Adolescent Obesity Associated With Hearing Loss

Obese adolescents are more likely than their normal-weight counterparts to have hearing loss, according to results of a new study. Findings showed that obese adolescents had increased hearing loss across all frequencies and were almost twice as likely to have unilateral (one-sided) low-frequency hearing loss. The study was recently e-published by The Laryngoscope, a journal published by the American Laryngological, Rhinological and Otological Society.

"This is the first paper to show that obesity is associated with hearing loss in adolescents," said study first author Anil K. Lalwani, MD, professor and vice chair for research, Department of Otolaryngology/Head & Neck Surgery, Columbia University Medical Center.

The study found that obesity in adolescents is associated with sensorineural hearing loss across all frequencies (the frequency range that can be heard by humans); sensorineural hearing loss is caused by damage to the inner-ear hair cells. The highest rates were for low-frequency hearing loss - 15.16 percent of obese adolescents compared with 7.89 percent of non-obese adolescents. People with low-frequency hearing loss cannot hear sounds in frequencies 2,000 Hz and below; they may still hear sounds in the higher frequencies (normal hearing range is from 20 Hz to 20,000 Hz). Often they can still understand human speech well, but may have difficulty hearing in groups or in noisy places.

"These results have several important public health implications," said Dr. Lalwani, who is also an otolaryngologist at NewYork-Presbyterian Hospital/Columbia University Medical Center. "Because previous research found that 80 percent of adolescents with hearing loss were unaware of having hearing difficulty, adolescents with obesity should receive regular hearing screening so they can be treated appropriately to avoid cognitive and behavioral issues."

Although the overall hearing loss among obese adolescents was relatively mild, the almost 2-fold increase in the odds of unilateral low-frequency hearing loss is particularly worrisome. It suggests early, and possibly ongoing, injury to the inner ear that could progress as the obese adolescent becomes an obese adult. Future research is needed on the adverse consequences of this early hearing loss on social development, academic performance, and behavioral and cognitive function.

"Furthermore, hearing loss should be added to the growing list of the negative health consequences of obesity that affect both children and adults - adding to the impetus to reduce obesity among people of all ages," said Dr. Lalwani.

In the United States, nearly 17 percent of children are obese, defined as having a body mass index (BMI) of =95 percentile. (BMI in children is expressed as a percentile; adult BMI is expressed as a number based on weight and height.) Obesity and its associated morbidities have been identified as a risk factor for hearing loss in adults.

The study analyzed data from nearly 1,500 adolescents from the National Health and Nutrition Examination Survey - a large, nationally representative sample of adolescents between the ages of 12 and 19, conducted from 2005 to 2006 by the National Center for Health Statistics of the Centers for Disease Control and Prevention. Participants were interviewed at home, taking into account family medical history, current medical conditions, medication use, household smokers, socioeconomic and demographic factors, and noise-exposure history.

Dr. Lalwani and his colleagues speculate that obesity may directly or indirectly lead to hearing loss. Although additional research is needed to determine the mechanisms involved, they theorize that obesity-induced inflammation may contribute to hearing loss. Low plasma levels of the anti-inflammatory protein adiponectin, which is secreted from adipose tissue, have been found in obese children, and low levels in obese adults have been associated with high-frequency hearing loss (which affects a person's ability to understand speech). Obesity also may contribute indirectly to hearing loss as a result of its comorbidities, including type 2 diabetes, cardiovascular disease, and high cholesterol - all of which have been reported to be associated with loss of peripheral hearing (relating to the outer, middle, and inner ear).

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Research Breakthrough Of Essential Molecule Reveals Important Targets In Diabetes And Obesity

Insulin is the most potent physiological anabolic agent for tissue-building and energy storage, promoting the storage and synthesis of lipids, protein and carbohydrates, and inhibiting their breakdown and release into the circulatory system. It also plays a major role in stimulating glucose entry into muscle tissue, where the glucose is metabolized and removed from the blood following meals. But gaps exist in understanding the precise molecular mechanisms by which insulin regulates glucose uptake in fat and muscle cells.

A research team led by Assia Shisheva, Ph.D., professor of physiology in Wayne State University's School of Medicine, has made breakthrough advancements on a molecule that may provide more answers to this mystery.

The conserved phospholipid enzyme, PIKfyve, was discovered in Shisheva's lab in 1999. Based on studies in cultured cells, the lab has implicated PIKfyve in the insulin-regulated glucose transport activation, which led to the development of a unique mouse model with PIKfyve ablation, or removal, in muscle (MPlfKO), the tissue responsible for the majority of postprandial glucose disposal.

In Shisheva's recent paper, "Muscle-specific PIKfyve gene distribution causes glucose intolerance, insulin resistance, adiposity and hyperinsulinemia but not muscle fiber-type switching," published online in the American Journal of Physiology - Endocrinology and Metabolism, Shisheva and her research team characterize whether this new model exhibits metabolic defects.

"Our team found a striking metabolic phenotype in the MPIfKO mice consisting of glucose intolerance and insulin resistance at an early age and on a normal diet," said Shisheva, a resident of Royal Oak. "We also revealed that PIKfyve is essential for normal insulin signaling to GLUT4/glucose transport in muscle and provided the first in vivo evidence for the central role of PIKfyve in the mechanisms regulating healthy blood glucose levels, or glucose homeostasis."

In addition, the research team found that these metabolic disturbances were followed by increased animal fat (adiposity) and elevated levels of insulin (hyperinsulinemia), but not abnormal amounts of lipids or cholesterol in the blood (dyslipidemia).

"The combined phenotype manifested by the MPlfKO mouse closely recapitulates the cluster of typical features in human prediabetes including systemic glucose intolerance and insulin resistance, hyperinsulinemia and increased visceral obesity without dyslipidemia," said Shisheva.

"Therefore, our mouse model, in addition to providing novel mechanisms of insulin resistance, represents a valuable tool for exploring new preclinical strategies to improve treatments in individuals with prediabetes."

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Your Weight, Eating Behavior, Likely Impacted By What You Believe Causes Obesity

Whether a person believes obesity is caused by overeating or by a lack of exercise predicts his or her actual body mass, according to new research published in Psychological Science, a journal of the Association for Psychological Science.

Obesity has become a pressing public health issue in recent years, with two-thirds of U.S. adults classified as overweight or obese and similar trends unfolding in many developed nations. Researchers Brent McFerran of the Ross School of Business at the University of Michigan and Anirban Mukhopadhyay of Hong Kong University of Science and Technology wondered whether individual beliefs might play a role in these trends.

From an initial online survey, they discovered that people seem to subscribe to one of two major beliefs about the primary cause of obesity:

"There was a clear demarcation," says McFerran. "Some people overwhelmingly implicated poor diet, and a roughly equal number implicated lack of exercise. Genetics, to our surprise, was a far distant third."

McFerran and Mukhopadhyay wanted to dig deeper to see if the pattern could be replicated and, if so, what implications it might have for behavior. They conducted a series of studies across five countries on three continents.

Data from participants in Korea, the United States, and France showed the same overall pattern: Not only did people tend to implicate diet or exercise as the leading cause of obesity, people who implicated diet as the primary cause of obesity actually had lower BMIs than those who implicated lack of exercise.

"What surprised me the most was the fact that we found lay theories to have an effect on BMI over and above other known factors, such as socio-economic status, age, education, various medical conditions, and sleep habits," says McFerran.

The researchers hypothesized that the link between people's beliefs and their BMI might have to do with how much they eat.

A study with Canadian participants revealed that participants who linked obesity to lack of exercise ate significantly more chocolates than those who linked obesity to diet. And a study with participants in Hong Kong showed that participants who were primed to think about the importance of exercise ate more chocolate than those primed to contemplate diet.

These findings provide evidence that our everyday beliefs about obesity may actually influence our eating habits - and our body mass.

According to Mukhopadhyay, this is "the first research that has drawn a link between people's beliefs and the obesity crisis, which is growing as fast as people's waistlines are."

The new findings suggest that, in order to be effective, public health campaigns may need to target people's beliefs just as much as they target their behaviors.

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Relationship Between Short-Term Antidepressant Use, Stress, High-Fat Diet And Long-Term Weight Gain

Short-term use of antidepressants, combined with stress and a high-fat diet, is associated with long-term increases in body weight, a new animal study finds. The results were presented Sunday at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Our study suggests that short-term exposure to stress and antidepressants, rather than a high-calorie, high-fat diet alone, leads to long-term body weight gain, accompanied with increased bone and spleen weights," said study lead author Suhyun Lee, a PhD candidate in the medical sciences at the John Curtin School of Medical Research at the Australian National University in Canberra, Australia.

Antidepressants are among the most prevalent medications today, accounting for millions of prescriptions each year. In the United States, physicians wrote more than 1.5 million prescriptions for antidepressants in 2009, while physicians in Australia wrote more than 12 million of these prescriptions in 2008.

At the same time, obesity rates are climbing in developed countries worldwide. Among adults in both the United States and Australia, two-thirds are overweight or obese. Being overweight or obese is a risk factor for many serious diseases, including heart disease, which is the leading cause of death among adults in the United States and Australia.

Unfortunately, weight gain is one of the main side effects associated with antidepressants. The amount of excess weight varies between patients, but some have reported increases as high as 7 percent of the amount they weighed at the start of their antidepressant treatment.

In this study, male rats treated with the antidepressant fluoxetine after induced stress had significantly increased body weight compared to control animals. In addition to greater overall body weight, animals in the antidepressant group also developed greater bone and spleen weights, compared to animals in the control group.

"These findings may implicate different pathophysiological mechanisms in stress and antidepressant related obesity when compared to obesity that is solely diet-induced," Lee said.

During the follow-up, investigators also compared behavior between the drug and control groups. This comparison showed that the antidepressants reduced anxiety among the animals in response to induced stress. After the stressful periods, which involved physical restraint, the fluoxetine-treated animals exhibited significantly fewer symptoms of anxiety, compared to the control animals.

The study involved a two-week period of repeated restraint stress, combined with antidepressant treatment among one group of animals, and saline administration among the control group. After the two-week period, both groups of animals received a high-fat diet for 295 days.

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The Importance Of A Father's Diet Before Conception

When fathers eat a high-fat diet before conception of offspring, the male offspring have increased body weight after weaning and high body fat in midlife despite eating a low-fat diet, a new study in mice finds. The results were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Many researchers have studied the effects of maternal diet on the risk of obesity in their children. We found that the father's diet also affects the offspring in ways that are inherited," said the study's principal investigator, Felicia V. Nowak, MD, PhD, associate professor of molecular endocrinology at Ohio University in Athens.

The inherited differences in metabolism in the offspring of obese fathers appear to be epigenetic - changes in how genes are expressed that are "not hardwired" into the genes, meaning that they are modifiable by internal and external environmental factors, Nowak said. The cause of these changes was not behavioral because the offspring did not observe what their fathers ate nor did they have access to a high-fat diet, she noted.

In their study, the researchers fed male mice a 13-week diet that was either high fat (45 percent of calories derived from fat) or low fat (10 percent of calories from fat; control mice) but contained the same number of calories. The mice that ate the high-fat food became obese. All mice were mated with females that had received the matched low-fat diet. All their offspring received standard laboratory mouse chow.

The mouse pups underwent testing of their body weight and fat at various ages: 20 days, which was right after weaning and is similar in age to human infants or toddlers, according to Nowak; 6 weeks, which is roughly equivalent to adolescence; 6 months, or young adulthood; and finally 12 months, or older adulthood.

Compared with offspring from control mice, the male offspring of paternal mice with diet-induced obesity had higher body weight starting at 6 weeks of age, and the increased weight was still present at 6 and 12 months, the authors reported. In addition, at 6 months, the male offspring of the obese paternal mice had a higher percentage of total body fat than control offspring did. There were, however, no observed differences in the amount of brown fat, the calorie-burning fat that both rodents and humans have.

Surprisingly, male offspring of the high-fat-fed paternal mice also showed increases in voluntary running at 6 weeks. Female offspring ran more than male offspring at 6 months and 12 months, Nowak said. She said they are studying possible causes for this behavior, which might offset the increased body fat and reduce the offspring's risk of metabolic disease such as diabetes and heart disease.

"Increasing numbers of children and adolescents are affected by obesity," Nowak said. "It is essential that we identify markers for early detection and prediction of obesity and diabetes. This will enable individuals to make healthy lifestyle choices and receive targeted health care interventions to delay or prevent the related disabilities and increase life expectancy."

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Causal Relationship Between Adiposity And Heart Failure, And Elevated Liver Enzymes

New evidence supports a causal relationship between adiposity and heart failure, and between adiposity and increased liver enzymes, according to a study published this week in PLOS Medicine. The study, conducted by Inga Prokopenko, Erik Ingelsson, and colleagues from the ENGAGE (European Network for Genetic and Genomic Epidemiology) Consortium, also provides additional support for several previously shown causal associations such as those between adiposity and type 2 diabetes, metabolic syndrome, dyslipidemia, and hypertension.

The authors investigated whether adiposity is causally related to various cardiometabolic traits using a Mendelian randomization analysis, in which the variation in genes associated with conditions is used to assess the causal relationship between conditions. It is known that a genetic variant (rs9939609) within the genome region that encodes the fat-mass- and obesity-associated gene (FTO) is associated with increased BMI. Using genetic and health data collected in 36 population-based studies of nearly 200,000 individuals of European descent, the authors measured the strength of the causal association between BMI and cardiometabolic traits and found that higher BMI had a causal relationship with heart failure, type 2 diabetes, metabolic syndrome, dyslipidemia, hypertension, increased blood levels of liver enzymes, and several other cardiometabolic traits.

As with all Mendelian randomization studies, the reliability of the causal associations reported here depends on several assumptions made by the researchers. The authors report, "The present study addressing the role of BMI in 24 traits in up to 198,502 individuals provides novel insights in the causal effect of obesity on heart failure and increased liver enzymes levels."

They also say that this study "provides robust support to the causal relationship between obesity and a number of cardiometabolic traits reported previously. These results support global public prevention efforts for obesity in order to decrease cost and suffering from [type 2 diabetes] and heart failure."

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Longest-Ever Intervention Study Investigating Whether Weight Loss Reduces The Risk Of Heart Disease For Patients With Type 2 Diabetes

A landmark study investigating the long-term effects of weight loss on the risks of cardiovascular disease among patients with Type 2 diabetes has now concluded, with significant results published in the New England Journal of Medicine.

Conducted at the University of Pittsburgh and at clinical facilities throughout the United States, the multicenter clinical trial investigated the effects of an intensive lifestyle intervention program, intended to achieve and maintain weight loss in overweight or obese people with Type 2 diabetes, on rates of cardiovascular disease. Begun in 2001, the trial enrolled more than 5,000 people at 16 clinical centers across the United States and is the longest intervention study of its type ever undertaken for patients with diabetes.

John Jakicic, chair and professor in the Department of Health and Physical Activity in Pitt's School of Education and Director of the Physical Activity and Weight Management Research Center, served as principal investigator for the University of Pittsburgh's role in the study. He, along with colleagues throughout the University, is among the researchers comprising the national Look AHEAD (Action for Health in Diabetes) Research Group, which carried out the study and authored the New England Journal of Medicine paper.

Among the study's main findings is that weight loss among members of the study's Intensive Lifestyle Intervention group, provided with a program of weight management and increased physical activity, resulted in no difference in heart attacks and strokes when compared with the study's control group, the Diabetes Support and Education group, which was provided with only general health information and social support.

The effect of the intervention program on weight loss, however, was significant: Participants in the intervention group lost 8.7 percent of their initial body weight after one year of the study versus 0.7 percent among the control group's members; the intervention group also maintained a greater weight loss, 6 percent of their initial weight, versus 3.5 percent for the control group, at the study's conclusion.

The Look AHEAD study is the first to achieve such sustained weight loss. A weight loss of 5 percent or more in short-term studies is considered to be clinically significant and has been shown to improve control of blood pressure, blood sugar, cholesterol, and other risk factors. Comparable weight loss can also help prevent the development of Type 2 diabetes in overweight and obese adults.

"While the findings from the Look AHEAD study did not support that engagement in a weight- loss intervention was effective for reducing the onset of cardiovascular disease incidence or mortality, this does not mean that overweight adults with diabetes should not lose weight and become more physically active," said Jakicic. "Rather, there is an overwhelming amount of evidence from this study to date that has shown that weight loss and physical activity were associated with numerous other health benefits.

"These include improving physical function and quality of life, reduction in risk factors such as lipids and blood pressure with less reliance on medication, better diabetes control with less reliance on medication, improved sleep, psychological and emotional health benefits, and many others," Jakicic said. "Thus, adults with diabetes can begin to realize many of these health benefits with even modest reductions in body weight and modest increases in physical activity."

The study sought to determine whether weight loss achieved with a lifestyle program would help individuals with diabetes live longer and develop less cardiovascular disease. While short-term studies had shown that weight loss improved control of blood sugar and mitigated risk factors for heart disease and stroke in overweight and obese individuals with Type 2 diabetes, the longer-term effects of weight loss were not well studied. In particular, it was unknown whether weight loss achieved with a lifestyle intervention alone could reduce the risk of heart disease in people with Type 2 diabetes.

Type 2 is the most common form of diabetes, affecting approximately 25 million Americans over the age of 20. Complications of Type 2 diabetes include heart disease and stroke, high blood pressure, blindness, kidney disease, the nervous system disease known as neuropathy, and amputations. The total cost of Type 2 diabetes in 2012 was estimated to be $245 billion. This disease, for which there is no cure but which involves ongoing treatment, can be managed with diet, physical activity including regular exercise equal to at least 30 minutes of brisk walking each day, modest weight loss, and a variety of medications. The Look AHEAD study has shown that these lifestyle factors are effective for improving the management of Type 2 diabetes.

Study participants were individuals between 45 and 75 years of age with Type 2 diabetes and a body-mass index of 25 or greater. Sixty percent of the study participants were women, while 37 percent were from ethnic and racial minority groups.

The University of Pittsburgh's General Clinical Research Center and Clinical Translational Research Center served as participating clinical sites, with researchers here recruiting more than 330 participants over a three-year span. Jakicic credited the Division of Endocrinology within the Department of Medicine and the Department of Psychiatry in Pitt's School of Medicine, and the Department of Epidemiology in Pitt's Graduate School of Public Health, with the success of the local clinical trials.

Participants were assigned randomly to the Intensive Lifestyle Intervention group or the Diabetes Support and Education group. Members of the Intensive Lifestyle Intervention group were enrolled in a weight management program that provided individual and group support for making changes in eating behaviors and engaging in physical activity. The intervention program focused on home-based, functional activities including helping participants balance, climb stairs, and get out of a chair, among other examples. Diabetes Support and Education group members received what Jakicic called "usual care, with some very infrequent support on general health topics that were not related to diet, physical activity, or weight loss."

Participants were required to have their own health care providers manage their diabetes and other conditions. Look AHEAD did not provide medical care, but it did assist participants in finding a health care provider if they did not have one.

The Look AHEAD study was intended to run for 13.5 years, the maximum length of time researchers had determined might be required to see a difference in heart disease between two groups. After 11 years, however, the Look AHEAD Data and Safety Monitoring Board, an independent monitoring board that provides recommendations to the National Institutes of Health, reviewed the data the study had collected and determined that Look AHEAD could reach the definite conclusion that there were no differences in cardiovascular disease rates between the study's two groups.

Speculating on the failure of weight loss to reduce the risk of cardiovascular disease, researchers suggested that even greater weight loss may be necessary to reduce cardiovascular risk in diabetes patients who are overweight or obese. They also suggested that by providing participants in both groups, and their health care providers, with annual feedback on the participants' blood pressure, lipids, and blood sugar control, the cardiovascular disease risks for all experiment participants may have been reduced at a comparable rate.

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In Animal Model, Dietary Fructose Found To Cause Liver Damage

The role of dietary fructose in the development of obesity and fatty liver diseases remains controversial, with previous studies indicating that the problems resulted from fructose and a diet too high in calories.

However, a new study conducted in an animal model at Wake Forest Baptist Medical Center showed that fructose rapidly caused liver damage even without weight gain. The researchers found that over the six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group.

The study is published in the American Journal of Clinical Nutrition.

"Is a calorie a calorie? Are they all created equal? Based on this study, we would say not," said Kylie Kavanagh, D.V.M., assistant professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study.

In a previous trial which is referenced in the current journal article, Kavanagh's team studied monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period. Not surprisingly, the animals allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group. They developed diabetes at three times the rate of the control group and also developed hepatic steatosis, or non-alcoholic fatty liver disease.

The big question for the researchers was what caused the liver damage. Was it because the animals got fat from eating too much, or was it something else?

To answer that question, this study was designed to prevent weight gain. Ten middle-aged, normal weight monkeys who had never eaten fructose were divided into two groups based on comparable body shapes and waist circumference. Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.

Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein.

Every week the research team weighed both groups and measured their waist circumference, then adjusted the amount of food provided to prevent weight gain. At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through fecal samples and intestinal biopsies.

"What surprised us the most was how quickly the liver was affected and how extensive the damage was, especially without weight gain as a factor," Kavanagh said. "Six weeks in monkeys is roughly equivalent to three months in humans."

In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there. It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate, Kavanagh said.

One of the limitations of the study was that it only tested for fructose and not dextrose. Fructose and dextrose are simple sugars found naturally in plants.

"We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can't say conclusively that fructose caused the liver damage," Kavanagh said. "What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.

"The liver damage began even in the absence of weight gain. This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems."

The Wake Forest Baptist team plans to begin a new study using the same controls but testing for both fructose and dextrose over a longer time frame.

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