Journal Evolution and Human Behaviour.
Dr Ian Stephen, from the School of Psychology, University of Nottingham, Malaysia Campus, led the research as part of his PhD at the University of St Andrews and Bristol University. He said: "Most people think the best way to improve skin colour is to get a suntan, but our research shows that eating lots of fruit and vegetables is actually more effective.
Dr Stephen and his team in the Perception Lab found that people who eat more portions of fruit and vegetables per day have a more golden skin colour, thanks to substances called carotenoids. Carotenoids are antioxidants that help soak up damaging compounds produced by the stresses and strains of everyday living, especially when the body is combating disease. Responsible for the red colouring in fruit and vegetables such as carrots and tomatoes, carotenoids are important for our immune and reproductive systems.
Dr Stephen said: "We found that, given the choice between skin colour caused by suntan and skin colour caused by carotenoids, people preferred the carotenoid skin colour, so if you want a healthier and more attractive skin colour, you are better off eating a healthy diet with plenty of fruit and vegetables than lying in the sun."
Dr Stephen suggests that the study is important because evolution would favour individuals who choose to form alliances or mate with healthier individuals over unhealthy individuals.
Professor David Perrett, who heads the Perception Lab, said: "This is something we share with many other species. For example, the bright yellow beaks and feathers of many birds can be thought of as adverts showing how healthy a male bird is. What's more, females of these species prefer to mate with brighter, more coloured males. But this is the first study in which this has been demonstrated in humans."
While this study describes work in Caucasian faces, the paper also describes a study that suggests the effect may exist cross culturally, since similar preferences for skin yellowness were found in an African population.
The work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and Unilever Research, and published with support from the Economic and Social Research Council (ESRC) and the British Academy and Wolfson Foundation.
See: http://perception.st-and.ac.uk/ for demos or to participate in face experiments.

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Ian D. Stephen, Vinet Coetzee, David I. Perrett. Carotenoid and melanin pigment coloration affect perceived human health☆☆☆. Evolution and Human Behavior, 2010; DOI: 10.1016/j.evolhumbehav.2010.09.003

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Eating vegetables gives skin a more healthy glow than the sun, study shows

Eating Vegetables Gives Skin a More Healthy Glow Than the Sun, Study Shows


ScienceDaily (Jan. 11, 2011) — New research suggests eating vegetables gives you a healthy tan. The study, led by Dr Ian Stephen at The University of Nottingham, showed that eating a healthy diet rich in fruit and vegetables gives you a more healthy golden glow than the sun.



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Health & Medicine

Staying Healthy
Skin Care
Vegetarian
Psoriasis
Diet and Weight Loss
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Reference

Vegetable
Food groups
South Beach diet
Mediterranean diet

The research, which showed that instead of heading for the sun the best way to look good is to munch on carrots and tomatoes, has been published in the Journal Evolution and Human Behaviour.
Dr Ian Stephen, from the School of Psychology, University of Nottingham, Malaysia Campus, led the research as part of his PhD at the University of St Andrews and Bristol University. He said: "Most people think the best way to improve skin colour is to get a suntan, but our research shows that eating lots of fruit and vegetables is actually more effective.
Dr Stephen and his team in the Perception Lab found that people who eat more portions of fruit and vegetables per day have a more golden skin colour, thanks to substances called carotenoids. Carotenoids are antioxidants that help soak up damaging compounds produced by the stresses and strains of everyday living, especially when the body is combating disease. Responsible for the red colouring in fruit and vegetables such as carrots and tomatoes, carotenoids are important for our immune and reproductive systems.
Dr Stephen said: "We found that, given the choice between skin colour caused by suntan and skin colour caused by carotenoids, people preferred the carotenoid skin colour, so if you want a healthier and more attractive skin colour, you are better off eating a healthy diet with plenty of fruit and vegetables than lying in the sun."
Dr Stephen suggests that the study is important because evolution would favour individuals who choose to form alliances or mate with healthier individuals over unhealthy individuals.
Professor David Perrett, who heads the Perception Lab, said: "This is something we share with many other species. For example, the bright yellow beaks and feathers of many birds can be thought of as adverts showing how healthy a male bird is. What's more, females of these species prefer to mate with brighter, more coloured males. But this is the first study in which this has been demonstrated in humans."
While this study describes work in Caucasian faces, the paper also describes a study that suggests the effect may exist cross culturally, since similar preferences for skin yellowness were found in an African population.
The work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and Unilever Research, and published with support from the Economic and Social Research Council (ESRC) and the British Academy and Wolfson Foundation.
See: http://perception.st-and.ac.uk/ for demos or to participate in face experiments.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Nottingham.




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Ian D. Stephen, Vinet Coetzee, David I. Perrett. Carotenoid and melanin pigment coloration affect perceived human health☆☆☆. Evolution and Human Behavior, 2010; DOI: 10.1016/j.evolhumbehav.2010.09.003

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Feast or famine: Researchers identify leptin receptor's sidekick as a target for appetite regulation

Feast or Famine: Researchers Identify Leptin Receptor's Sidekick as a Target for Appetite Regulation


ScienceDaily (Jan. 11, 2011) — A study by researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine adds a new twist to the body of evidence suggesting human obesity is due in part to genetic factors. While studying hormone receptors in laboratory mice, neuroscientists identified a new molecular player responsible for the regulation of appetite and metabolism.



See Also:
Health & Medicine

Obesity
Diet and Weight Loss
Nervous System

Mind & Brain

Dieting and Weight Control
Nutrition Research
Disorders and Syndromes

Reference

Appetite
Sensory neuron
Blood sugar
Astrocyte

In the Jan. 11 online issue of PLoS Biology, the authors report that mice engineered not to express the lipoprotein receptor LRP1, in the brain's hypothalamus, began to eat uncontrollably, growing obese as well as lethargic. They found that LRP1, a major transporter of lipids and proteins into brain cells, is a "co-receptor" with the leptin receptor -- meaning that both the leptin and LRP1 receptors need to work together to transmit leptin signals.
Leptin decides whether fat should be stored or used, resulting in lethargy or energy. When working properly, the hormone, which is made when body cells take in fat from food, travels to the brain to tamp down appetite.
"If a person is born with too little gene expression in the leptin pathway, which includes its receptors, or the circuitry is not functioning well, then leptin will not work as well as it should," says the study's lead investigator, neuroscientist Guojun Bu, Ph.D., of Mayo Clinic. "Appetite will increase, and body fat will be stored."
Given these results, Dr. Bu says it may be possible to develop a treatment that increases gene expression in one or both of the protein receptors, which then increases the messages meant to decrease appetite sent to the brain.
The serendipitous findings were born out of Dr. Bu's primary research focus, Alzheimer's disease. He has been studying how cholesterol, essential to the smooth functioning of neurons, is carried from star-shaped astrocytes to the surface of neurons by apolipoprotein E (APOE). There are two major receptors for APOE on brain neurons, and LRP1 is one of them.
Inheriting one version of APOE -- APOE4 -- is a known risk factor for development of Alzheimer's disease, and Dr. Bu has found that APOE4 is less effective at transporting cholesterol. To understand what role LRP1 plays in bringing APOE4 into neurons, he created a knockout mouse model with no expression of LRP1 in its forebrain neurons; the rest of its body expressed the receptor normally.
He found neurons lacking LRP1 had even less ability to absorb cholesterol, and that they lost synaptic contact with other neurons, impairing their ability to retain memory.
But Dr. Bu was surprised to find the mice suddenly gained weight. "This is the opposite of what had been observed in mice who did not have the receptor in their body fat cells," he says. "Those animals became skinny because they couldn't absorb enough lipoproteins."
The knockout mice were indistinguishable from control mice for the first six months of life but then gained weight rapidly, a phenomenon that correlated with a decrease in LPR1 expression in the central nervous system. At 12 months old, the genetically engineered mice had twice as much body fat as control mice, lacked energy, and were insulin resistant. "Together, these results indicate that LRP1, which is critical in lipid metabolism, also regulates food intake and energy balance in the adult central nervous system," Dr. Bu says.
The study was funded by the National Institutes of Health and the Alzheimer's Association.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Mayo Clinic.




Journal Reference:

Stephen O'Rahilly, Qiang Liu, Juan Zhang, Celina Zerbinatti, Yan Zhan, Benedict J. Kolber, Joachim Herz, Louis J. Muglia, Guojun Bu. Lipoprotein Receptor LRP1 Regulates Leptin Signaling and Energy Homeostasis in the Adult Central Nervous System. PLoS Biology, 2011; 9 (1): e1000575 DOI: 10.1371/journal.pbio.1000575

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High sugar consumption may increase risk factors for heart disease in American teenagers

High Sugar Consumption May Increase Risk Factors for Heart Disease in American Teenagers


ScienceDaily (Jan. 11, 2011) — Teenagers who consume a lot of added sugars in soft drinks and foods may have poor cholesterol profiles -- which may possibly lead to heart disease in adulthood, according to first-of-its-kind research reported in Circulation: Journal of the American Heart Association.



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"Added sugars" are any caloric sweeteners added to foods or beverages by the manufacturer during processing or the consumer. The National Health and Nutrition Survey (NHANES) of 2,157 teenagers (ages 12 to 18) found the average daily consumption of added sugars was 119 grams (28.3 tsp or 476 calories), accounting for 21.4 percent of their total energy.
The American Heart Association recently recommended a specific upper limit for added sugars intake, based on the number of calories an individual needs throughout the day, according to their energy expenditure, sex and age. For example, an appropriate amount for an individual with an energy requirement of 1,800 calories per day (an average teenage girl ages 14-18 might be in this calorie range) would be no more than 100 calories from added sugars. An individual with a requirement of 2200 calories per day should eat or drink no more than 150 calories from added sugars.
Teens consuming the highest levels of added sugars had lower levels of high density lipoprotein levels (HDL), the good cholesterol, and higher levels of triglycerides and low density lipoproteins (LDL), the bad cholesterol.
"This is the first study to assess the association of added sugars and the indicators of heart disease risk in adolescents," said Jean Welsh, MPH, PhD, R.N., study author and post-doctoral fellow at Emory University in Atlanta, Ga. "The higher consumers of added sugar have more unfavorable cholesterol levels. The concern is long-term exposure would place them at risk for heart disease later in adulthood."
Teenagers with the highest levels of added sugar consumption at more than 30 percent of total energy had 49.5 milligrams/deciliter (mg/dL) compared to 54 mg/dL of HDL levels in those with the lowest levels of added sugar consumption -- a 9 percent difference. Previous studies indicate that the largest contributors of added sugars to the diet are sugary beverages such as sodas, fruit drinks, coffees and teas, Welsh said.
"Adolescents are eating 20 percent of their daily calories in sugars that provide few if any other nutrients," she said. "Sweet things have lost their status as treats."
The study included dietary recall from one 24-hour period that researchers merged with sugar content data from the U.S. Department of Agriculture My Pyramid Equivalents Databases. Researchers estimated cardiovascular risk by added sugar consumption of less than 10 percent up to more than 30 percent of daily total energy. Two days of dietary data were used among a subsample of 646 adolescents and the key findings remained consistent:

Those with higher intake of added sugar had higher LDL levels of 94.3 mg/dL compared to 86.7 in those with the lowest levels, a 9 percent difference.
Triglyceride levels in those with the highest consumption were 79 mg/dL compared to 71.7 mg/dL among the lowest, a 10 percent difference.
Overweight or obese adolescents with the highest level of added sugar consumption had increased signs of insulin resistance.

"While Americans appear to be working hard to lower their intake of saturated fats, there is not the same awareness when it comes to added sugars," Welsh said. "The intake of added sugars is positively associated with known cardiovascular risk factors. Added sugars play a significant role in the U.S. diet, contributing substantially to energy intake without contributing important nutrients to the diet." Adolescents and adults should "use the labels of the drinks and food they consume to become familiar with the amount of sugar in them," Welsh said. "Replacing sugar laden drinks with water is one way to substantially reduce sugar and calorie intake."
Physicians also need to ask adolescents about their sugars intake and guide them to better choices, she said.
Because the researchers used cross-sectional data, they don't know if added sugars intake caused the differing cholesterol levels, only that they are linked. They also assessed the diet using one 24-hour recall of intake, which may not reflect on a person's usual intake. Long-term studies are needed to fully understand the effect that added sugars consumption in adolescence has on cardiovascular disease risk in adulthood, Welsh said.
Co-authors: are Andrea Sharma, Ph.D., M.P.H.; Solveig A.Cunningham, Ph.D.; and Miriam B. Vos, M.D., M.S.P.H. Author disclosures are on the manuscript.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Heart Association.




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Jean A. Welsh, Andrea Sharma, Solveig A. Cunningham, and Miriam B. Vos. Consumption of Added Sugars and Indicators of Cardiovascular Disease Risk Among US Adolescents. Circulation, 2011; DOI: 10.1161/CIRCULATIONAHA.110.972166

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Study evaluates prevalence of age-related macular degeneration in the United States

Study Evaluates Prevalence of Age-Related Macular Degeneration in the United States


ScienceDaily (Jan. 10, 2011) — An estimated 6.5 percent of Americans age 40 and older have the eye disease age-related macular degeneration, a lower rate than was reported 15 years ago, according to a report in the January issue of Archives of Ophthalmology, one of the JAMA/Archives journals.



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"Despite new medical and surgical interventions, age-related macular degeneration (AMD) remains an important cause of loss of vision in the United States," the authors write as background information in the article. The last nationally representative estimates of prevalence of AMD were based on the 1988-1994 Third National Health and Nutrition Examination Survey (NHANES III).
To update these estimates, Ronald Klein, M.D., M.P.H., of University of Wisconsin School of Medicine and Public Health, Madison, and colleagues analyzed data from the 2005 to 2008 NHANES. A total of 7,081 individuals age 40 or older were selected to participate and had photographs taken of both eyes. Digital images of the eyes were assessed for signs of AMD, including drusen (tiny yellow or white deposits in the retina), pigment changes and atrophy in the retina and surrounding tissue.
The overall prevalence of AMD among adults age 40 and older was an estimated 6.5 percent, which represented a decrease from the 9.4 percent reported in the 1988 to 1994 survey. The estimated prevalence of late (more advanced) AMD was 0.8 percent. Non-Hispanic black individuals age 60 and older had a lower prevalence of any AMD than non-Hispanic white individuals of the same age.
"These estimates are consistent with a decreasing incidence of AMD reported in another population-based study and have important public health implications," the authors conclude. "The decreasing prevalence of AMD may reflect recent change in the frequency of smoking and other exposures such as diet, physical activity and blood pressure associated with AMD. It remains to be seen whether public health programs designed to increase awareness of the relationships of these exposures to AMD in patients at risk and their physicians and eye care providers will continue to result in further decline of the prevalence of AMD in the population."
Editor's Note: This research was supported by a National Health and Nutrition Examination survey contract, which provided funding for the entire study including collection and analyses of data. Additional support was provided by Senior Scientific Investigator Awards from Research to Prevent Blindness.

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R. Klein, C.-F. Chou, B. E. K. Klein, X. Zhang, S. M. Meuer, J. B. Saaddine. Prevalence of Age-Related Macular Degeneration in the US Population. Archives of Ophthalmology, 2011; 129 (1): 75 DOI: 10.1001/archophthalmol.2010.318

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