Archive for the ‘Loss fat’ Category

Lower muscle mass and an increase in body fat are common consequences of growing older.

While exercise is a proven way to prevent the loss of muscle mass, a new study led by McMaster researcher Dr. Mark Tarnopolsky shows that taking a combination of creatine monohydrate (CrM) and conjugated linoleic acid (CLA) in addition to resistance exercise training provides even greater benefits.

The study to be published on Oct. 3 in PLoS One, an international, peer-reviewed online journal of the Public Library of Science, involved 19 men and 20 women who were 65 years or older and took part in a six-month program of regular resistance exercise training.

In the randomized double blind trial, some of the participants were given a daily supplement of creatine (a naturally produced compound that supplies energy to muscles) and linoleic acid (a naturally occurring fatty acid), while others were given a placebo. All participants took part in the same exercise program.

The exercise training resulted in improvements of functional ability and strength in all participants, but those taking the CrM and CLA showed even greater gains in muscle endurance, an increase in fat-free mass and a decrease in the percentage of body fat.

“This data confirms that supervised resistance exercise training is safe and effective for increasing strength and function in older adults and that a combination of CrM and CLA can enhance some of the beneficial effects of training over a six month period,” said Tarnopolsky, a professor of pediatrics and medicine.

This study provides functional outcomes that build on an earlier mechanistic study co-led by Tarnopolsky and Dr. S. Melov at the Buck Institute of Age Research, published in PLoS One this year, which provided evidence that six months of resistance exercise reversed some of the muscle gene expression abnormalities associated with the aging process.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Veronica McGuire
McMaster University

Myostatin (MSTN) is a transforming growth factor-ß (TGF-ß) family member that plays a critical role in regulating skeletal muscle mass [1]. Mice engineered to carry a deletion of the Mstn gene have about a doubling of skeletal muscle mass throughout the body as a result of a combination of muscle fiber hyperplasia and hypertrophy [2]. Moreover, loss of myostatin activity resulting either from postnatal inactivation of the Mstn gene [3], [4] or following administration of various myostatin inhibitors to wild type adult mice [5][7] can also lead to significant muscle growth. Hence, myostatin appears to play as least two distinct roles, one to regulate the number of muscle fibers that are formed during development and a second to regulate growth of muscle fibers postnatally. The function of myostatin appears to have been conserved across species, as inactivating mutations in the myostatin gene have been demonstrated to cause increased muscling in cattle [8][11] , sheep [12], dogs [13] and humans [14]. As a result, there has been considerable effort directed at developing strategies to modulate myostatin activity in clinical settings where enhancing muscle growth may be beneficial. In this regard, loss of myostatin activity has been demonstrated to improve muscle mass and function in dystrophic mice [15][17] and to have beneficial effects on fat and glucose metabolism in mouse models of obesity and type II diabetes [18].

Myostatin is synthesized as a precursor protein that undergoes proteolytic processing to generate an N-terminal propeptide and a C-terminal dimer, which is the biologically active species. Following proteolytic processing, the propeptide remains bound to the C-terminal dimer and maintains it in an inactive, latent complex [6], [19], [20], which represents one of the major forms of myostatin that circulates in the blood [21], [22]. In addition to the propeptide, other binding proteins are capable of regulating myostatin activity in vitro, including follistatin [19], [21], FLRG [22], and Gasp-1 [23]. We previously showed that follistatin can also block myostatin activity in vivo; specifically, we showed that follistatin can ameliorate the cachexia induced by high level expression of myostatin in nude mice [21] and that transgenic mice expressing follistatin in muscle have dramatic increases in muscle mass [19]. Here, I show that overexpression of follistatin can also cause substantial muscle growth in mice lacking myostatin, demonstrating that other TGF-ß related ligands normally cooperate with myostatin to suppress muscle growth and that the capacity for enhancing muscle growth by targeting this signaling pathway is much larger than previously appreciated.

Results

Increased muscle mass in transgenic mice expressing FLRG

Previous studies have identified several proteins that are normally found in a complex with myostatin in the blood [22], [23]. One of these is the follistatin related protein, FLRG, which has been demonstrated to be capable of inhibiting myostatin activity in vitro. To determine whether FLRG can also inhibit myostatin activity in vivo, I generated a construct in which the FLRG coding sequence was placed downstream of a myosin light chain promoter/enhancer. From pronuclear injections of this construct, a total of four transgenic mouse lines (Z111A, Z111B, Z116A, and Z116B) were obtained containing independently segregating insertion sites. Each of these four transgenic lines was backcrossed at least 6 times to C57 BL/6 mice prior to analysis in order to control for genetic background effects. Northern analysis revealed that in three of these lines the transgene was expressed in skeletal muscles but not in any of the non-skeletal muscle tissues examined (Figure 1); in the fourth line, Z111B, the expression of the transgene was below the level of detection in these blots. As shown in Table 1, all four lines exhibited significant increases in muscle weights compared to wild type control mice. These increases were observed in all four muscles that were examined as well as in both sexes. Moreover, the rank order of magnitude of these increases correlated with the rank order of expression levels of the transgene; in the highest-expressing line, Z116A, muscle weights were increased by 57–81% in females and 87–116% in males compared to wild type mice. Hence, FLRG is capable of increasing muscle growth in a dose-dependent manner when expressed as a transgene in skeletal muscle.

The research was funded by grants from the NIH and the Muscular Dystrophy Association and by a gift from Merck Research Laboratories.

See http://www.jhu.edu/sejinlee/%20for%20more%20information for more information.
Citation: Lee S-J (2007) Quadrupling Muscle Mass in Mice by Targeting TGF-ß Signaling Pathways. PLoS ONE 2(8): e789. doi:10.1371/journal.pone.0000789

LINK TO THE PUBLISHED ARTICLE http://www.plosone.org/doi/pone.0000789

Source: Nick Zagorski
Johns Hopkins Medical Institutions

The majority of non-medical anabolic-androgenic steroid (AAS) users are not cheating athletes or risk-taking teenagers. According to a recent survey, containing the largest sample to date and published in the online open access publication, Journal of the International Society of Sports Nutrition, the typical male user is about 30 years old, well-educated, and earning an above-average income in a white-collar occupation. The majority did not use steroids during adolescence and were not motivated by athletic competition or sports performance.

The study, conducted by a collaboration of researchers from around the country coordinated by Jason Cohen, Psy.D. candidate, used a web-based survey of nearly 2,000 US males. Whereas athletes are tempted to take anabolic steroids to improve sports performance, the study suggests that physical self-improvement motivates the unrecognized majority of non-medical AAS users who particularly want to increase muscle mass, strength, and physical attractiveness. Other significant but less highly ranked factors included increased confidence, decreased fat, improved mood and attraction of sexual partners.

Although often considered similar to abusers of narcotics and other illicit drugs (e.g., heroin or cocaine), non-medical AAS users are remarkably different. These users follow carefully planned drug regimens in conjunction with a healthy diet, ancillary drugs and exercise. As opposed to the spontaneous and haphazard approach seen in abusers of psychotropic drugs, everything is strategically planned to maximize benefits and minimize harm. “This is simply not a style or pattern of use we typically see when we examine substance abuse” said Jack Darkes, Ph.D., one of the authors. “The notions of spontaneous drug seeking and loss of control do not apply to the vast majority of AAS users,” added co-author Daniel Gwartney, M.D.

“These findings question commonly held views of typical AAS users and their underlying motivations,” said Rick Collins, one of the study’s authors. “The focus on ‘cheating’ athletes and at risk youth has led to irrelevant policy as it relates to the predominant group of non-medical AAS users. The vast majority of AAS users are not athletes and hence, are not likely to view themselves as cheaters. The targeting of athletes through drug testing and other adolescent or sports-based interventions has no bearing on non-competitive adult users.” The study concludes that these AAS users are a driven and ambitious group dedicated to gym attendance, diet, occupational goals and educational attainment. “The users we surveyed consider that they are using directed drug technology as one part of a strategy for physical self-improvement within a health-centered lifestyle,” said Collins. “Effective public policy should begin by accurately identifying who’s using steroids and why. We hope our research – the largest adult survey of non-medical AAS use we know of – is a significant step forward in that direction.”

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: Charlotte Webber
BioMed Central

Article:
A League of Their Own: Demographics, Motivations and Patterns of Use of 1,955 Male Adult Non-Medical Anabolic Steroid Users in the United States
Jason Cohen, Rick Collins, Jack Darkes and Dan Gwartney
Journal of the International Society of Sports Nutrition (in press)

During embargo, article available at: http://www.jissn.com/imedia/1374735248154681_article.pdf?random=454689

After the embargo, article available from the journal website at: http://www.jissn.com

Female athletes often lose their menstrual cycle when training strenuously, but researchers have long speculated on whether this infertility was due to low body fat, low weight or exercise itself. Now, researchers have shown that the cause of athletic amenorrhea is more likely a negative energy balance caused by increasing exercise without increasing food intake.”A growing proportion of women are susceptible to losing their menstrual cycle when exercising strenuously,” says Dr. Nancy I. Williams, assistant professor of kineseology and physiology at Penn State. “If women go six to 12 months without having a menstrual cycle, they could show bone loss. Bone densities in some long distance runners who have gone for a prolonged time period without having normal menstrual cycles can be very low.”

In studies done with monkeys, which show menstrual cyclicity much like women, researchers showed that low energy availability associated with strenuous exercise training plays an important role in causing exercise-induced amenorrhea. These researchers, working at the University of Pittsburgh, published findings in the Journal of Clinical Endocrinology and Metabolism showing that exercise-induced amenorrhea was reversible in the monkeys by increasing food intake while the monkeys still exercised.

Williams worked with Judy L. Cameron, associate professor of psychiatry and cell biology and physiology at the University of Pittsburgh. Dana L. Helmreich and David B. Parfitt, then graduate students, and Anne Caston-Balderrama, at that time a post-doctoral fellow at the University of Pittsburgh, were also part of the research team. The researchers decided to look at an animal model to understand the causes of exercise-induced amenorrhea because it is difficult to closely control factors, such as eating habits and exercise, when studying humans. They chose cynomolgus monkeys because, like humans, they have a menstrual cycle of 28 days, ovulate in mid-cycle and show monthly periods of menses.

“It is difficult to obtain rigorous control in human studies, short of locking people up,” says Williams.

Previous cross-sectional studies and short-term studies in humans had shown a correlation between changes in energy availability and changes in the menstrual cycle, but those studies were not definitive.

There was also some indication that metabolic states experienced by strenuously exercising women were similar to those in chronically calorie restricted people. However, whether the increased energy utilization which occurs with exercise or some other effect of exercise caused exercise-induced reproductive dysfunction was unknown.

“The idea that exercise or something about exercise is harmful to females was not definitively ruled out,” says Williams. “That exercise itself is harmful would be a dangerous message to put out there. We needed to look at what it was about exercise that caused amenorrhea, what it was that suppresses ovulation. To do that, we needed a carefully controlled study.”

After the researchers monitored normal menstrual cycles in eight monkeys for a few months, they trained the monkeys to run on treadmills, slowly increasing their daily training schedule to about six miles per day. Throughout the training period the amount of food provided remained the standard amount for a normal 4.5 to 7.5 pound monkey, although the researchers note that some monkeys did not finish all of their food all of the time.

The researchers found that during the study “there were no significant changes in body weight or caloric intake over the course of training and the development of amenorrhea.” While body weight did not change, there were indications of an adaptation in energy expenditure. That is, the monkeys’ metabolic hormones also changed, with a 20 percent drop in circulating thyroid hormone, suggesting that the suppression of ovulation is more closely related to negative energy balance than to a decrease in body weight.

To seal the conclusion that a negative energy balance was the key to exercise-induced amenorrhea, the researchers took four of the previous eight monkeys and, while keeping them on the same exercise program, provided them with more food than they were used to. All the monkeys eventually resumed normal menstrual cycles. However, those monkeys who increased their food consumption most rapidly and consumed the most additional food, resumed ovulation within as little as 12 to 16 days while those who increased their caloric intake more slowly, took almost two months to resume ovulation.

Williams is now conducting studies on women who agree to exercise and eat according to a prescribed regimen for four to six months. She is concerned because recreational exercisers have the first signs of ovulatory suppression and may easily be thrust into amenorrhea if energy availability declines. Many women that exercise also restrict their calories, consciously or unconsciously.

“Our goal is to test whether practical guidelines can be developed regarding the optimal balance between calories of food taken in and calories expended through exercise in order to maintain ovulation and regular menstrual cycles,” says Williams. “This would then ensure that estrogen levels were also maintained at healthy levels. This is important because estrogen is a key hormone in the body for many physiological systems, influencing bone strength and cardiovascular health, not just reproduction.”

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: A’ndrea Elyse Messer
Penn State

Women who undertake a long-term weight training program produce more biologically active growth hormone, a finding that allows physiologists to understand why weight training improves muscle tone and optimizes metabolic function.A study published in the December issue of the American Journal of Physiology-Endocrinology and Metabolism looked at different forms of growth hormone, used different testing methods, and varied weight training regimens. The research found that the role of growth hormone in women’s muscle development may be more complicated than previously thought.

“We found that growth hormone was responsive to moderate and heavy exercise regimens having 3-12 repetitions with varying weight loading,” said the study’s principal author, William J. Kraemer. “Women need to have heavy loading cycle or workout in their resistance training routines, as it helps to build muscle and bone.”

The study, “Chronic resistance training in women potentiates growth hormone in vivo bioactivity: characterization of molecular mass variants,” was carried out by Kraemer, Jeff S. Volek, Barry A. Spiering and Carl M. Maresh of the University of Connecticut, Storrs; Bradley C. Nindl, U.S Army Research Institute of Environmental Medicine, Natick, Mass.; James O. Marx, The University of Pennsylvania, Philadelphia; Lincoln A. Gotshalk, University of Hawaii at Hilo; Jill A. Bush, University of Houston, Texas; and Jill R. Welsch, Andrea M. Mastro and Wesley C. Hymer, The Pennsylvania State University, University Park, Penn. The The American Physiological Society published the study.

Hormone comes in different formsGrowth hormone, produced in the pituitary, plays an important role in bone and muscle development, particularly in women. Men, on the other hand, rely to a greater extent on muscle-building testosterone. Since women rely on growth hormone to increase muscle and bone strength, the more growth hormone stimulated by a type of exercise, the better its outcome. Growth hormone also plays a role in fighting tissue breakdown, staving off stress fractures and improving metabolic function.

The growth hormone molecule is composed of 191 amino acids, but sometimes the molecules break apart to form smaller pieces. Other times these smaller pieces join together into larger pieces, including pieces that are larger than the original molecule. In addition, growth hormone can attach to binding proteins. It has been shown that there are more than 100 variants of the growth hormone molecule.

This study looked at growth hormone variants using two different tests that measured an immune response, known as immunoassays. Immunoassays are the tests physiologists have traditionally used in such studies. The researchers added a third test, the tibia line rat growth assay, to detect the biological action of the hormones, a novel approach to the study of growth hormones in exercise.

Type of growth hormone varies with exerciseThe researchers divided the participants into two groups: an upper body training group and a total body training group. The two groups were then subdivided: Half used heavier weights with fewer repetitions (up to eight) while the other half used lighter weights with a greater number of repetitions (up to 12).

The researchers took blood samples before and after the initial training (acute exercise) session that all participants did as the start of the study. They also obtained blood samples before and after the final training session 24 weeks later (chronic exercise). One of the unique aspects of the study was that it continued over a relatively long time.

The researchers made these findings:

  • The presence of growth hormone varied with the training regimen.
  • The presence of growth hormone varied with the test used to detect it. This suggests that pituitary function and the release of different sizes of growth hormone is altered with weight training.
  • The body can adapt and produce more or less of certain sizes of growth hormone with weight training. In this study, the larger sized growth hormone variants appear to increase with heavy resistance training.

“This study shows that not every form of growth hormone responds in the same way, but is dependent upon the exercise protocol,” Kraemer explained. “This may forever change the way we look at growth hormone in the circulation with exercise and training.”

Next stepThe researchers will next examine growth hormone and weight training in women who are using oral contraceptives.

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: Christine Guilfoy
American Physiological Society

Funding

This study was supported by a grant from the US Department of Defense Women’s Health Initiative.

The American Physiological Society was founded in 1887 to foster basic and applied bioscience. The Bethesda, Maryland-based society has 10,500 members and publishes 14 peer-reviewed journals containing almost 4,000 articles annually.

APS provides a wide range of research, educational and career support and programming to further the contributions of physiology to understanding the mechanisms of diseased and healthy states. In 2004, APS received the Presidential Award for Excellence in Science, Mathematics and Engineering Mentoring.

What is testosterone?

Testosterone is a vital sex hormone that plays an important role in puberty. But contrary to what some people believe, testosterone isn’t exclusively a male hormone. Women produce small amounts of it in their bodies as well. In men, testosterone is produced in the testes, the reproductive glands that also produce sperm. The amount of testosterone produced in the testes is regulated by the hypothalamus and the pituitary gland.

What is a hormone?

Hormones, such as testosterone, are powerful chemicals that help keep our bodies working normally. The term hormone is derived from the Greek word, hormo, which means to set in motion. And that’s precisely what hormones do. They stimulate, regulate, and control the function of various tissues and organs. Made by specialized groups of cells within structures called glands, hormones are involved in almost every biological process, including sexual reproduction, growth, metabolism, and immune function. These glands, including the pituitary, thyroid, adrenals, ovaries and testes, release various hormones into the body as needed. Do testosterone levels diminish with age? Does “male menopause occur?”

There is scant evidence that “male menopause,” a condition supposedly caused by diminishing testosterone levels in aging men, exists. As men age, their testes often produce somewhat less testosterone than they did during adolescence and early adulthood, when production of this hormone peaks. But it is important to keep in mind that the range of normal testosterone production is large. Many older men have testosterone levels within the normal range of healthy younger men. Others have levels well below this range. However, the likelihood that a man will ever experience a major shut down of hormone production, similar to a woman’s menopause, is remote.

In fact, many of the changes that take place in older men often are incorrectly blamed on decreasing testosterone levels. Some men who have erectile difficulty (impotence), for instance, may be tempted to blame this problem on lowered testosterone. However, in many cases, erectile difficulties are due to circulatory problems, not low testosterone.

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Article adapted by MD Only Sports Weblog from original press release.
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U.S. NATIONAL INSTITUTES OF HEALTH

American consumers have long been skeptical about weight-loss supplements, and rightly so. With dozens of nutrients, herbs, and food extracts being marketed as aids for weight loss, there is shockingly little reliable information available concerning the safety and efficacy of any given product. What is more, many so-called miracle pills and quick fixes fail to deliver on the grand weight-loss promises they make, others come with unpleasant side effects, and some have even proven to be dangerous when used incorrectly.

According to Georgetown medical professor Harry Preuss, MD, MACN, CNS, however, there are a number of non-drug weight-loss aids available that do work and can help people shed pounds, build muscle, and burn fat. Based on his own research as well as hundreds of previously recorded scientific studies conducted at major universities and published in leading medical journals, in Dr. Preuss’s new book new book with Bill Gottlieb, THE NATURAL FAT-LOSS PHARMACY (Broadway Books, January 2007), he helps consumers separate the good from the bad and the helpful from the hype and lists the safe, effective, and natural weight-loss supplements on the market.

* HCA (hydroxycitric acid): An extract from the rind of the tamarind fruit, HCA interferes with an enzyme that triggers the formation of fatty acids, cholesterol and triglycerides. It helps lower blood levels of leptin (the substance that triggers hunger), increases serotonin and fat oxidation, and increases production of glycogen, leading to a filling of “fullness.” Study participants taking HCA ate up to 30% less food at every meal.

* MCT (medium chain triglycerides): This class of fatty saturated acids found naturally in coconut and butter help the body burn more calories – up to 25-30% more. The supplement leads to a drop in LDL (bad) cholesterol and reduction in body fat.

* Green and oolong tea extract: One of the antioxidants in green tea is EGCG, which beside possibly preventing cancer, high blood pressure, and diabetes, can also cut down on the creation of body fat and help destroy it through increased oxidation. Studies show that supplements containing EGCG increase calorie-burning by up to 180 calories a day.

* CLA (conjugated linolenic acid): In a study reported in the June 2004 issue of the American Journal of Clinical Nutrition, 180 healthy, overweight men and women were given either CLA or a placebo for one year. On average the CLA group lost 5 pounds of fat and gained 2 pounds of firming muscle – without diet or exercise.

* Chromium: Twenty-five years of research shows that taking supplements of this “trace mineral” can improve the insulin system, which regulates blood sugar levels. With enough chromium, muscle cells can make muscle, there’s less extra sugar to be stored as fat, and excess fat can be burned as fuel. In a study, women who took chromium lost 84% of their weight as fat, while women not taking the supplements lost 92% of their weight as muscle.

* Starch blockers (bean, wheat, hibiscus) and sugar blocker (L-arabinose): Many scientists now agree that cutting down on refined carbohydrates can not only help you get and stay trim, but also help you avoid diabetes, stroke, heart disease, and cancer. It may even slow the aging process. But low-carbohydrate diets are only one option. A smart alternative: carb-blockers made from a bean or wheat or hibiscus flower extract, which block the absorption of refined carbs in the digestive tract if taken before or during a high-carb meal, like pasta or pizza. L-arabinose, a simple sugar found in foods like corn, works to block the absorption of sucrose, meaning you can have your cake and lose the carbohydratess and calories.

* Chitosan and other soluble fibers: In an effort to clean up oil spills, scientists discovered chitosan, a pulverized powder made from the shells of shrimp and crab. This ultra-absorbent powder soaks up oil, grease, and heavy metals, both in the oceans and in the intestinal track. In 1995 Italian researchers gave either chitosan or a placebo to 150 people, who were on a 1,000-calorie-a-day diet for 4 weeks. Those on the placebo lost 4% of their weight, while those on chitosan lost 13%. Other studies show that chitosan can lower cholesterol by 29%. Psyllium, pectin, and guar gum are other soluble fibers that work similarly.

* 5-HTP (5-Hydroxyl-L-tryptophan): Due to high-stress, many people in America have low levels of serotonin, a brain chemical that controls appetite and mood. The result: overeating. 5-HTP is a natural amino acid that boosts serotonin, helping decrease food cravings and also creating a calm state of mind that is less vulnerable to emotional overeating. In an Italian study, overweight women who took serotonin spontaneously began to cut their calories – by more than 1000 calories per day.

* Cacti (Hoodia and Caralluma): The bushmen of the Kalahari desert rely on Hoodia, a form of cactus, to relieve hunger and thirst pangs. Caralluma is an edible Indian cactus that is used in chutneys and pickles and to control appetite, particularly in times of famine. As with Hoodia, scientists speculate that unique molecules in Caralluma affect the hypothalamus, switching off appetite. It can also normalize blood sugar, and after thousands of years of use, there are no known side effects.

* HMB (Hydroxy methylbutyrate): HMB is a metabolite, or a breakdown product of leucine, a component of protein that aids muscle-building. Although found in foods like alfalfa sprouts and catfish, only a supplement can provide enough to protect and build muscle. You do have to exercise to get the benefit of this supplement, but it is especially helpful to those 70 or older as well as AIDS and cancer patients and can lower blood pressure and high cholesterol.

* BCAA (Branched-chain amino acids – leucine, valine, soleucine): Branched chain amino acids comprise 35% of the amino acids in muscle tissue. Supplying muscles with extra BCAA can help prevent exercise-related muscle damage, soreness after exercise, and can build more calorie-burning muscle.

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Article adapted by MD Only Weblog from original press release.
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Contact: Ellen Folan
Random House/Broadway Books

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