Posts filed under 'Weight Guides'
By UTA HARNISCHFEGER
Associated Press Writer
November 16, 2005, 8:14 AM EST
GENEVA — Efforts so far by the food and drink industry to improve the nutritional value of their products to help fight childhood obesity are simply not good enough, the World Health Organization said.
“The industry’s efforts are commendable, but inadequate. They are only a drop in the ocean,” Colin Tukuitonga, who oversees the WHO’s global strategy on diet and physical activity, said before a meeting with representatives of the food and soft drink industry on Wednesday.
Some industry giants such as Kraft, Nestle and Unilever have recently reviewed their recipes and reduced the salt, sugar and fat content of some of their products. They have also pledged to change some of their advertising and marketing practices.
“These are selected companies doing one-off changes,” Tukuitonga said. “They are making a genuine effort … but we need an industry-wide approach.”
The meeting Wednesday is part of WHO’s global strategy on diet and physical activity launched last year after health ministers from around the world approved the plan.
The agency believes profound changes in the way food is processed and marketed are essential to the turning the tide of the growing obesity epidemic, which is predicted to cause millions of people worldwide to suffer an early death or disability.
Officials want companies to make additional commitments or set specific targets.
“We are already doing a lot on a company level,” said Nina Backes, spokeswoman at Nestle. “I am not aware that we will make a specific commitment toward the WHO.”
Backes said Nestle has cut fat, salts and sugars in some 700 products in recent years and changed its labeling policy to provide additional information to the consumer.
Tukuitonga said he hoped the food industry “would voluntary agree on some self-imposed actions and targets,” particularly for processed foods. “We are a long way from what we consider healthy foods,” he said.
Neville Rigby of the International Obesity Task Force, a network of eminent obesity scientists and policy experts, lauded some companies for making “pretty strong statements,” but said it was hard to monitor how they delivered on their pledges.
Source: newsday.com
November 17th, 2005
Tuesday, Nov 08, 2005
TORONTO (CP) - In a discovery with implications for fighting obesity in humans, Canadian scientists have discovered a molecular switch in specially bred laboratory mice that makes the animals skinnier than their normal brethren.
The altered mice, which lack a certain gene, have half as much fat as normal mice - and the fat they do have isn’t the kind that piles on the weight, say researchers at the Ottawa Health Research Institute.
Anthony Scime, a molecular biologist at the University of Ottawa institute, said the leaner mice have a higher proportion of what are known as brown fat cells, which burn up fat and release it as heat.
Normal mice - and humans and other mammals, for that matter - have mostly white fat cells, which metabolize fat as energy to fuel muscles and other bodily functions.
So when food intake exceeds energy output, these white fat cells multiply and expand in girth, Scime said Tuesday from Ottawa. “You just keep on getting bigger and bigger.”
The knocked-out gene in the mice - called P107 - seems to act as a switch on precursor cells, causing them to develop into heat-producing brown fat cells instead of lipid-storing white fat cells, said lead investigator Michael Rudnicki, director of molecular medicine at the institute.
“The P107 knockout mice eat just as much as normal mice, but they burn off all the extra calories (as heat),” Rudnicki said.
The discovery could have big implications for treating human obesity, a ballooning public health risk in Canada, where more than five million people are considered obese and many more are overweight. A growing proportion of the country’s children also are overweight or obese, setting the stage for cardiovascular disease, diabetes and some cancers later in life.
“What it’s done is open up a new pathway or new way of looking at how the precursor (cell) that decides to make white or brown fat switches on one way or the other,” said Scime. “Especially in light of P107 seeming not to have any other deleterious effect on the mice, perhaps in humans, P107 would be a good target for obesity therapy.”
That could mean designing a drug that in effect flips the P107 switch, although Scime predicts such a medication could take 10 to 20 years to come to market.
“Drugs that inhibit P107 might be able to prevent the body from making white fat,” he said. “This could be a particularly effective strategy because previous studies have shown that once white fat cells are created, they are very difficult to get rid of.
“Also, once brown fat is created, it would continue to burn extra calories off as heat.”
As newborns, about five per cent of our body weight is made up of heat-producing brown fat cells - nature’s way of keeping little bodies warm after they leave the womb. But as we age, the proportion of brown fat cells drops dramatically, giving way to more white fat cells.
“The sole purpose is to keep the body warm,” said Rudnicki. “So this brown fat is typically located between the shoulder blades, wrapped around our internal organs close to the heart, and babies have lots of it. People who live outdoors, the homeless or Inuit, have a lot more of it and those people burn a lot of fat to keep warm.”
But compared to humans, most other mammal species are loaded with brown fat cells. It’s these cells that allow bears, for instance, to hibernate over the winter, producing enough heat to maintain internal body temperature at a level to keep the bear alive until spring.
Scime said the P107 knockout mice were originally bred about six years ago so scientists could investigate how certain cells differentiate into muscles. But when no anomalies were found in the muscles of the mice, they “were kind of shelved, put on the back burner,” he said.
But during other experiments using the genetically flawed mice a few years ago, Scime noticed that they were skinnier than their normal counterparts and began trying to find out why.
“And our study showed that they had a lot of fat precursors (cells) that were not differentiating into fat, and this is why they were lean.”
A paper on the discovery is published in the November issue of Cell Metabolism.
© The Canadian Press, 2005
Source: mytelus.com
November 9th, 2005
THURSDAY, Oct. 27 (HealthDay News) — A diet high in fat and sugar triggered immune system abnormalities — including reduced levels of natural killer T (NKT) cells — in the livers of mice, says a study led by Johns Hopkins University in Baltimore.
The study authors said these diet-related changes may contribute to obesity-related liver disease. The findings appear in the October issue of the journal Hepatology.
Natural killer T (NKT) cells in the liver regulate production of cytokines, which are cell proteins.
The study found that the mice on the high-fat diet gained much more weight than mice fed a normal diet. The mice on the high-fat diet also developed fatty livers and had increased production of IL-12, a cytokine that reduces NKT cell viability, and had increased NKT cell death.
The high-fat diet also promoted production of pro-inflammatory cytokines. When the researchers induced liver injury in the mice, they found that those on the high-fat diet experienced more liver inflammation and damage than mice on the normal diet.
The findings show that high-fat diets are associated with a chronic inflammatory state in the liver, which promotes chronic liver disease, the study authors said. They said this may be the result of diet-induced depletion of NKT cells that normally balance production of pro- and anti-inflammatory cytokines.
“Further evaluation of other mouse strains, different age groups and genders will be necessary to clarify if any of these factors modulate susceptibility to diet-related changes in hepatic NKT cells,” the authors said. “Nevertheless, our findings are important because they clearly demonstrate significant dietary effects on ‘classic’ NKT cells and cytokine production by other liver mononuclear cells.”
October 31st, 2005
By Megan Rauscher
Fri Oct 28, 4:10 PM ET
NEW YORK (Reuters Health) - A condition involving abnormally high levels of androgens (steroid hormones) known in medical circles as “hyperandrogenemia” starts early in obese children, a study shows, possibly placing them at increased risk for the metabolic syndrome — a cluster of conditions such as high blood pressure and high blood sugar levels that raise the risk of heart disease and diabetes.
The study also shows that weight loss leads to decreasing androgen levels. Weight loss is the “therapy of choice” for obese children with elevated androgen levels, Dr. Thomas Reinehr who led the study told Reuters Health.
“Androgens,” Reinehr explained, “are steroid hormones such as testosterone or androsterone, which control the development and maintenance of masculine characteristics in both males and females.”
“Obesity is known to be associated with increased androgen production in adult females, while studies of obese adult males have linked obesity to low androgen production,” Reinehr from the University of Witten/Herdecke in Datteln, Germany added. “There has been minimal study into the role of androgens in obese children, and it has, until now, remained unknown whether the (levels) of these hormones change after obese children lose weight,” he also pointed out.
To investigate, Reinehr and colleagues compared androgen levels in 273 obese and 79 normal weight children of the same age and pubertal stage, and studied the effect of weight loss on these hormone levels.
Weight loss was achieved via a 12-month intervention program that incorporated exercise, behavior and nutrition therapy consisting of a high-carbohydrate low-fat diet.
The study revealed that obese children, regardless of their gender or pubertal stage, show significantly higher testosterone and DHEAS levels as compared to children who are lean or normal weight.
In girls, and also in boys who were prepubertal, there was a positive link between body mass index and androgen levels. However, obese pubertal boys did not demonstrate increased androgen levels in this study.
“Overall, weight loss led to a decrease in testosterone among obese prepubertal children and pubertal girls,” Reinehr said. Therefore, “although obesity tends to be associated with an increase in androgens, this increase is reversible pending weight loss,” he concluded.
SOURCE: Journal of Clinical Endocrinology and Metabolism October 2005.
Taken From: http://news.yahoo.com
October 31st, 2005
FRIDAY, Oct. 28 (HealthDay News) — A new initiative to combat obesity in U.S. black and Hispanic children is ready for launch in 2006, according to sponsors at the American Council for Fitness and Nutrition (ACFN) and the American Dietetic Association Foundation (ADAF).
Both groups plan to analyze data from the U.S. Centers for Disease Control and Prevention and other sources to assess the need for, and the best methods of, combating obesity among black and Hispanic children. Statistics have long showed these minority youngsters to be at especially high risk for obesity.
Based on the information they receive, the two organizations will create separate detailed guides for black and Hispanic community leaders, to help create and expand programs to help families adopt healthier lifestyles. The ACFN and ADAF plan to enlist respected organizations in the black and Hispanic communities to take part in the development and distribution of these guides.
“ACFN and the ADA Foundation are ideal partners to address a need that goes beyond putting great nutrition and physical activity resources into the hands of community leaders. We intend to show how to achieve collaboration in communities - the key to getting more families and children involved,” registered dietitian Cecilia Pozo Fileti, a member of the ACFN advisory board, the ADA, and head of the Latinos and Hispanics in Dietetics and Nutrition, said in a prepared statement.
Taken From: http://news.yahoo.com
October 31st, 2005
Fri Oct 21, 7:29 AM ET
VANCOUVER, Canada (AFP) - Following just a few simple rules regarding moderate exercise, healthy eating and lifestyle can ensure weight control and lower the risk of disease, say the world’s leading researchers on obesity.
“There’s been a hysteria in place over the last many years,” said Dr Steven Blair, who presented a key speech on the state of the art in exercise to an international science conference on obesity here Friday.
“We have a public health problem of overweight and obesity, but it’s been blown out of proportion,” said Blair. “We focus on obesity and not on other health habits and other risk factors.”
Scientists concur that there’s a crisis in soaring rates of obesity and related diseases, like diabetes, in most developed countries. Current treatments, especially for extreme obesity, are few, have limited success and, in the case of surgery, can be radical and invasive.
But there was also good news for the majority of people at the annual conference of NAASO, The Obesity Society, held in this western Canadian city.
As long as people don’t smoke, eat healthy foods and get enough exercise, excess weight may not be as much of a health risk as is commonly thought.
New research in sleep, nutrition, stress, social and consumer factors in obesity and the chemical triggers of weight gain could soon lead to better prevention and treatment.
Findings by scientists at the US Centers for Disease Control show that being merely “overweight” does not, by itself, increase the risk of disease and death. While obesity remains a major cause of early death, fewer people die because of excess fat than previous research indicated.
Meanwhile, scientists now believe that a healthy amount of exercise is attainable for most people.
Despite the enormous range of exercise programs and gear for sale in developed countries, keeping fit simply requires a daily total of 30 minutes of brisk walking, just five days a week, said Blair.
Blair, whose Texas-based Cooper Institute studies and designs physical activity programs around the world and trains fitness instructors for the US military, cited dramatics effects from a simple walk routine.
Walking “cuts the risk of dying in half over next eight to ten years,” he said. “It cuts the risk of diabetes, hypertension, metabolic syndrome, and colon cancer … sometimes in half.”
“It cuts your risk of becoming depressed, and if you are depressed, it helps ameliorate the symptoms,” said Blair.
“If you exercise, you call into action nearly every body system including your heart and lungs, and molecules and hormones dash madly around the body.”
“A whole cascade of many body functions are affected by exercise,” even if the 30-minute daily walks are divided into three 10-minute or two 15-minute walks.
For the 25 percent of Americans who get no exercise at all and who may be discouraged by complex fitness programs, the fact that almost all benefits of exercise are attained in the walk program may be encouraging.
Blair noted that the health benefits do increase during more intense or prolonged exercise, but that the extra benefit from more exercise is relatively small.
Meanwhile, for people who are extremely obese and for whom walking is not possible, treatment options are few but improving.
There are only two effective drugs for obesity currently on the market, said psychologist Thomas Wadden, president of The Obesity Society. “But we will have a lot of new medications in the next ten to 20 years.”
And as research shows bariatric surgery, sometimes known as “gut stapling”, increases life expectancy, the procedure has rapidly increased. Wadden said about 125,000 such surgeries are now performed each year in the US, up from less than 75,000 in 2002.
Taken from: news.yahoo.com
October 24th, 2005
October 19, 2005
When babies receive shots against diseases like polio and measles, their vaccinations may in the future include protection against getting fat, according to researchers.
Infection by certain pathogens triggers rapid increases in fatty tissue in animals, Nikhil Dhurnadha told the annual meeting of NAASO, the Obesity Society, in this western Canadian city.
At the same time, the discovery that many more obese people than normal-weight people have been exposed to a certain virus suggests a link between obesity and viral infection.
“Not all obesity can be explained by infection,” said Dhurandhar, of the Pennington Biomedial Research Center at Louisiana State University in Baton Rouge. “Infections can be one of the causes.”
Popular opinion has long held that most obesity is caused simply by overeating, underexercise and a lack of will power. But viruses are just one of many contributing factors that scientists have recently discovered.
Researchers are reporting at the conference on other fat triggers that include a genetic tendency to store fat among groups whose ancestors survived famines, medications such as treatments for psychotic mental disorders, toxins in the environment like organochlorines, and infectious agents like bacteria, viruses and prions.
“Obesity is multifactoral,” Dhurandhar told scientists at the conference.
In an interview with AFP, he said there is proof that at least 10 different pathogens cause obesity in animals. They include canine distemper virus, RAV7 and MAM1 avian viruses, the Borna virus in rats — which is also linked with depression in humans, types of scrapie, three adeno viruses including AD5, AD36 and AD37 which cause fat gain in several species, and chlamydia pneumonae bacteria.
Scientists have also found that when mice are infected by general bacteria from the guts of other mice, the recipients body fat increases.
Dhurandhar became interested in viral causes of obesity while working as a family physician in Bombay in the 1980s, during a severe outbreak of SMAM1, an adeno virus that kills chickens.
A friend noticed that the dead chickens were unusually fat, with enlarged livers, kidneys, low cholesterol levels and an atrophied thymus gland.
Dhurandhar wondered how the virus affected people. He tested his own patients, and found 20 per cent of his obese patients had been exposed to SMAM1, and that those people were significantly heavier with lower cholesterol levels.
He moved to the United States to conduct more research, and started working with Richard Atkinson at the University of Wisconsin. Because US authorities refused permission to import the Indian avian virus, the pair decided to work with adeno virus AD36.
First, they infected laboratory chickens, mice and monkeys, all of which grew significantly fatter and had lower cholesterol.
Then, because they could not test the virus on humans, they examined stored blood from 500 people in Wisconsin, Florida and New York. They found antibodies for AD36 in 30 per cent of the obese people, but only in 11 per cent of people with normal body weight.
And, just as Dhurandhar earlier discovered among his Indian patients, the obese who had been exposed to the virus were 20 per cent heavier than other overweight people.
Further tests on tissue from lab monkeys taken over a nine-year period showed that healthy monkeys newly infected by AD36 “gained 15 per cent body weight in six months, and dropped their cholesterol by 30 per cent.”
The scientists also studied 26 pairs of twins, and found that in cases where one twin had been exposed to AD36, in all cases their weight was significantly greater.
“In 10 years, people may be able to walk into a clinic and be told that their obesity is due to X cause, such as genes, the endocrine system, or pathogens. That may have a more productive outcome than a blanket treatment right now, (which) is not very successful,” said Dhurandhar.
And because viruses are hard or impossible to treat, he said, prevention through vaccines will be key.
Taken from: http://www.terra.net.lb
October 19th, 2005
October 19, 2005
Listening to music during physical activity may be the key to motivating people who dislike exercise, new research suggests.
US scientists reported their findings from a study of overweight and obese women to a conference on obesity. The research showed that the patients who were given a portable CD player to listen to music while walking lost more weight and body fat than the group who walked without music.
The group with CD players also followed the exercise program more faithfully, while fewer of them dropped out of the program, said psychology professor Christopher Capuano, of Fairleigh Dickinson University in Teaneck, New Jersey.
“Walking to music seemed to really motivate the women in our study to get out there,” he told the annual meeting of NAASO, The Obesity Society, in Vancouver, in western Canada.
Carpuano’s group studied 41 women during a 24-week program of dieting, walking exercise three times each week, and weekly group meetings.
Carpuano noted that one of the biggest problems with long-term weight control programs is the drop-out rate, and music may prompt participants to stick with their regime.
Taken from: http://www.terra.net.lb
October 19th, 2005
What kind of diet will help me lose weight?
Many diets can help you lose weight. However, “going on a diet” is not the best answer to losing weight. Usually you gain the weight back after you “go off” the diet. If you want to lose weight and keep it off, you have to change much more than just what you eat. You have to change how and when you eat, and you have to start exercising or exercise more often. Most people who lose weight and keep it off do 3 things. First, they find out why they are overweight. Second, they follow a healthy eating plan. Third, they exercise regularly.
Why am I overweight?
There may be many reasons for your weight problem. Weight problems often run in families. Or you may be eating to make yourself feel better when you are sad, stressed or lonely. Sometimes a low body metabolism (the rate you burn calories) or a problem with hormone levels may be the cause.
A new diet may help you lose weight for a little while. But the weight often comes back unless you find new ways to deal with the problems that are leading to your weight gain. This may mean learning new ways to handle stress, finding ways to feel less lonely or talking with a counselor about your feelings.
What kind of diet should I follow?
You should follow a healthy diet that you like and that you can stick to. The diet should be low in fats and sugars, and high in fiber.
Your doctor or a nutritionist can give you advice on what kinds of foods are healthy choices. Remember to watch portion sizes. A healthy portion of meat is the size of a deck of cards. A healthy portion of rice or pasta is about the size of your fist. Most restaurants tend to double or even triple these amounts.
Read the nutrition labels on foods before you buy them. If you need help understanding the labels, ask your doctor or a nutritionist to explain them.
Won’t it be hard to change my diet?
It might be hard, and it will also take time, so try not to get discouraged. Your effort will be worth it. The key is to keep trying to eat the right foods. The following are a few suggestions to help you change your diet:
* Make small, slow changes. Then it will be easier to make the changes a part of your everyday life.
* Every few days, write down what you eat and drink that day. Use this record to help you see if you need to eat more from any food groups, such as fruits, vegetables, or low-fat dairy products.
* Ask for help from your family doctor or a nutritionist, especially if you have a medical problem that requires a special diet.
* Read the nutrition labels on foods before you buy them. If you need help understanding the labels, ask your doctor or a nutritionist to explain them.
July 22nd, 2005
Conclusion
Achieving and maintaining healthy lifestyle behaviors including activity and food intake can help weight management by helping to prevent weight gain. Prevention of weight gain and achieving modest amounts of weight loss can improve overall health.
In today’s society, the environment is conducive to less activity than previous decades, more food availability in larger quantities, and higher caloric density. Therefore, concentrating on factors to limit the environmental influences is critical. It is important to acknowledge those factors we can change and those we cannot. It is also important that dietitians and other health care providers be in the forefront of lobbying for public health policy, third party reimbursement for treatment and management, and adequate community resources to address weight status and weight-related illness. We need to document our outcomes, develop flexible and individualized goals for patients, and continue to support research efforts to improve the efficacy of treatment. Such documentation requires thorough assessments and follow-up: medically, nutritionally, be-haviorally, and psychologically. Based on current available treatment approaches, goals need to stay focused on a “healthy lifestyle” targeting the environmental factors that allow for gene expression, particularly physical activity and food choices directed toward less calorically dense foods.
We must educate ourselves and the medical community as to the physical and psychological impact of our recommendations. We must include our patients in the decision making process and inform them of the known positive outcomes they can achieve.
ADA Position adopted by the House of Delegates October 20, 1996, and reaffirmed on September 12,1999. This position is in effect until December 31, 2005. The American Dietetic Association authorizes republication of the position paper, in its entirety, provided full and proper credit is given. Requests to use portions of the position must be directed to ADA Headquarters at 800/877-1600, ext 4835 or ppapers@eatright.org.
Recognition is given to the following for their contributions:
Authors:
Sue Cummings, MS, RD (Massachusetts General Hospital Weight Center, Boston, MA); EUen S. Parham, PhD, RD (Northern Illinois University, DeKalb, IL); Gladys W. Strain, PhD, RD (Mt. Sinai School of Medicine, New York, NY)
Reviewers:
Gaston P. Bathalon, PhD, RD, FADA (US Army, Natick, MA); Ann M. Coulston, MS, RD, FADA (nutrition consultant, Woodside, CA); Sharron Dalton, PhD, RD (New York University, New York, NY); Dayle Hayes, MS, RD (nutrition consultant, Billings, MT); Joanne P. Ikeda, MA, RD (University of California, Berkeley, CA); Melinda Manore, PhD, RD (Oregon State University, Corvallis, OR)
Members of the Association Positions Committee Workgroup: Barbara Baron, MS, RD (Chair); Mary Marian, MS, RD; Lillie Williams, PhD, RD, FADA; James 0. Hill, PhD (content advisor)
References
1. US Department of Health, Human Services, Center for Disease Control and Prevention; National Center for Health Statistics, Maryland. Prevalence of Overweight and Obesity Among Adults: United States, 1999.
2. Wolf AM, Colditz GA. Current estimates of the economic cost of obesity in the United States. Obes Res 1998;6:97-106.
3. Allison DB, Fontaine KR, Manson JE, Stevens J, Vanltallie TB. Annual deaths attributable to obesity in the United States. JAMA 1999;282:1530-1538.
4. Dheeksha M. National Institute of Health, National Heart, Lung, and Blood Institute Clinical guidelines on the identification evaluation, and treatment of overweight and obesity in adults—the evidence report. Obes Res 1998;6:121S-122.
5. Anderson JW, Kontz EC, Frederich RC, Wood CL. Long-term weight-loss maintenance: a meta-analysis of US Studies. Am J Clin Nutr 2001;74:579-584.
6. Schick SM, Wing RR, Klem ML, McGuire Tetal. Persons successful at long-term weight loss and maintenance continue to consume a low energy, low fat diet. JADA 1998;98:408-413.
7. Wing RR, Hill JO. Successful weight loss maintenance. Ann Rev Nutr 2001;21:323-341.
8. Kassirer JP, Angell M. Losing weight—An ill-fated New Year’s Resolution. N Engl J Med 1998;338:52-54.
9. National Institutes of Health and National Heart, Lung and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res. 1998:xi.
10. Leibel R, Rosenbaum M, Hirsch J. Changes in Energy Expenditure Resulting from Altered Body Weight. N Engl J Med 1995;332:621-628.
11. Schwartz MW, Woods SC, Porte D, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature 2000;404:661-671.
12. Bray GA, York DA. Clinical review 90: Leptin and clinical medicine: a new piece in the puzzle of obesity. J Clin Endocrinol Metab 1997;82:2771-2776.
13. Erlanson-Albertsson C, York D. Enterostatin—a peptide regulating fat intake. Obes Res 1997;5:360-372.
14. Barsh G, Farooqi I, O’Rahilly S. Genetics of body weight regulation. Nature 2000;404:644-651.
15. Perusse L, Chagnon YC, Weisnagel SJ, Rankinen T, Snyder E, Sands J, Bouchard C. The human obesity gene map: The 2000 Update. Obes Res 2001;9. 8135–169.
16. Maes HH, Neale MC, Eaves IJ. Genetics and environmental factors in relative body weight and human adiposity. Behav Genet 1997;27. 325–35.
17. Stunkard AJ, Sorensen TIA, Hanis C, Teasdale TW, Chakraborty R, Schull WJ, Schulsinger F. An adoption study of human obesity. N Engl J Med 1986;314:193-198.
18. Stunkard AJ, Harris JR, Pedersen NL, McClearn GE. The body mass index of twins who have been reared apart. N Engl J Med 1990;322:1483-1487.
19. Bouchard C, Trembley A, Despres JP, et al. The response of long-term overfeeding in identical twins. N Engl J Med 1990;322:1477-1482.
20. Zhang YY, Proenca R, Marffei M, et al. Positional cloning of the mouse obese gene and its human homologue. Nature 1994;372:425-432.
21. Montague CT, Farooqi IS, Whitehead JP, et al. Congenital leptin deficiency is associated with severe early o
July 5th, 2005
Conclusion
Achieving and maintaining healthy lifestyle behaviors including activity and food intake can help weight management by helping to prevent weight gain. Prevention of weight gain and achieving modest amounts of weight loss can improve overall health.
In today’s society, the environment is conducive to less activity than previous decades, more food availability in larger quantities, and higher caloric density. Therefore, concentrating on factors to limit the environmental influences is critical. It is important to acknowledge those factors we can change and those we cannot. It is also important that dietitians and other health care providers be in the forefront of lobbying for public health policy, third party reimbursement for treatment and management, and adequate community resources to address weight status and weight-related illness. We need to document our outcomes, develop flexible and individualized goals for patients, and continue to support research efforts to improve the efficacy of treatment. Such documentation requires thorough assessments and follow-up: medically, nutritionally, be-haviorally, and psychologically. Based on current available treatment approaches, goals need to stay focused on a “healthy lifestyle” targeting the environmental factors that allow for gene expression, particularly physical activity and food choices directed toward less calorically dense foods.
We must educate ourselves and the medical community as to the physical and psychological impact of our recommendations. We must include our patients in the decision making process and inform them of the known positive outcomes they can achieve.
ADA Position adopted by the House of Delegates October 20, 1996, and reaffirmed on September 12,1999. This position is in effect until December 31, 2005. The American Dietetic Association authorizes republication of the position paper, in its entirety, provided full and proper credit is given. Requests to use portions of the position must be directed to ADA Headquarters at 800/877-1600, ext 4835 or ppapers@eatright.org.
Recognition is given to the following for their contributions:
Authors:
Sue Cummings, MS, RD (Massachusetts General Hospital Weight Center, Boston, MA); EUen S. Parham, PhD, RD (Northern Illinois University, DeKalb, IL); Gladys W. Strain, PhD, RD (Mt. Sinai School of Medicine, New York, NY)
Reviewers:
Gaston P. Bathalon, PhD, RD, FADA (US Army, Natick, MA); Ann M. Coulston, MS, RD, FADA (nutrition consultant, Woodside, CA); Sharron Dalton, PhD, RD (New York University, New York, NY); Dayle Hayes, MS, RD (nutrition consultant, Billings, MT); Joanne P. Ikeda, MA, RD (University of California, Berkeley, CA); Melinda Manore, PhD, RD (Oregon State University, Corvallis, OR)
Members of the Association Positions Committee Workgroup: Barbara Baron, MS, RD (Chair); Mary Marian, MS, RD; Lillie Williams, PhD, RD, FADA; James 0. Hill, PhD (content advisor)
References
1. US Department of Health, Human Services, Center for Disease Control and Prevention; National Center for Health Statistics, Maryland. Prevalence of Overweight and Obesity Among Adults: United States, 1999.
2. Wolf AM, Colditz GA. Current estimates of the economic cost of obesity in the United States. Obes Res 1998;6:97-106.
3. Allison DB, Fontaine KR, Manson JE, Stevens J, Vanltallie TB. Annual deaths attributable to obesity in the United States. JAMA 1999;282:1530-1538.
4. Dheeksha M. National Institute of Health, National Heart, Lung, and Blood Institute Clinical guidelines on the identification evaluation, and treatment of overweight and obesity in adults—the evidence report. Obes Res 1998;6:121S-122.
5. Anderson JW, Kontz EC, Frederich RC, Wood CL. Long-term weight-loss maintenance: a meta-analysis of US Studies. Am J Clin Nutr 2001;74:579-584.
6. Schick SM, Wing RR, Klem ML, McGuire Tetal. Persons successful at long-term weight loss and maintenance continue to consume a low energy, low fat diet. JADA 1998;98:408-413.
7. Wing RR, Hill JO. Successful weight loss maintenance. Ann Rev Nutr 2001;21:323-341.
8. Kassirer JP, Angell M. Losing weight—An ill-fated New Year’s Resolution. N Engl J Med 1998;338:52-54.
9. National Institutes of Health and National Heart, Lung and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res. 1998:xi.
10. Leibel R, Rosenbaum M, Hirsch J. Changes in Energy Expenditure Resulting from Altered Body Weight. N Engl J Med 1995;332:621-628.
11. Schwartz MW, Woods SC, Porte D, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature 2000;404:661-671.
12. Bray GA, York DA. Clinical review 90: Leptin and clinical medicine: a new piece in the puzzle of obesity. J Clin Endocrinol Metab 1997;82:2771-2776.
13. Erlanson-Albertsson C, York D. Enterostatin—a peptide regulating fat intake. Obes Res 1997;5:360-372.
14. Barsh G, Farooqi I, O’Rahilly S. Genetics of body weight regulation. Nature 2000;404:644-651.
15. Perusse L, Chagnon YC, Weisnagel SJ, Rankinen T, Snyder E, Sands J, Bouchard C. The human obesity gene map: The 2000 Update. Obes Res 2001;9. 8135–169.
16. Maes HH, Neale MC, Eaves IJ. Genetics and environmental factors in relative body weight and human adiposity. Behav Genet 1997;27. 325–35.
17. Stunkard AJ, Sorensen TIA, Hanis C, Teasdale TW, Chakraborty R, Schull WJ, Schulsinger F. An adoption study of human obesity. N Engl J Med 1986;314:193-198.
18. Stunkard AJ, Harris JR, Pedersen NL, McClearn GE. The body mass index of twins who have been reared apart. N Engl J Med 1990;322:1483-1487.
19. Bouchard C, Trembley A, Despres JP, et al. The response of long-term overfeeding in identical twins. N Engl J Med 1990;322:1477-1482.
20. Zhang YY, Proenca R, Marffei M, et al. Positional cloning of the mouse obese gene and its human homologue. Nature 1994;372:425-432.
21. Montague CT, Farooqi IS, Whitehead JP, et al. Congenital leptin deficiency is associated with severe early onset obesity in humans. Nature 1997;387:903-908.
22. Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. Nature 1998;395:763-770.
23. Ravussin E, Bogardus C. Relationship of genetics, age, and physical fitness to daily energy expenditure and fuel utilization. Amer J Clin Nutr 1989;49. 968–75.
24. Bradford BL, Spiegelman BM. Towards a molecular understanding of adaptive thermogenesis. Nature 2000;404:652-660.
25. Bray GA.ContemporaryDiagnosis, Management of Obesity Health Care Co.Newtown, PA: 1998. 35-67.
26. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991-1998. JAMA 1999;282:1519-1522.
27. Casas YG, Schiller BC, DeSouza CA, Seals DR. Total and regional composition across age in healthy Hispanic and white women of similar socioeconomic status. Am J Clin Nutr 2001;73:13-18.
28. Jakicic JM, Wing RR. Differences in resting energy expenditure in African Americans vs Caucasian overweight females. Int J Obes Relat Metab Disord 1998;22. 236–42.
29. Hill JO, Peters JC. Environmental contributions to the obesity epidemic. Science 1998;280:1371-1374.
30. Young LR, Nestle M. The contribution of expanding portion sizes to the US obesity epidemic. Am J Public Health 2002;92:246-249.
31. Devlin MJ, Yanovski SZ, Wilson GT. Obesity: What mental health professionals need to know. Am J Psychiatry 2000;157:854-866.
32. Stahl SM. How to appease the appetite of psychotropic drugs. J Clin Psychiatry 1998;59:500-501.
33. Ackerman S, Nolan LJ. Body weight gain induced by psychotropic drugs: incidence, mechanism, and management. CNS Drugs 1998;9:135-151.
34. DiPietro L, Anda RF, Williamson DF, Stunkard AJ. Depressive symptoms and weight change in a national cohort of adults. IntJ Obes 1992;16:745-753.
35. Stunkard AJ, Fernstrom MH, Frank E, Kupfer DJ. Direction of weight change in recurrent depression: consistency across episodes. Arch Gen Psychiatr 1990;47:857-860.
36. Wurtman RJ, Wurtman JJ. Serotoninergic mechanisms and obesity. J Nutr Biochem 1998;9:511-515.
37. Dheeksha M. National Institutes of Health and National Heart, Lung and Blood Institute Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res 1998;6:108S-109S.
38. Willett WC, Dietz WH, Colditz GA. Primary Care: Guidelines for healthy weight. N Engl J Med 1999;341:427-434.
39. Kuczmarski RJ, Flegal KM. Criteria for definition of overweight in transition: background and recommendations for the United States. Am J Clin Nutr 2000;72:1074-1081.
40. Flegal KM, Troiano RP, Ballard-Barbash R. Aim for a healthy weight: What is the target. J Nutr 2001;131:440S-450S.
41. Bray GA. Clinical Evaluation and Introduction to Treatment of Overweight Contemporary Diagnosis and Management of Obesity, Handbooks in Health Care Co, Newtown, PA 1998.
42. Dheeksha M. National Institutes of Health and National Heart, Lung and Blood Institute. Clinical Guidelines on the Identification Evaluation and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res 1998;6:54S.
43. World Health Organization. Obesity: Preventing and Managing the Global Epidemic. Report of a WHO Consultation on Obesity, Geneva, June 1997. 1998, pp 43-72.
44. Cummings S, Pratt J, Kaplan L. Evaluation and Management of Obesity. In: Carlson K, Eisenstat S. Primary Care of Women. 2nd ed. New York, NY: Mosby Yearbook; 2002.
45. Yanovski SZ, Nelson JE, Dubbert BK. Spitzer Rl. Association of binge eating disorder and psychiatric comorbidity in obese subjects. Am J Psychiatry 1993;150:1472-1479.
46. Molijari E, Ragazzoni P, Morosin A. Psychopathology in obese subjects with and without binge-eating disorder and in bulimic subjects. Psychol Rep 1997;80:1327-1335.
47. Dheeksha M, National Institutes of Health and National Heart, Lung and Blood Institute.. Clinical Guidelines on the Identification, evaluation and treatment of Overweight and Obesity in Adults—The Evidence Report. Obesity Research, 1998;6:110S.
48. Bertram SR, Venter I, Stewart RI. Weight loss in obese women—exercise vs dietary education. S Afr Med J 1990;78:15-18.
49. Gordon NF, Scott CB, Levine BD. Comparison on single versus multiple lifestyle interventions: are the antihypertensive effects of exercise training and diet-induced weight loss additive?. Am J Cardiol 1997;79:763-767.
50. Stefanick MI, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD. Effects of the NCEP Step 2 diet and exercise on lipoprotein in postmeno-pausal women and men with low HDL-cholesterol and high LDL-cholesterol. N Engl J Med 1998;329:12-20.
51. Grommet J. Weight management: Framework for changing behavior In: Dalton S. Overweight and Weight Management. Gaithersburg, MD: Aspen; 1997.332-347.
52. Van Gaal LF. Dietary treatment of obesity. In Handbook of Obesity, eds Bray GA, Bouchard C and James WPT. Marcel Dekker, NY 1998, 875-890.
53. McFarlane T, Polivy J, McCabe RE. Help, not harm: Psychologic foundation for a nondieting approach toward health. J Social Issues 1999;55:261-276.
54. Dheeksha M, National Institutes of Health and National Heart, Lung and Blood Institute.. Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res 1998;6:110S.
55. Foster GD, Wadden TA, Vogt RA, Brewer G. What is a reasonable weight loss Patients?’ expectations and evaluations of obesity treatment outcome. J Consult Clinl Psychol 1998;65:79-85.
56. Allison D. A Handbook of Assessment Methods for Eating Behaviors and Weight-related Problem: Measures Theory and Research, Sage, Thousand Oaks CA 1995.
57. St Jeor ST. Obesity Assessment: Tools, Methods and Interpretations. NY: Chapman &. Hall. 1997.
58. Parham ES. Promoting body size acceptance in weight management counseling. JADA 1999;99:920-925.
59. Strain GW. Response to promoting size acceptance to weight management counseling. JADA 1999;99:926-928.
60. Lyons P, Miller WC. Effective healthcare for large people. Healthy Weight J 2000;14:71-73.
61. Berg F. Women Afraid to Eat: Breaking Free in Today’s Weight Obsessed World. Hettinger ND: Healthy Weight Network; 2000.265-282.
62. Kant AK. Consumption of energy-dense, nutrient-poor foods by adult Americans: nutritional and health implications The third National Health and Nutrition Examination Survey, 1988-1994. Am J Clin Nutr 2000;72:929-936.
63. Dheeksha M. National Task Force on the Prevention and Treatment of Obesity, National Institutes of Health. Very low-calorie diets. JAMA 1993;270:967-974.
64. Wadden TA. Treatment of obesity by moderate and severe caloric restriction: results of clinical research trials. Ann Intern Med 1993;119. 688–93.
65. . NIH Technology Assessment Conference Panel, 1993. Methods for voluntary weight loss and control: Technology Assessment Conference Statement. Ann Intern Med 119:764-770.
66. In Contemporary Diagnosis and Management of Obesity, ed Bray G. Handbooks in Health Care Co, Newtown, Pa 1998, 192-202.
67. Wadden TA, Foster GD, Letizia KA. One-year behavioral treatment of obesity: comparison of moderate and severe caloric restriction and the effects on weight maintenance therapy. J Consult Clin Psychol 1994;62:165-171.
68. Stein K. High-protein, low carbohydrate diets: Do they work?. JADA 2000;100:760-761.
69. United States Dept of Agriculture.Dietary Guidelines for Americans, 2000. 5th ed. 2000 Home and Garden Bulletin 232; 28-31.
70. National Institutes of Health and National Heart, Lung and Blood Institute.. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report 1998;6:114S.
71. Flechtner-Mors M, Ditschuneit HH, Johnson TD, Suchard MA, Adler G. Metabolic and weight loss effects of long-term dietary intervention in obese patients: Four year results. Obes Res 2000;8:399-402.
72. Wadden TA, Frey DL. A multicenter evaluation of a proprietary weight loss program for the treatment of obesity: A five-year follow-up. Int J Eat Disord 1997;22:203-212.
73. Freedman MR, King J. Kennedy Popular diets: a scientific review. Obes Res 2001;9:1S-40S.
74. Rippe JM. Hess St The role of physical activity in the prevention and management of obesity. J Am DietAssoc 1998;98:S31-S38.
75. Mclnnis KY. Exercise and obesity. Coron Artery Dis 2000;11:111-116.
76. Pavlou KN, Krey S, Steffee WO. Exercise as an adjunct to weight loss and maintenace in moderately obese subjects. Am J Clin Nutr 1989;49:1115-1123.
77. Schulz LO, Schoeller DA. A compilation of total daily energy expenditures and body weights in healthy adults. Am J Clin Nutr 1994;60:676-681.
78. Bailor DL, Katch VL, Becque MD, Marks CR. Resistance weight training during caloric restriction enhances lean body weight maintenance. Am J Clin Nutr 1988;319:1173-1179.
79. Porcari J, Ward A, Morris D, Maher M, Cuneo P, O’Hanley S, Rippe J. Comparison of weight loss in males and females after 16 weeks of fitness walking and/or diet [abstract]. Med Sci Sports Exers 1986;21:S102.
80. Ross R, Dagnone D, Jones PJH, Smith H, Paddags A, Hudson R, Janssen I. Reduction in obesity and related comorbid conditions after diet-induced weight loss or exercise-induced weight loss in men. Ann Intern Med 2000;133:92-103.
81. Mourier A, Gautier JF, De Kerviler E, Bigard AX, Villette JM, Gamier JP, Duvallet A, Guezennec CY, Cathelineau G. Mobilization of visceral adipose tissue related to the improvement in insulin sensitivity in response to physical training in NIDDM. Effects of branched-chain amino acid supplements. Diabetes Care. 1997;20:385-391.
82. Wing RR, Matthews KA, Kuller LH, Meilahn EN, Plantinga P. Waist to hip ratio in middle-aged women: Associations with behavioral and psychosocial factors and with changes in cardiovascular risk factors. Arterioscler Thromb Vase Biol 1991;11:1250-1257.
83. Blair SN, Kampert JB, Kohn HWsrd, Barlow CE, Macera CA, Paffenbarger RS J, Gibbon LW. Influences of cardiorespiratory fitness and other precursors on cardiovascular disease an all-cause mortality in men and women. JAMA 1996;276:205-210.
84. Bartlow CE, Kohl HW, Gibbons LW, Clair SF. Physical fitness, mortality, and obesity. Int J Obesity 1995;19:S41-S44.
85. Wood P, Stefanick M, Dreon D, Frey-Hewitt B, Garay SC, Williams PT, Superko HR, Fortmann SP, Albers JJ, Branizan KM, Willsworth NM, Terry RB, Haskell WL. Changes in plasma lipids and liproproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med 1988;319:1173-1179.
86. Yanovski S, Yanovski JA. Drug Therapy: Obesity. N Engl J Med 2002;346:591-602.
87. NIH, NAASO. The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. NIH Publication Number DO-4084, 2000. 35-38.
88. Stein, K. Herbal supplements and prescription drugs. JADA. 2000; 1 00:4.
89. Nortier JL, Martinez M-CM, Schmeiser HH, Arlt VM, Bieler CA, Petein M, Depierreux MF, DePauw L, Abramowicz D, Vereerstraeten P, Vanherweghem J-L. Urothelial carcinoma associated with the use of a Chinese herb (Aristolochia Fangchi). N Engl J Med 2000;342. 1686–92.
90. Kernan WN, Viscoli CM, Brass LM, Broderick JP, Brott T, Feldman E, Morgenstern LB, Wilterdink JL, Horwitz Rl. Phenylpropanolamine and risk of hemorrhagic stroke. N Engl J Med 2000;343. 1686–92.
91. Haller CA, Benowitz NL. Adverse cardiovascular and central nervous system events associated with dietary supplements containing ephedra alkaloids. N Engl J Med 2000;343. 1833–8.
92. National Institutes of Health and National Heart, Lung, and Blood Institute.. Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity — The Evidence Report. Obes Res1 1998;6:120S.
93. Campbell LA, Smith FJ, Burn P. Strategies and potential molecular targets for obesity treatment. Science. 1998; 1383-1387.
94. Heymsfield SB, Greenberg AS, Fujioka K, Dixon RM, Kushner R, Hunt T, Lubina JA, Patane J, Hunt P, McCamish M. Recombinant leptin for weight loss in obese and lean adults. A randomized, controlled, dose-escalation trial. JAMA 1999;282:1568-1575.
95. MacLean LD, Rhode BM, Nohr CW. Late outcome of isolated gastric bypass. Ann of Surg 2000;231:524-528.
96. Marceau P, Hould FS, Simard S, et al. Biliopancreatic diversion with duodenal switch. World J Surg 1998;22:947-954.
97. MacLean LD, Rhode BM. Does genetic predisposition influence surgical results of operations for obesity?. Obes Surgery 1996;6:132-137.
98. Kellum JM, DeMaria EJ, Sugarman HJ. The surgical treatment of morbid obesity. Curr Prob Surg 1998;35:791-858.
99. Sumall AJ. A review of liposuction as a cosmetic surgical procedure. J Nat Med Assn 1987;79:1275-1279.
100. Miller WC. How effective are traditional dietary and exercise interventions for weight loss?. Med Sci Sports Exerc 1999;31:1129-1131.
101. Dheeksha M. National Institute of Health, National Heart, Lung, and Blood Institute Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults — the evidence report. Obes Res 1998;6:111S.
102. National Institute of Health,National Heart, Lung, and Blood Institute.. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults — the evidence report. Obes Res 1998;6:127S.
103. Marlatt GA, Gordon JR. Relapse Prevention: Maintenance Strategies in Addictive Behavior Change, Guilford Press, NY 1985.
104. Wing RR. Behavioral approaches to the treatment of obesity In: Bray GA, Bouchard C, James WPT, Handbook of Obesity. New York, NY: Marcel Dekker; 1998. 855-1999874.
105. Wadden TA. The management of obesity: From past failure to future attainment In: Guy-Grand B, Ailhaud G, Progress in Obesity Research 8. London: John Libbey &. Co; 1999. 713-719.
106. Jeffery RW, Drewnowski A, Epstein LH, Stunkard AJ, Wilson GT, Wing RR, Hill DR. Long-term maintenance of weight loss: current status. Health Psychology 2000;1:5-16.
107. International Classification of Diseases. 9th Rev. ICD-9-CM. Chicago, IL: American Medical Association; 2000.
108. National Institutes of Health and National Heart, Lung and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res. 1998:xii.
109. Byfield C. A lifestyle physical activity intervention for obese sedentary women: Effect on cardiovascular disease risk factors. American College of Sports Med: Indianapolis IN; 2000.
110. Helm KK, Klawiller B. Nutrition Therapy: Advanced counseling Skills. Lake Dallas, Texas: Helm Seminars; 1995. 135-161.
111. Beck JS. Cognitive Therapy-.Basics and Beyond, Guilford Press, New York, NY 1995.
112. Rosen JC. Improving body image in obesity. In: Thompson, JK, Body Image, Eating Disorders and Obesity. Washington, DC: American Psychological Association; 1996. 425-550.
July 5th, 2005
Responsibilities of Dietitians in Weight Management
Dietetic practice in weight management is complex and challenging; specialized training is desirable. It is important to focus upon long-term as well as short-term outcomes while respecting the patient’s goals and values. Since many patients are looking for fast and large weight losses, it is important to convey realistic expectations. Tracking treatment outcomes and sharing these with patients, help to clarify expectations at the outset. It is also important for dietitians to maintain currency in their own professional development; including continuing education and training and, if feasible, obtaining specialized supervision when needed. Dietetic professionals need to stay within appropriate scope of practice; they must know their limitations and respect them; making referrals as needed.
Role of the Dietetics Professional in a Team Approach to Weight Management
The physician is usually the first member of the health care team to see patients in need of weight management. It is essential that physicians use this contact effectively, reflecting the complexity of the challenge and making referral to other health care professionals to activate successful intervention. The dietitian has primary responsibility for assessment and recommendations related to food behavior. Given the relationship of physical activity to energy expenditure and weight maintenance, the dietitian may also be involved in assessment and recommendation of activity, provided the patient is cleared for exercise by his or her medical doctor. For example, Byfield was able to show significant and sustained improvements in energy expenditure and cardiorespiratory fitness in heavy women who participated in a program designed to address barriers to exercise and encourage daily physical activity (109).
It may also fall on the dietitian to be the provider who can interpret the results from the initial assessment and make appropriate, patient-matched treatment recommendations.
The dietitian should be attentive to the patient’s concerns, being aware of feelings, values, behaviors, and worries beyond food behaviors and assume an active role in communicating these to the other care providers.
Dietitians are the primary nutrition practice professionals and, as such, have a responsibility for exerting leadership for reducing the prevalence of obesity. Clearly prevention is a complex matter requiring the cooperation of private and public sectors. Currently there is no clear path of action to prevent excessive body weight, which increases health risks. Research has identified certain groups at particular risk; evidently interventions have to start with very young children (26,110).
Dietitians can contribute to the prevention of obesity, not only in their own practice but also by pointing out the seriousness of the increasing weight of the entire population. Dietitians must advocate public policies to support increased opportunigties for healthy eating, exercise, and research into improved strategies for intervention and prevention. As professionals with daily close contact with individuals struggling with weight management, dietitians need to remind policy makers of the difficulty and complexity of the situation. They must resist efforts to further stigmatize obesity, pointing out the lack of evidence of any benefit of this approach, as well as the danger of increasing the risk of eating disorders. It has been suggested that successful weight management is in need of fresh ideas (93); dietitians with their broad educational preparation and intense patient contact may be a rich source of such ideas.
Knowledge and Skills Required
A thorough knowledge of weight management and appreciation of its complexity is imperative. The dietitian will benefit from a working knowledge of theories of behavior change and how to build upon these in designing interventions. Weight management requires the dietitian to have specialized assessment and screening skills in order to make appropriate treatment recommendations. When providing counseling it is important to involve the patient as an active partner. In addition to nutrition education and guidance, nutrition counseling strategies include cognitive-behavioral interventions (111,112). These interventions often involve the ability to assist patients in finding resources within themselves and their community so as to continue behaviors independent of continued intervention by health care professionals.
July 5th, 2005
Pharmacotherapy
Currently there are few pharmacotherapy options available for long term usage. Medications that have been approved by the PDA for treatment of “clinically significant” obesity (BMI > 30 or BMI 27-29 with one or more obesity-related disorders.), include sibutramine and orlistat. Sibutramine (Meridia) is a centrally acting serotonin and adrenergic reuptake inhibitor. It has the potential complication of hypertension and increased heart rate. Orlistat (xenical) is a pancreatic lipase inhibitor which inhibits the absorption of up to 30% of dietary fat. Steatorrhea, bloating and distension, and anal leakage are potential complications, and one must be alert for possible fat-soluble vitamin deficiencies. Reported losses with these medications combined with a low-calorie diet average 2-10kg per year, and if the medications are discontinued weight gain results (86). Amphetamine-like derivitives: mazindol, phentermine, benzphetamine, phendimetrazine are available only for short-term use. When weight loss drugs are prescribed they should be only as part of a comprehensive treatment plan including behavior therapy, diet, and physical exercise (87). The herbal preparations for weight loss do not have standardized amounts of active ingredients and have been reported to have harmful effects (88,89). Certain over-the-counter preparations containing propanolamine (Dexatrim and related compounds) have no proven efficacy for short- or long-term weight loss and are being recalled because of the incidence of hemor-rhagic stroke (90,91). Ephedrine plus caffeine, and fluoxetine have been tested for weight loss, but not approved and over-the-counter and herbal preparations are currently not recommended (92).
Pharmacotherapy research is currently focusing on three approaches, a) inhibitors of energy intake (appetite suppressants, orexins/hypocretin antagonists); b) enhancers of energy expenditure, UCP2 and UCP3 uncoupling proteins; and c) stimulators of fat mobilization (93). Leptin is now in the process of phase 2 testing, but to date, data do not indicate leptin has the potential for being the much sought after magic bullet to modify weight status (94).
Surgery
During the past 25 years, gastric surgery has been shown to be the most effective approach for generating long-term weight loss in extremely heavy persons. More than 90% of patients experience significant (> 20% to 25%) weight loss, and between 50% and 80% maintain weight loss for over 5 years; in contrast, the 5-year efficacy of other approaches is approximately 5% (95). Surgical procedures promote weight loss both by restricting food intake and causing malabsorption. Food intake may be reduced by the placement of a band (gastric banding), which allows only a small amount of food to enter the stomach or by the placement of a band plus staples to create a small pouch (vertical banded gastroplasty). Gastric bypass operations, Roux-en-Y gastric bypass, and the extensive gastric bypass (biliopancreatic diversion, with duodenal switch), create a small pouch by stapling or removal of portions of the stomach, and also bypass the duodenum and other segments of the small intestines thus producing some extent of malabsorption. These procedures have acceptable operative risk, 1% to 2.5% death rate, but require lifelong medical follow-up and monitoring to avoid and manage possible complications (4). Although bariatric surgery has made major advancements in the last 30 years, the effect on the human body of the weight loss produced requires investigation.
Prior to surgery, patients should be fully evaluated by a multidisciplinary team, including but not limited to a medical doctor, psychiatrist, and a dietitian. The role of the dietitian is important in screening to evaluate weight history, efforts to lose weight, food preferences, and food related behaviors, ie, binge eating to assist in electing the optimal procedure for the patient. The patient should be motivated to accept the responsibility for sustaining lifestyle changes to maintain weight loss and decrease post-operative complications.
The development of laparoscopic techniques has significantly reduced the frequency of complications with wound infection, which was the most common complication (5% to 20%), and the length of hospital stay. Data is available for a 5-year follow-up for standard open procedures but long-term follow-up of laparoscopic procedures is not yet available (96). It is of note that surgery appears to rule over genetics in weight loss responses and maintenance (97).
Accepted indications for surgical weight loss therapy are having a BMI > 40 or BMI 35-39 with one or more obesity-related disorders; and having previously unsuccessful non-surgical attempts at long-term weight management. Weight loss surgery is most effective when accompanied by pre- and post-operative comprehensive therapy to modify eating and exercise behavior. Such adjunctive therapy increases the likelihood of long-term success and should be a standard component of surgical weight management (98).
Liposuction is another form of surgery with a focus on adipose tissue. Its purpose is cosmetic, to alter body contours, and it should not be considered as a surgical procedure for weightless (99).
Relapse Prevention
Clearly, preventing regain of fat losses is the major challenge of weight maintenance. Among the limited numbers of programs that do long-term follow-up, many find that losses are completely regained within 3-5 years (100). A successful program is often defined as one that produces maintenance of loss of at least 5%, or 6.6kg of body weight (101). NIH recommends that maintenance efforts be continued indefinitely (102). Dietary and physical activity modifications need to be integrated and accepted as a way of life.
Unfortunately, we have limited knowledge of what behaviors are necessary for successful maintenance. The National Weight Control Registry involves individuals who have lost at least 30 pounds and sustained the loss for a least a year; the typical registrant has, in fact, lost more than that minimum and sustained the loss for more than five years. The successful maintainers in the Registry report very careful attention to a reduced calorie, low-fat diet, increased levels of physical activity, and frequent weighing (5–7). It is not established that these behaviors represent what is minimally necessary for weight loss maintenance; however, these proposed lifestyle modifications on an ongoing basis have produced long-term weight loss maintenance.
Experts in the prevention of relapse have developed models to explain the environmental, emotional, and behavioral aspects of relapse (103). Unfortunately, these models do not address the biological factors impacting metabolic rate and hunger and satiety, thereby contributing to weight regain. Improvements in weight loss maintenance are shown when the risks of relapse are addressed as part of the intervention. Even with extended contacts and relapse prevention education, the reported programs are not able to produce maintenance of all losses in all participants (104). It is difficult to sustain the commitment and participation in long-term treatment programs or with follow-up programs (105), but this is what has been shown to be effective.
Dietitians, because of their close work with patients and clients, are ideally placed to exert leadership in combating weight management relapse. In every patient interaction, they should emphasize the goal of long-term change. Dietitians may help their patients come to view dealing with their weight as a multi-stage process. Regain should not be framed as a personal failure but rather as an indication of a need for another phase of active management. Not all patients will be able to maintain the behaviors that are necessary to sustain losses. Dietitians can anticipate this reality and help their patients to salvage some benefits from their efforts.
Dietitians should address the problems by collecting data initiating alternative strategies and using other resources in the community. An ongoing problem continues to be the cost of providing expanded and extended programs. Currently there is no funding for long-term maintenance services. We must find creative new ways to exert our influences. These might be online programs, phone contacts, utilization of lay leadership, and others.
Cost of Weight Management
Although ideally a long-term, multidisciplinary program is more effective than a short-term program (106), ideal programs are expensive to run. Multifaceted programs can better address the complexity of issues related to achievement of goals; these programs require the services of several health care professionals, increasing the financial cost and time commitment from patients. In addition, access to exercise facilities and/or equipment and purchasing more appropriate food may add to to the overall expense. All approaches to weight management, including pharmaceutical and surgical interventions, ultimately require a comprehensive lifestyle program that focuses on nutrition, exercise, cognitive behavioral changes and medical monitoring to increase the likelihood of long-term success and healthy outcomes.
However, there currently exist barriers to implementing lifestyle programs of maximum effectiveness. Even though health care costs are acknowledged, and NHLBI and the International Classification of Diseases list obesity as a disease, many other organizations do not consider it a disease for reimbursement purposes (9,107). For example, third party reimbursement is not universal and rare for programs to modify weight status; reimbursement when it is provided is frequently limited in duration. Since the prevalence of obesity is rapidly increasing and becoming a major public health concern, it is imperative that private and public sectors work together to obtain third party reimbursement to support treatment for changes in weight status for obesity treatment as well as funding for further research. Obesity must be acknowledged as a disease for reimbursement purposes since data clearly support its association with increased morbidity and mortality (108). Until such data is accepted by both third party payers and the medical community, the obesity epidemic will not be effectively controlled, and a significant barrier will be maintained. Also, there is limited understanding among both lay and health care professionals of the complexity and difficulty of the need for intensive and extensive weight management support. Cost-containment strategies that may improve efficiency may also compromise outcome. These strategies include: triage or stepped approaches; limitations of treatment length and/or frequency of sessions; use of groups; and/or coordination with self-help, lay-led, and for-profit resources.
July 5th, 2005
Interventions
Diet and Lifestyle Modifications
There exists a continuum in philosophy and clinical practice as to what extent externally controlled modification of weight status should be attempted (58,59). This continuum ranges from complete reliance on internal control to increased external structural supports provided by the prescription of diets, meal plans and exercise protocols. Internally regulated approaches are referred to by various names including non-dieting, normalized eating, or intuitive eating. These approaches are based on an assumption that the body knows best and have in common that they urge that food intake be guided by internal clues to hunger and satiety. There may be great variability among individuals in the extent to which they are able to perceive and act upon internal cues. Lengthy intervention may be required to learn to perceive internal signals of hunger and satiety and to develop the trust to allow these signals to guide food intake. Emotional associations with food and eating complicate the sensations that offer internal guidance; when these associations are extreme, therapy for emotional issues is indicated. The body’s regulatory systems resist changes in fatness by adjusting control systems. In addition, there may be a failure of the regulatory system in the body that controls either hunger or satiety or both, making it difficult for an individual to rely on this method. Internal regulation of food intake is most often used with patients who are seeking to stabilize their weight and to address other issues associated with their eating and weight. Programs that have utilized it have demonstrated short-term improvements in self-esteem, body image, and other parameters associated with psychological well-being (53,60). Long-term, randomized, controlled studies with sufficient numbers of participants are not available to validate this approach.
Moderate or mixed approaches promote internally guided eating in combination with limited external guidance systems. Based on the observation that internal guidance of food behavior is difficult given most peoples’ experiences and environment, this moderate approach provides structural supports even while urging that individuals respond to their own cues of hunger and satiety. There is no available data to support the proposition that adults experience food or nutrient-specific appetites that lead infallibly to a balanced diet. Readily available foods tend to be high in fat, calories, salt, and sugar, making the consumption of such foods more likely. A moderate approach would teach patients to provide themselves with high volume, nutrient-dense but not calorie-dense foods in a balanced array and to then allow their hunger and satiety to guide them in choosing quantities. Teaching awareness of one’s eating, both the amount eaten and the sensations produced, is important. This approach emphasizes moderation, balance, and common sense and should reduce feelings of deprivation (61). It is most often accompanied by advice concerning exercise, stress management, and self-acceptance. The outcomes of these approaches depend upon the original goals. Theoretically, such a moderated approach should lead to changes in eating and exercise behaviors that can be sustained and will lead to slow continued weight losses. There has been little documentation of the long-term effectiveness of this combined approach. However, data from the Continuing Survey of Food Intakes by Individuals 1994-1996 was analyzed to look at dietary patterns and selected measures of nutritional status and Body Mass Index. This analysis found that individuals on a moderate fat, high-carbohydrate diet as recommended by the Food Pyramid Guide were more likely to maintain weight loss (62).
Externally based systems range from severe caloric restriction, very low calorie diets (< 800 calories per day), to low-calorie diets (estimated energy expenditure minus 500-1,000 calories per day) to guide food intake. These systems are based on the assumption that not all individuals are able to internally control their food intake to the extent of achieving a healthier weight and therefore must rely on external guidance and increased structural supports. Data regarding severe energy restricted diets, such as very low calorie diets (VLCDs), show that despite the short-term success of achieving significant weight losses, there is poor long-term maintenance of losses (63). It has been well documented that use of the low-calorie diets, typical of a modified approach, can produce mean weight losses in the range of 8% to 10% of body weight over a period of 6-12 months (64). Unfortunately, it is also well documented that unless individuals sustain the diet plus exercise indefinitely, most of the losses are regained (65). Patients who have realistic weight loss goals (5% to 10% weight loss), have never dieted, are trying to modify very poor food habits, are seeking external supports and increased structure, and accept the need for a sustained effort may benefit from diets mildly reduced in calories accompanied by a regular exercise program.
Diets
Multiple approaches to the modification of caloric intake have been tried. Diets can be classified as: starvation (0-200 kcals/ day); very-low calorie (200-800 kcals/day) or low calorie (>800 kcal/day) (66). Starvation diets include fasting, which has been used for centuries and results in a loss of lean body mass and mineral loss due to diuresis. VLCDs are protein-sparing modified fasts using either a premixed liquid or meat, fish, or poultry. VLCDs come and go in popularity often according to the push of a commercial program or book. Generally, in a medical environment, they are reserved for patients who have BMIs > 30 and have failed other approaches. Patients should be under medical supervision and must receive supplemental vitamins and minerals (63). It has been established that the weight losses over time are not greater than a mixed diet of equal caloric content, and the resumption of eating solid foods frequently disrupts maintenance efforts (67,68).
More commonly used interventions are low-calorie diets that modify the macronutrient composition of the diet. Low-calorie diets emphasize portion control in an effort to reduce energy intake below the level of energy expended. For balanced, deficit diets, the treatment protocol must be adapted to the needs of the patient. However, usually an energy deficit of 500-1000 calories per day is planned for individuals with the expectation that a weight loss of 1-2 pounds per week will occur. The reduction of saturated fat is advised with a total fat intake of less than 30% (69). It is important that total calories are reduced, not just total fats, or little weight change will result (70). Of greatest importance is stressing “healthy eating” advised for all Americans according to the Food Pyramid Guide and the US Dietary Guidelines. Dietary planning and employing caloric dilution to keep the volume of food up while reducing total calories, may decrease feelings of deprivation and restriction.
Meal replacements are another category of calorie-controlled diets. Individuals replace a meal with a liquid drink that contains approximately 200 calories per serving and approximately 50% to 60% carbohydrate, 30% protein, and 10% fat or a pre-measured frozen meals of a set caloric value. The replacements help keep calories under control and probably, more importantly, reduce sensory stimulation and the need to make decisions about portion size. The patient must be individually motivated to adhere to a pre-measured meal plan on a long-term basis and accepting of the small sustained changes in weight status, 3.2% to 8.4% over four years (71).
Patients often are attracted to diets and programs that promise magical, no-stress weight loss. Although these programs have no metabolic validity, their promises are appealing. This has led to a weight loss industry in this country in excess of $30 billion per year. It must be acknowledged that such programs do modify food intake and produce weight loss not because of the claims given, but because of the energy deficit. Although many have short-term success, these diets are often unbalanced and deficient in certain nutrients and may be excessive in others (72). A recent Obesity Research supplement “Popular Diets: A Scientific Review,” by Freedman, King, and Kennedy provides a compendium of the scientific data regarding the implementation of these popular diets (73).
Physical Activity
The lack of energy expenditure in our society today is one component of energy balance which underlies the pathogen-esis of obesity and the overall principles for treatment. Physical activity or exercise is highly recommended as an essential component of the intervention plan to promote weight loss (74,75). Not only does physical activity contribute to weight loss by altering energy balance, but also favorably affects body composition, risk for disease, mood and quality of life. Regular physical activity also appears to be one of the best predictors of successful weight maintenance (76). Therefore, the importance of physical activity in the role of weight management and overall health cannot be overlooked.
It is well established that physical activity during weight loss can favorably affect energy balance and body composition (74,77). Weight gain results from a positive energy balance. Daily physical activity alters energy balance not only by increasing energy expended, but without exercise, loss of lean body mass with dieting alone contributes to a decrease in metabolic rate. Physical activity has been shown to aid in the preservation of lean body mass during weight loss (78,79). The addition of moderate physical activity to restriction of energy intake in promoting weight loss, has been shown to limit the loss of lean body mass to less than 10% (79). Maintaining or minimizing the loss of fat-free mass during periods of restricted energy intake appears to be particularly beneficial, since fat-free mass is the most important factor influencing resting metabolism (74). Furthermore, the addition of resistance training to aerobic activity reportedly enhances body composition further (78).
Physical activity also may positively influence the distribution of body fat independent of its effect on body weight (74). Although an increase in overall body fat is considered a risk for chronic disease, an increase in visceral abdominal fat has been identified as even a stronger independent risk factor for the development of type 2 diabetes, coronary heart disease, hypertension and some cancers than general obesity (80). Despite the fact that the combination of dieting and physical activity has been shown to reduce visceral abdominal fat, several studies have shown the benefit of exercise alone in reducing visceral abdominal fat. This is particularly important since the risk for disease is thereby reduced. (80,81). Physically active individuals have also been found to have lower waist-to-hip ratios in comparison to sedentary individuals (80,82).
The combination of weight loss and physical activity has consistently been shown to convey additional health benefits by improving the metabolic parameters associated with chronic disease. Weight loss and exercise together reduce total cholesterol, low-density cholesterol, triglyceride, plasma insulin, and blood glucose levels thereby reducing the risks for metabolic syndrome, type 2 diabetes, and heart disease (74,80,75,83). It is important to note however, that regardless of whether weight is lost or not, overweight and obese individuals receive significant health benefits associated with daily physical activity (83,84). Overweight or obese individuals who achieve cardiorespiratory fitness have been shown to have a lower all-cause morbidity and mortality risk than sedentary individuals of normal weight (83,84). Many times, despite the lack of weight loss, metabolic parameters such as insulin, glucose, and triglyceride levels are also improved with exercise alone (80,85). Therefore, daily physical activity should be encouraged for all individuals not only for weight loss or weight maintenance but to improve overall general health through the prevention and reduction of risks for chronic disease.
July 5th, 2005
Goals of Weight Management Interventions
At the outset of treatment, the patient and health care provider should discuss and agree upon goals. The clinician needs to avoid overpowering advice inferring “do as I say” versus empowering advice such as “pay attention to what you want to do; trust yourself in this process.” With such an attitude the provider and the patient will develop a relationship of shared responsibility. Realistic expectations, short- and long-term, may be fostered by a discussion of a healthy weight versus an ideal body weight. Goals of weight management interventions may include:
* prevention of weight gain or stopping weight gains in the individual who has been seeing a steady increase in his or her weight (51);
* varying degrees of improvements in physical and emotional health (52);
* small maintainable weight losses or more extensive weight losses achieved through sensible and tolerable eating and exercise behaviors (53); and
* improvements in eating, exercise, and other behaviors apart from any weight loss.
Expectations and recognition of the time required to make sustainable behavior changes must also be discussed. To enable potential patients to make an informed decision to begin treatment, the program’s success in assisting patients in meeting various types of goals needs review.
Health can be improved with relatively minor weight losses. A weight loss of 10% may ameliorate health risks associated with excessive body weight (54). A challenge to health care providers is helping patients to accept a 10% weight loss. Some patients, encouraged by a “thin obsessed” society, want to set unrealistically low weight goals (55). Size acceptance, which emphasizes the positive aspects of one’s body and its appearance, while realistically appraising and accepting the more negative aspects, may need to be addressed. This requires challenging value systems that make appearance one of the most important aspects of life. Appearance, in many patients, will be an important motivator; however, it is critical that the dietitian and other health care providers emphasize the goal of achieving a healthier weight and lifestyle, while de-emphasizing cosmetic goals.
Setting treatment goals and documenting before and after measures is an important aspect of patient care. Whatever goals of treatment are set by the practitioner and the patient, before and after measures of those goals should be tracked to encourage positive health behaviors and acknowledge progress toward those goals. Clinical measures such as before and after weight, laboratory values, and blood pressure should be documented. Batteries of measurement tools are needed to monitor progress in self-esteem, self-efficacy, body image, size acceptance, and sense of control over eating (56–57). Tracking outcomes will not only allow the dietitian and patient to monitor change but can contribute to the evaluation of the efficacy of the program. Outcomes measures, other than absolute weight, should provide the patient with continued motivation and demonstrate to the individual that he or she has achieved positive behavior change.
July 5th, 2005
Next Posts
Previous Posts
