Isolated aerobic exercise and weight loss: a systematic review and meta-analysis of randomized controlled trials.

Thorogood A, Mottillo S, Shimony A, Filion KB, Joseph L, Genest J, Pilote L, Poirier P, Schiffrin EL, Eisenberg MJ.

Source

Divisions of Cardiology and Clinical Epidemiology, Jewish General Hospital/McGill University, Montreal, Quebec, Canada; Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada.

Abstract

BACKGROUND:

Aerobic exercise is a common nonpharmacological intervention for the management of obesity. However, the efficacy of isolated aerobic exercise at promoting weight loss is unclear. We conducted a systematic review and meta-analysis to evaluate the efficacy of isolated aerobic exercise programs in overweight and obese populations.

METHODS:

We searched for published randomized controlled trial reports of aerobic exercise through January 20, 2010. Trials with an isolated aerobic exercise intervention were included. A random-effect model was used to synthesize the results of each intervention.

RESULTS:

We identified 14 trials involving 1847 patients. The duration of aerobic exercise programs ranged from 12 weeks to 12 months. Results were pooled for programs with 6-month duration and programs with 12-month duration. Six-month programs were associated with a modest reduction in weight (weighted mean difference [WMD]=-1.6 kg; 95% confidence interval [CI], -1.64 to -1.56) and waist circumference (WMD=-2.12 cm; 95% CI, -2.81 to -1.44). Twelve-month programs also were associated with modest reductions in weight (WMD=-1.7 kg; 95% CI, -2.29 to -1.11) and waist circumference (WMD=-1.95 cm; 95% CI, -3.62 to -0.29).

CONCLUSION:

Moderate-intensity aerobic exercise programs of 6-12 months induce a modest reduction in weight and waist circumference in overweight and obese populations. Our results show that isolated aerobic exercise is not an effective weight loss therapy in these patients. Isolated aerobic exercise provides modest benefits to blood pressure and lipid levels and may still be an effective weight loss therapy in conjunction with diets.

Copyright © 2011 Elsevier Inc. All rights reserved.

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New Link Found Between Obesity and Insulin Resistance

Obesity is the main culprit in the worldwide avalanche of type 2 diabetes. But how excess weight drives insulin resistance, the condition that may lead to the disease, is only partly understood. Scientists at Joslin Diabetes Center now have uncovered a new way in which obesity wreaks its havoc, by altering the production of proteins that affect how other proteins are spliced together.

Their finding, published in Cell Metabolism, may point toward novel targets for diabetes drugs.
Scientists in the lab of Mary-Elizabeth Patti, M.D., began by examining the levels of proteins in the livers of obese people, and finding decreases in number for certain proteins that regulate RNA splicing.

"When a gene is transcribed by the cell, it generates a piece of RNA," explains Dr. Patti, who is also an Assistant Professor of Medicine at Harvard Medical School. "That piece of RNA can be split up in different ways, generating proteins that have different functions."

"In the case of these proteins whose production drops in the livers of obese people, this process changes the function of other proteins that can cause excess fat to be made in the liver," she adds. "That excess fat is known to be a major contributor to insulin resistance."

Additionally, the researchers showed that these RNA splicing proteins are diminished in samples of muscle from obese people.

The investigators went on to examine a representative RNA-splicing protein called SFRS10 whose levels drop in muscle and liver both in obese people and in over-fed mice. Working in human cells and in mice, they demonstrated that SFRS10 helps to regulate a protein called LPIN1 that plays an important role in synthesizing fat. Among their results, mice in which they suppressed production of SFRS10 made more triglycerides, a type of fat circulating in the blood.

"More broadly, this work adds a novel insight into how obesity may induce insulin resistance and diabetes risk by changing critical functions of cells, including splicing," says Dr. Patti. "This information should stimulate the search for other genes for which differences in splicing may contribute to risk for type 2 diabetes. Ultimately, we hope that modifying these pathways with nutritional or drug therapies could limit the adverse consequences of obesity."

Jussi Pihlajamäki and Carles Lerin of Joslin are co-first authors on the paper. Markku Laakso of the University of Eastern Finland co-supervised the project. Other contributors include Tanner Boes, Joshua Schroeder, Farrell Dearie, Sarah Crunkhorn, Furkan Burak, Josep C. Jimenez-Chillaron and Allison B. Goldfine of Joslin; Paula Itkonen, Tiina Kuulasmaa and Pekka Miettinen of the University of Eastern Finland; Thomas Floss and Wolfgang Wurst of the Technical University of Munich; Peter Park of Children's Hospital Boston; Imad Nasser of Beth Israel Deaconess Medical Center; Zhenwen Zhao and Yan Xu of Indiana University Schoolf of Medicine; and Zhaiyi Zhang, Hongmei Ren, Andrew J. Morris and Stefan Stamm of University of Kentucky/Lexington. Lead funders were the National Institutes of Health and the Lilly Foundation.

http://www.sciencedaily.com/releases/2011/08/110802125551.htm

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Study Explains Why Muscles Weaken With Age and Points to Possible Therapy

Researchers at Columbia University Medical Center have discovered the biological mechanism behind age-related loss of muscle strength and identified a drug that may help reverse this process. Their findings were published in the August 2 online edition of Cell Metabolism.

As we grow older, our skeletal muscles tend to wither and weaken, a phenomenon known as sarcopenia. Sarcopenia, which begins to appear at around age 40 and accelerates after 75, is a major cause of disability in the elderly. Exercise can help counter the effects of age-related muscle loss. Otherwise, there are no established treatments.

According to the new study, conducted in mice, sarcopenia occurs when calcium leaks from a group of proteins in muscle cells called the ryanodine receptor channel complex. These leaks then trigger a chain of events that ultimately limits the ability of muscle fibers to contract, reports study leader Andrew R. Marks, M.D., chairman and professor of physiology and cellular biophysics, the Clyde and Helen Wu Professor of Medicine, and director of the Wu Center for Molecular Cardiology at Columbia University Medical Center (CUMC).

Ryanodine receptors, which are calcium channels found in most body tissues, have been the focus of Dr. Marks' research since 1989. After cloning the ryanodine receptor gene, he later discovered, in studies of mice, that leaky ryanodine receptors are involved in the development of heart failure and arrhythmias. In 2009, he showed that leaks in these channels also contribute to Duchenne muscular dystrophy, a genetic disorder characterized by rapidly progressing muscle weakness and early death.
Since muscular dystrophy and sarcopenia have some commonalities, Dr. Marks suspected that ryanodine receptor leakage may also be involved in age-related muscle loss, which the present study shows is the case.

"This is a completely new concept -- that the damage that occurs in aging is very similar to what happens in muscular dystrophy," says Dr. Marks, "thus as we age we essentially develop an acquired form of muscular dystrophy."

Both the aging process and the genetic defect responsible for muscular dystrophy cause an increase in the production of oxygen free radicals, highly reactive and harmful molecules. "Our data suggest that this sets up a vicious cycle, in which the free radicals cause ryanodine receptors to leak calcium into the cell. The calcium poisons mitochondria -- organelles that power the cell -- leading to the release of even more free radicals. This, in turn, causes more calcium leakage. With less calcium available for contraction, the muscles get weaker," says first author Daniel C. Andersson, M.D., Ph.D., a postdoctoral fellow in physiology and cellular biophysics at CUMC.

The study also points to a possible therapy for sarcopenia: an experimental drug called S107, developed by Dr. Marks and his colleagues. The drug acts by stabilizing calstabin1, a protein that binds to ryanodine receptors and prevents calcium leakage.

In the study, 24-month-old mice (roughly the equivalent of 70-year-old humans) were given S107 for four weeks. The mice showed significant improvements in both muscle force and exercise capacity, compared with untreated controls. "The mice ran farther and faster during voluntary exercise," says Dr. Andersson. "When we tested their muscles, they were about 50 percent stronger." The drug had no effect on younger mice with normal ryanodine receptors.

A similar drug is now in phase II clinical trials for the treatment of heart failure.
"Most investigators in the field of aging have been saying that the way to improve muscle strength is to build muscle mass, using such therapies as testosterone, growth hormone, and insulin-like growth factor-1," says Dr. Marks. "But an increase in muscle mass is not necessarily accompanied by an increase in muscle function. Our results suggest that you can improve muscle function by fixing leaky calcium channels. And in fact, treating aged mice with S107 enhanced muscle strength without increasing muscle size, at least during the four-week treatment period."

Dr. Marks' paper is titled, "Ryanodine Receptor Oxidation Causes Intracellular Calcium Leak and Muscle Weakness in Aging." In addition to Dr. Andersson, his coauthors include Mathew J. Betzenhauser, Steven Reiken, Albano C. Meli, Alisa Umanskaya, Wenjun Xie, Takayuki Shiomi, and Ran Zalk at CUMC, and Alain Lacampagne at Universités Montpellier, Montpellier, France.
A.R. Marks is a consultant for a start-up company, ARMGO Pharma, Inc., which is targeting ryanodine receptors to improve exercise capacity in muscle diseases.

This research was supported by grants from the National Heart, Lung, and Blood Institute and the Swedish Research Council.

http://www.sciencedaily.com/releases/2011/08/110802125549.htm

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Why Diets Don't Work: Starved Brain Cells Eat Themselves, Study Finds

A report in the August issue of the Cell Press journal Cell Metabolism might help to explain why it's so frustratingly difficult to stick to a diet. When we don't eat, hunger-inducing neurons in the brain start eating bits of themselves. That act of self-cannibalism turns up a hunger signal to prompt eating.

"A pathway that is really important for every cell to turn over components in a kind of housekeeping process is also required to regulate appetite," said Rajat Singh of Albert Einstein College of Medicine.
The cellular process uncovered in neurons of the brain's hypothalamus is known as autophagy (literally self-eating.) Singh says the new findings in mice suggest that treatments aimed at blocking autophagy may prove useful as hunger-fighting weapons in the war against obesity.

The new evidence shows that lipids within the so-called agouti-related peptide (AgRP) neurons are mobilized following autophagy, generating free fatty acids. Those fatty acids in turn boost levels of AgRP, itself a hunger signal.

When autophagy is blocked in AgRP neurons, AgRP levels fail to rise in response to starvation, the researchers show. Meanwhile, levels of another hormone, called -melanocyte stimulating hormone, remain elevated. That change in body chemistry led mice to become lighter and leaner as they ate less after fasting, and burned more energy.

Autophagy is known to have an important role in other parts of the body as a way of providing energy in times of starvation. However, unlike other organs, earlier studies had shown the brain to be relatively resistant to starvation-induced autophagy.

"The present study demonstrates the unique nature of hypothalamic neurons in their ability to upregulate autophagy in response to starvation that is consistent with the roles of these neurons in feeding and energy homeostasis," the researchers wrote.

Singh said he suspects that fatty acids released into the circulation and taken up by the hypothalamus as fat stores break down between meals may induce autophagy in those AgRP neurons. Singh's research earlier showed a similar response in the liver.

On the other hand, he says, chronically high levels of fatty acids in the bloodstream, as happens in those on a high-fat diet, might alter hypothalamic lipid metabolism, "setting up a vicious cycle of overfeeding and altered energy balance." Treatments aimed at the pathway might "make you less hungry and burn more fat," a good way to maintain energy balance in a world where calories are cheap and plentiful.

The findings might also yield new insight into metabolic changes that come with age given that autophagy declines as we get older. "We already have some preliminary evidence there might be changes with age," Singh said. "We are excited about that."

http://www.sciencedaily.com/releases/2011/08/110802125546.htm

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What's in a Kids Meal? Not Happy News

High-calorie, high-sodium choices were on the menu when parents purchased lunch for their children at a San Diego fast-food restaurant. Why? Because both children and adults liked the food and the convenience.

However, the study of data compiled by researchers in the Department of Pediatrics at the University of California, San Diego, appearing this week in the new journal, Childhood Obesity, showed that convenience resulted in lunchtime meals that accounted for between 36 and 51 percent of a child's daily caloric needs. In addition, 35 to 39 percent of calories came from fat and the meals provided more than 50 percent of the recommended total daily sodium intake for most children- and as high as 100 percent of sodium levels recommended for pre-schoolers.

"We found that families perceived fast-food restaurants as easy and cheap, and many were using fast food as a reward for their children," said Kerri N. Boutelle, PhD, Behavioral Director of the Weight and Wellness Clinic at the University of California, San Diego and Rady Children's Hospital-San Diego, who has studied childhood obesity, its causes and treatment for over 15 years. "Considering the high prevalence of fast-food consumptions by adults as well as kids, it's important to recognize the impact of fast food and its impact on the current obesity epidemic in the U.S."

The UC San Diego researchers surveyed 544 families with children entering a fast-food chain restaurant located inside Rady Children's Hospital in San Diego, California at lunch time over a six-week period. Families were asked to retain and present their receipts from food purchases and complete a brief survey. Families were provided a $2 incentive to participate.

Families were asked to clarify their purchases: for whom each item was purchased, if items were shared, sizes of individual items (small, medium, large), whether soft drinks were regular or diet, what items were included in any combination meals purchased, and if there were any modifications to their order. For every purchased item, the surveyors asked for age and gender of the person eating it.
"The number of meals and snacks eaten away from home is believed to contribute to excess calories consumed by children, and this number has increased dramatically in the past 30 years," said Boutelle. "On a typical day, a remarkable 30 percent of youth report consuming fast food."

The purpose of the study was to evaluate the nutritional content and quality of food, as well as the reasons reported for dining at a fast-food restaurant. Perhaps unsurprisingly, the top reasons for going to this restaurant were "the children like the food" and it was "convenient." Just over half the families reported the choice as "a reward for visiting the hospital" (about the same number as replied "hungry with no other options").

But adults also overwhelmingly reported that they liked the food. The toys included with the children's meals did not appear to be a top reason (49 percent said it didn't enter into their decision "at all").
The nutritional content of the food choices supported other published data on fast-food and dietary intake on children. The highest percentage of daily caloric needs represented by these meals (51 percent) was in the age 2 to 5 years. Menu items most frequently purchased for preschoolers were French fries, soda, chicken nuggets, cheeseburgers and hamburgers. Meals for older children years were similar, with the addition of hot apple pies (ages 6 to 11) and chocolate chip cookies (ages 12 to 18).

Of note, soda was purchased much more often than milk or juice when a drink was purchased. The researchers also observed that while healthier options such as apple dippers or fruit parfaits were available, families did not seem to choose them over more typical fast foods.

Strengths of this study were that purchase receipts were an objective measure of meal choices, and a large number of families -- both economically and ethnically diverse -- was polled. However, limitations included the lack of data on what was actually consumed, and that the study may have been influenced by the restaurant's location inside a children's hospital, limiting the choice of restaurants if not the food choices themselves.

"Bottom line, we need to educate families on making health decisions when in a fast-food restaurant," said Boutelle, acknowledging that any intervention to decrease fast-food consumption will need to take into account that people of all ages simply like fast food.

http://www.sciencedaily.com/releases/2011/08/110802180827.htm

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