Weight Loss Blog

A too-fast heartbeat in early adulthood is a warning sign for increased risk of cardiovascular problems decades later on, a Japanese study suggests.

The study of 614 residents of a rural farming community in southwestern Japan found that a heart rate greater than 80 beats a minute during a first examination in 1979 predicted the development of obesity and diabetes, which contribute to heart problems.

The findings, from Kurume University School of Medicine, were published online Dec. 11 in the American Journal of Hypertension.

A fast heart rate is a signal from the sympathetic nervous system, a part of the autonomic nervous system, which is the body’s automatic pilot that governs instinctive responses, explained Mercedes Carnethon, assistant professor of preventive medicine at Northwestern University’s Feinberg School of Medicine. She found the same rapid heartbeat association in a group of Americans she studied.

“If someone has a consistently fast heart rate, it is because of increased input from the sympathetic part of the nervous system because the body is preparing to respond to stress,” Carnethon said. “There is an increase in levels of blood glucose — essentially because the body is storing energy to prepare for fight or flight, so that predisposes to diabetes.”

Carnethon’s study followed Chicago residents even longer than the Japanese researchers. “Over a 33-year follow-up, we showed that people with a higher heart rate were more likely to have Medicare claims for diabetes-related conditions,” she said.

There’s a possible clinical use for the findings, Carnethon said, since doctors routinely listen to the heart rate.

“It is a very simple measure, regularly taken in clinical practice, that could be potentially useful because it suggests where there might be a higher incidence of heart risk and mortality,” she said. “It is a first stage to alert the clinician that there might be something worth investigating.”

The similar findings in the two studies half a world apart are noteworthy, Carnethon said. “We are always happy to see findings replicated by different investigators in different settings,” she said.

Meanwhile, researchers are reporting a different built-in mechanism that protects a lucky few individuals from heart disease — a genetic mutation that seems to reduce blood levels of the fats called triglycerides.

The mutation was found in members of the Old Order Amish community in Pennsylvania, said the lead investigator, Toni I. Pollin, an assistant professor of medicine at the University of Maryland School of Medicine.

Pollin and her colleagues looked through the complete genetic complement of more than 800 members of the Amish community. “We looked at genes involved in the response to dietary fat,” she said. “One region came up strong on chromosome 11. This genetic marker was not too far from a cluster of genes involved in lipid metabolism.”

The researchers closed in on one gene, designated APOC-3, according to a report in the Dec. 12 issue of the journal Science. That gene makes a protein that inhibits the breakdown of triglycerides. About 5 percent of the Amish in the study had a mutated form of the gene that limited production of the protein, and so they had low blood lipid levels.

“It is an apparent cardioprotective mechanism,” Pollin said. “It raises the hope that by decreasing production of APOC-3 it could potentially be therapeutic.”

It’s possible that a drug designed to target the gene could be used to reduce levels of blood fats and thus reduce coronary risk, Pollin said.

The mutation has not been found outside the Amish community, Pollin said. “We have looked at 200 healthy individuals and have not found it, she said.

High heart rates linked to obesity, diabetes

High resting heart rates may be linked to the development of obesity and diabetes, a Japanese study shows.
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Researchers have identified at least six new gene mutations linked to obesity and said on Sunday they point to ways the brain and nervous system control eating and metabolism.

Joel Hirschhorn at Children’s Hospital and Harvard Medical School in Boston led a team called Genetic Investigation of Anthropometric Traits or GIANT to screen 15 different studies of the entire human genetic map and pinpoint the six new genetic variations.

“Today’s findings are a major step forward in understanding how the human body regulates weight,” Dr. Alan Guttmacher, Acting director of the National Human Genome Research Institute, said in a statement.

“This study essentially doubles in one fell swoop the number of known and replicated genetic factors contributing to obesity as a public health problem,” added Dr. Kari Stefansson, Chief Executive Officer of DeCODE Genetics of Iceland, who led a team that made similar findings in a separate study.

The GIANT team found variations in six genes — TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 — were strongly associated with a height-to-weight ratio known as body mass index or BMI.

“One of the most notable aspects of these discoveries is that most of these new risk factors are near genes that regulate processes in the brain,” added Stefansson, whose company hopes to sell genetic tests based on such discoveries.

“This suggests that as we work to develop better means of combating obesity, including using these discoveries as the first step in developing new drugs, we need to focus on the regulation of appetite at least as much as on the metabolic factors of how the body uses and stores energy,” Stefansson said.

“These new variants may point to valuable new drug targets,” he added.

Nearly a third of U.S. adults are considered obese with a BMI of 30 or more. Obesity is associated with more than 100,000 deaths each year in the U.S. population and trends are similar in many other countries.
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Breast cancer patients who are overweight have more aggressive disease and are likely to die sooner, U.S. researchers reported on Friday.

A dangerous type of breast cancer, known as inflammatory breast cancer, was seen in 45 percent of obese patients, compared with 30 percent of overweight patients and 15 percent of patients of healthy weight.

“The more obese a patient is, the more aggressive the disease,” said Dr. Massimo Cristofanilli of the University of Texas M.D. Anderson Cancer Center, who led the study.

“We are learning that the fat tissue may increase inflammation that leads to more aggressive disease.”

Writing in the journal Clinical Cancer Research, Cristofanilli and colleagues said they studied 606 women with breast cancer that had spread within the breast.

They classified them according to body mass index or BMI, a globally accepted measure of obesity. People with BMIs of below 25 are considered normal, while 25-29 marks overweight and 30 or above is clinically obese.

After five years, 56.8 percent of obese women and 56.3 percent of overweight women were still alive. But 67.4 percent of the normal weight women had survived.

More than 56 percent of women of normal weight survived 10 years, compared to 42.7 percent of obese women and 41.8 percent of overweight women.

“Obesity goes far beyond just how a person looks or any physical strain from carrying around extra weight. Particular attention should be paid to our overweight patients,” Cristofanilli said.

Many studies have shown that the obese have a greater risk of several types of cancer. Last month British researchers reported in the Lancet medical journal that obesity can double the risk of leukemia, multiple myeloma, thyroid cancer, colon and kidney cancers.

Fat cells produce a range of hormones that could fuel cancer, researchers say.

Locally advanced breast cancer more deadly in obese

Women with locally advanced breast cancer who are overweight have a worst prognosis than their slimmer counterparts, US researchers reported.

An aggressive type of breast cancer, known as inflammatory breast cancer, was also seen in significantly more obese and overweight patients than in normal-weight patients, according to the study, published in the journal Clinical Cancer Research.

“The more obese a patient is, the more aggressive the disease,” said principal investigator Dr. Massimo Cristofanilli of the University of Texas M.D. Anderson Cancer Center in Houston. “We are learning that the fat tissue may increase inflammation that leads to more aggressive disease.”

Cristofanilli and colleagues studied 602 women with locally advanced breast cancer. They classified the patients by body mass index (BMI), the ratio of height to weight, frequently used to measure obesity. (People with BMIs of less than 18.5 are underweight; between 18.5 and 24.9 is considered normal; 25.0 to 29.9 is overweight; and 30 or higher is obese.)

After fiveyears, the researchers report that 58.6 per cent of the obese women, 58.3 per cent of the overweight women and 69.3 per cent of the normal-weight women were still alive.

After ten years, 57.3 per cent of normal- or underweight had survived compared with 42.4 per cent of obese women and 44.1 per cent of overweight women.

“Obesity goes far beyond just how a person looks or any physical strain from carrying around extra weight. Particular attention should be paid to our overweight patients,” Cristofanilli said.

Many studies have shown that the obese have a greater risk of several types of cancer. Last month British researchers reported in The Lancet medical journal that obesity can double the risk of leukemia, multiple myeloma, thyroid cancer, colon and kidney cancers.

Breast cancer, blood sugar and body fat

“Big C risk is worse if you’re fat” reads the headline in The Sun today. The news story it refers to goes on to say that fat women are “less likely to get low-risk breast cancer – but more prone to life-threatening versions”. The researchers have “discovered a link between the fiercest types [of breast cancer] and high blood sugar”, the newspaper adds.

The newspaper report is based on a Swedish study investigating metabolic factors and breast cancer risk. There were few results of statistical significance this study so it is impossible to reach firm conclusions. Although this study adds evidence to previous research which suggests a complex link between metabolism and breast cancer, more studies are needed to identify what this risk is. This study is not conclusive and The Sun and other news sources have overstated its significance.

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The mix of bacteria in a baby’s gut may predict whether that infant will become overweight or obese later in life, a new study suggests.

Babies with high numbers of bifidobacteria and low numbers of Staphylococcus aureus may be protected from excess weight gain, according to a team of researchers from the University of Turku in Finland.

Their study was published in the March issue of The American Journal of Clinical Nutrition.

The researchers suggested their findings may help explain why breast-fed babies are at lower risk for later obesity, since bifidobacteria are prevalent in the guts of breast-fed babies.

Other studies repeatedly have found that being breast-fed is associated with a reduced risk of excess weight or obesity in childhood, with the risk lowered from 13 percent to 22 percent.

In the new study, researchers evaluated children who had been part of a long-term study to evaluate the effect of probiotics on allergic disease. Probiotics are potentially beneficial bacteria found in foods such as yogurt and in dietary supplements.

The children had been evaluated at birth, five more times before age 2, and then again at ages 4 and 7. The researchers in the original study had also tested for intestinal microbes in fecal samples collected at 6 months and 12 months.

For this latest study, the Finnish researchers selected 49 participants from the larger study — 25 of them were overweight or obese at age 7 years, and 24 were normal weight at the same age.

When they looked at the fecal samples, the average bacterial counts of bifidobacteria when taken at 6 months and 12 months were twice as high in those who were a healthy weight as in those who got heavy.

Those who stayed at a healthy weight also had lower fecal S. aureus levels at 6 months and 12 months than did those who got heavy.

The S. aureus may trigger low-grade inflammation, the authors speculated, and that may also contribute to developing obesity.

In other research, gut bacteria in adults have been found to be altered in obese adults who lost weight. Someday, the Finnish researchers speculated, tinkering with gut flora may help prevent or treat obesity.

The latest study doesn’t pinpoint exactly why intestinal bacteria are linked with the development of obesity, said Connie Diekman, director of university nutrition at Washington University in St. Louis and president of the American Dietetic Association.

“The exact role that bacteria in the intestine play in development of obesity is still the subject of much research,” she said, “but the benefits of breast-feeding are clear. Breast-feeding provides not only the proper nutrition for your infant, but it provides benefits that may impact long-term health and weight issues as well.”

However, she added that, “while breast-feeding may play a role in the weight of children, so many other factors influence weight that parents shouldn’t ignore good role modeling of healthy food choices, proper portions and regular physical activity. Healthy weight is a combination of factors, and no single issue will be the cause of weight gain or the magic answer to weight loss.”

Another expert who has studied how obesity changes microbes in the gut calls the new study unique, because it collected information over several years and could look for differences in gut microflora. “The finding, that the lean children harbored higher levels of bifidobacteria at younger ages, is very intriguing,” says Ruth Ley, a research assistant professor at Washington University School of Medicine in St. Louis.

Still, she says, research on the role of gut bacteria in regulating body weight is in the very early stages.

Research Links Obesity to Mix of Bacteria in Digestive Tract

Obese people have a distinctive mix of bacteria in their digestive systems that seems to make them prone to gaining weight, a startling discovery that could lead to new ways to fight the obesity epidemic, researchers reported yesterday.

Obese people have more digestive microbes that are especially efficient at extracting calories from food, the researchers said, and the proportion of these super-digesting organisms ebbs as the people lose weight. Moreover, when the scientists transplanted these bacteria from obese mice into lean mice, the thin animals start getting fat. This provides more support for the provocative theory that the bacteria that populate the intestine play an important role in regulating weight.

“There appears to be a link between obesity and the type of bugs in your gut,” said Jeffrey I. Gordon of Washington University School of Medicine in St. Louis, who led the series of experiments being published in today’s issue of the journal Nature. “The difference in the structure of microbial ecology of our gut may set us up for susceptibility to obesity.”

Gordon and his colleagues stressed that more work is needed to explore the findings. And they cautioned against trying to manipulate “gut flora” with antibiotics or microbial “probiotic” pills sold in health-food stores. But if the findings are confirmed and better understood, they could lead to profound new insights into one of the nation’s biggest health problems, the researchers said.

“In the future, we could potentially manipulate the structure and function of these microbial societies as a new approach toward preventing and treating obesity,” Gordon said.

The findings produced enthusiasm and caution from other researchers. Some praised the work for possibly offering a long-sought alternative explanation for the obesity epidemic. Perhaps some change, such as a food additive or antibiotic use, has caused a fundamental shift in gut flora, making it easier for many people to gain weight.

“This is very exciting,” said Barbara Corkey, an obesity researcher at Boston University. “We don’t know why the obesity epidemic is happening. People say it’s because of gluttony and sloth. I think there must be something else. It’s exciting to see some work being done on alternative explanations.”

Others suspect that if gut microbes do play a role, it is a minor one.

“This is extremely interesting,” said Hans-Rudolf Berthoud of the Pennington Biomedical Research Center in Baton Rouge. “But lifestyle and the environment are still the major factors in the obesity epidemic.”

On a broader level, the findings highlight the symbiotic relationship humans maintain with the trillions of microorganisms that populate our bodies, Gordon and others said.

“This strengthens the notion that the indigenous organisms in the human body are probably intimately involved in our health,” said David A. Relman of Stanford University. “The ways they are involved remain unclear, but this underscores the idea that it behooves us to figure it out.”

Scientists have long known that the human body is teeming with germs, primarily bacteria, which cover the skin and inhabit every orifice. By some estimates only one out of every 10 cells in the human body is human. These organisms perform a host of functions, especially in the digestive tract, where they help digest food.

“There’s growing interest in the idea that humans are more than just human cells,” said Martin Jack Blaser of New York University. “These cells are not just passengers. They are part of the human metabolism.”

To explore the role of the organisms in weight regulation, Gordon’s team first compared the gut flora of 12 obese people to lean subjects’. The obese tended to have a significantly greater proportion of one of the two main types of bacteria found in the gut, known as Firmicutes, than the other, known as Bacteroidetes.

Next, the researchers spent a year meticulously measuring the gut flora of the obese volunteers as they tried to lose weight by eating low-calorie diets that restricted either their fat or carbohydrate intake. As volunteers lost weight, the proportion of Firmicutes in their digestive tracts fell and the proportion of Bacteroidetes rose, the researchers found.

When the researchers conducted detailed molecular analyses of the two types of bacteria in the laboratory, they discovered the Firmicutes were much better at extracting calories from food.

Moreover, when the researchers examined the gut flora of obese laboratory mice, they found a similar pattern in their ratios of Firmicutes to Bacteroidetes. And when researchers transferred gut flora from obese mice to mice devoid of gut flora, the recipient animals tended to gain weight, confirming that the pattern was associated with weight gain.

“This attribute of being able to harvest and store more energy appeared to be transmissible,” Gordon said. “For the first time, we see that there is a correlation between the microbial gut ecology and the obese state.”

Among other things, the findings could help explain why it becomes harder and harder to lose weight as people get fat, Gordon said.

“That’s part of the pathology of obesity. When you shift the amount of fat tissue, the amount of energy you can harvest becomes somewhat greater, and that’s going to fuel the obese state,” he said.

The researchers acknowledged that the difference in the number of calories extracted by the microbes is relatively small. But over time even a small differential could be significant, they said.

Many questions remain, however. It is unclear what determines the make-up of a person’s gut flora. It might be the microbes they pick up from their mothers; it might be their exposure to antibiotics. It is also unclear how fat tissue and gut flora might affect one another, and whether the change in gut bacteria causes or is a result of the weight loss.

Despite those and other questions, scientists said the findings are sure to inspire more investigation.

“They open up a completely new hypothesis,” said Randy Seeley, an obesity researcher at the University of Cincinnati who wrote a commentary accompanying the research. “There are a lot of hurdles here that we have to deal with in terms of our basic understanding. But it’s fascinating.”

Researchers in Sweden have discovered a protein that stimulates the formation of fat cells, a finding that could potentially be used to treat obesity, the Karolinska Institute said.

The protein, called TRAP (tartrate-resistant acid phosphatase), “stimulates the formation of new fat cells and can thus precipitate the development of obesity,” the Institute said in a statement.

The research was based on cell cultures and mice studies, and showed that patients with obesity have excessive levels of the protein.

“This protein is potentially useful in the treatment of conditions involving morbid cachexia (weight loss), such as cancer diseases,” professor Goeran Andersson, who led the study, said.

“The discovery can also lead to new ways of treating obesity based on the inhibition of this protein’s effect,” he said.

The study lasted four years and followed 14 obese women, Andersson told AFP.

The news of the research comes just two days after experts in UK raised hope for new obesity treatment.

They said new treatments could be in the pipeline to give obese people a full feeling after eating just a small meal.

Experts at University College London identified two cell proteins that relax the stomach and help it expand to accommodate large meals.

By targeting the protein receptors, they hope to be able to develop drugs which make people feel “full up” quicker. They identified two protein receptors — P2Y1 and P2Y11 — involved in fast and slow relaxation of the gut.

World governments focus too much on fighting terrorism while obesity and other “lifestyle diseases” are killing millions more people, an international conference heard Monday.

Overcoming deadly factors such as poor diet, smoking and a lack of exercise should take top priority in the fight against a growing epidemic of preventable chronic disease, legal and health experts said.

Global terrorism was a real threat but posed far less risk than obesity, diabetes and smoking-related illnesses, prominent US professor of health law Lawrence Gostin said at the Oxford Health Alliance Summit here.

“Ever since September 11, we’ve been lurching from one crisis to the next, which has really frightened the public,” Gostin told AFP later.

“While we’ve been focusing so much attention on that, we’ve had this silent epidemic of obesity that’s killing millions of people around the world, and we’re devoting very little attention to it and a negligible amount of money.”

The fifth annual conference of the Oxford Health Alliance — co-founded by Oxford University — has brought together world experts from academia, government, business, law, economics and urban planning to promote change.

An estimated 388 million people will die from chronic disease worldwide over the next 10 years, according to World Health Organisation figures quoted by the alliance.

“There’s a political paralysis in dealing with the issue,” said Gostin, an adviser to the US government and a professor at Georgetown and Johns Hopkins universities.

He noted that prevention of obesity and its effects had hardly rated a mention in the current campaign for the US presidency.

“Yet the human costs are frightening when we consider that obesity could shorten the average lifespan of an entire generation, resulting in the first reversal in life expectancy since data collecting began in 1900,” he said.

Like terrorism, some passing health threats get major government attention and media coverage, while heart and lung disease, diabetes and cancer account for 60 percent of the world’s deaths, the meeting was told.

“It is true that new and re-emerging health threats such as SARS, avian flu, HIV/AIDS, terrorism, bioterrorism and climate change are dramatic and emotive,” said Stig Pramming, the Oxford group’s executive director.

“However, it is preventable chronic disease that will send health systems and economies to the wall.”

The conference is due to end Wednesday with a “Sydney Resolution” calling on governments and big business among others to take action to avert millions of premature deaths due to chronic disease.

“The way we live now is making us sick, it’s making our planet sick and it’s not sustainable,” said Asia-Pacific co-director Ruth Colagiuri.

The Sydney resolution focuses on four key areas, including the need to make towns and cities healthier places in which to live by urban design which promotes walking and cycling and reduces carbon emissions from motor vehicles.

Insufficient physical exercise is a risk factor in many chronic diseases and is estimated to cause 1.9 million deaths worldwide each year, said Tony Capon, professor of health studies at Australia’s Macquarie University.

“We need to build the physical activity back into our lives and it’s not simply about bike paths, it’s about developing an urban habitat that enables people to live healthy lives: ensuring that people can meet most of their daily needs within walking and cycling distance of where they live,” he said.

The resolution also calls for a reduction in sugar, fat and salt content in food, making fresh food affordable and available and increasing global efforts to stop people smoking.

World governments are focussing too much on fighting terrorism while obesity and other “lifestyle diseases” are killing millions more people?

Overcoming deadly factors such as poor diet, smoking and a lack of exercise should take top priority in the fight against a growing epidemic of chronic disease, legal and health experts said.

Global terrorism was a real threat but posed far less risk than obesity, type two diabetes and smoking-related illnesses, US law professor Lawrence Gostin said at the Oxford Health Alliance Summit here.

“Ever since September 11 we’ve been lurching from one crisis to the next which has really frightened the public,” Gostin told media later.

“While we’ve been focussing so much attention on that we’ve had this silent epidemic of obesity that’s killing millions of people around the world and we’re devoting very little attention to it and a negligible amount of money.”

The fifth annual conference of the Oxford Health Alliance — co-founded by Oxford University — has brought together world experts from academia, government, business, law, economics and urban planning to promote change.

Like terrorism, some passing health threats get major government attention and media coverage, while heart and lung disease, diabetes and cancer account for 60 percent of the world’s deaths, the meeting was told.

“It is true that new and re-emerging health threats such as SARS, avian flu, HIV/AIDS, terrorism, bioterrorism and climate change are dramatic and emotive,” said Stig Pramming, the Oxford group’s executive director.

“However, it is preventable chronic disease that will send health systems and economies to the wall.”

The conference is due to end Wednesday with a call on governments and big business among others to take action to avert the millions of premature deaths due to chronic disease.

Now look. Two years ago (!) we had this article published:

Obesity Bigger Threat Than Terrorism?

America’s obesity epidemic will dwarf the threat of terrorism if the nation does not reduce the number of people who are severely overweight, the surgeon general said Wednesday.

“Obesity is the terror within,” Richard Carmona said during a lecture at the University of South Carolina. “Unless we do something about it, the magnitude of the dilemma will dwarf 9-11 or any other terrorist attempt.”

Obesity rates have tripled over the past 40 years for children and teens, raising their risk of diabetes and other diseases. For the first time, Carmona said, children are being diagnosed with high blood pressure.

“Where will our soldiers and sailors and airmen come from?” he said. “Where will our policemen and firemen come from if the youngsters today are on a trajectory that says they will be obese, laden with cardiovascular disease, increased cancers and a host of other diseases when they reach adulthood?”

Lowering the nation’s obesity rate depends on changing behaviors, but too many Americans are health illiterate, meaning they cannot understand medical terms and directions from doctors, Carmona said.

The surgeon general offered few specific solutions but said public policy reforms would not be helpful in curbing obesity, explaining that common-sense health decisions cannot be legislated.

Reducing the amount of salt that children eat could provide a short-cut to keeping them slim, British researchers reported on Wednesday.

They found that children who ate less salt drank fewer sugary soft drinks and could reduce their risk of high blood pressure and obesity.

Writing in the journal Hypertension, they said this could lower rates of heart attack and stroke in later life.

“Sugar-sweetened soft drinks are a significant source of calorie intake in children,” said Dr. Feng He of St. George’s University of London.

“It has been shown that sugar-sweetened soft drink consumption is related to obesity in young people,” He added in a statement.

“If children aged 4 to 18 years cut their salt intake by half, there would be a decrease of approximately two sugar-sweetened soft drinks per week per child, so each child would decrease calorie intake by almost 250 kilocalories per week.”

One pound of body weight equals 3,500 calories.

He and colleagues analyzed data from a 1997 national survey of more than 2,000 people between 4 and 18 in Britain. More than 1,600 boys and girls had salt and fluid intake recorded in a diary, with everything they ate and drank weighed.

“We found that children eating a lower-salt diet drank less fluid,” He said. “From our research, we estimated that 1 gram of salt cut from their daily diet would reduce fluid intake by 100 grams per day.”

The children who ate less salt also drank fewer sugar-sweetened soft drinks, and He predicted that a 1 gram reduction in salt would reduce sugar-sweetened soft drink consumption by 27 grams a day, after factoring in age, gender, body weight and level of physical activity.

He said parents should check labels, choose low-salt food products and not add salt during cooking and at the table.

“Small reductions in the salt content of 10 percent to 20 percent cannot be detected by the human salt taste receptors,” she said.

According to the American Heart Association, healthy adults should reduce their sodium intake to less than 2,300 milligrams or 2.3 grams per day. This is about 1 teaspoon of salt.

Americans and Britons consume up to 75 percent of their sodium from processed foods like tomato sauce, soups, canned foods and prepared mixes.

Salt may fuel child obesity

Salt-rich diets could be the key to why some children battle with obesity, University of London researchers say.

In a study of data on 1,600 children, they found that children eating a salty diet tended to drink more, including more fattening, sugary soft drinks.

They reported in journal Hypertension that halving the average daily salt intake of six grams a day could cut 250 calories a week from a child’s diet.

They called for further work by the food industry on reducing salt content.

One in five children in the UK is overweight and there are fears that this will contribute to a rising trend in adult obesity, heart disease and stroke in years to come.

Eating products high in salt tends to make people thirsty and it is known that in adults, a salt-laden diet tends to increase the amount of sugary soft drinks consumed.

First in children

This is the first study to see if the same effect was found in children.

The team from St George’s, University of London, looked at data from the National Diet and Nutrition Survey, conducted in 1997.

They used a sample of 1,600 four to 18-year-olds who had all had their salt and fluid intake measured precisely.

They found that children eating a lower-salt diet drank less fluid and estimated that one gram of salt cut from a daily diet would reduce fluid intake by 100 grams per day.

Approximately a quarter of those 100 grams would be sugary soft drinks, they predicted.

The researchers estimated that if children cut their salt intake by half - an average reduction of three grams a day - there would be a decrease of approximately two sugar-sweetened soft drinks per week per child.

That, in turn, would decrease each child’s calorie intake by almost 250 calories per week.

They urged parents to check the salt content of their children’s meals and manufacturers to find ways to reduce this content.

They said reductions in the salt content of 10% or 20% cannot be detected by human salt taste receptors and do not cause any “technological or safety problems”.

Professor Graham McGregor, one of the paper’s authors and the chairman of Consensus Action on Salt and Health, said that while some manufacturers had acted to reduce salt levels in bread and cereals - the main sources of salt for children - there was still plenty left for the industry to do.

“Unfortunately some food specifically targeted at children has to be laced with salt otherwise it would be inedible, because it is made from mechanically-recovered meat,” he said.

“The salt levels in some of these products have been brought virtually up to the level of sea water.

“This is evidence of another, hidden way in which eating too much salt may harm the health of children and the industry needs to do a lot more.”

Label call

Dr Myron Weinberger, from the Indiana University Medical Center, wrote that reductions in salt and soft drink consumption in children, coupled with an increase in physical activity, could help reduce the “scourge of cardiovascular disease” in western society.

A spokesman for the British Heart Foundation said that better food labelling would help parents to choose healthier foods for their families.

“When children regularly swill down salty foods with sugary, calorie-laden soft drinks, it can mean double trouble for their future heart health.

“This report is yet more proof that children must be supported to make healthier food choices to avoid becoming obese or increasing their blood pressure.”

Salty Snacks Mean More Sodas for Kids

Kids who load up on salty meals and snacks get thirsty, and too often they turn to calorie-filled sodas. So maybe cutting back on the salt is a good way to cut the calories. That’s the idea coming from a British study published Wednesday in an American Heart Association journal.

Salt is “a hidden factor in the obesity epidemic,” said Graham MacGregor, a co-author of the study by researchers at St. George’s University of London.

And researchers say all that salt isn’t coming from the salt shaker: About 80 percent comes from manufactured food.

“Most people think that sodium comes from the salt shaker. The salt shaker contributes less than 10 to 15 percent,” said Dr. Myron Weinberger, a professor of medicine at Indiana University School of Medicine.

“Fast foods, for example, are just loaded with sodium. Processed foods are all very high in sodium,” said Weinberger, who wrote an editorial related to the study published in the online journal Hypertension.

Not only could less salt translate to fewer soft drinks and therefore fewer calories, but a modest reduction in salt has already been shown to lower blood pressure, which increases the risk of later-in-life heart attack and stroke, researchers say.

Also, several studies have shown a link between sugary soft drinks and obesity in children.

Reducing salt in manufactured foods can be done gradually, without the public even noticing, said Dr. Feng He, lead author of the study and cardiovascular research fellow at St. George’s. She said a 10 to 20 percent reduction in salt isn’t even detectable.

“It’s important for the food industry to make a reduction,” she said.

The study suggested that cutting in half the amount of salt British children consume — a decrease of about half a teaspoon a day — would lead to an average reduction of about 18 ounces of sugar-sweetened soft drinks per week.

The study was based on diet data from Great Britain’s National Diet and Nutrition Survey. Researchers looked at 1,688 British boys and girls — ages 4 to 18 — over a seven-day period in 1997.

They noted that the amount of salt eaten might be underestimated in the study because it didn’t include salt added during cooking or at the table. The researchers also found that more than half the fluids drunk by the children were soft drinks, and more than half of those were sugar-sweetened.

MacGregor, a professor of cardiovascular medicine at St. George’s, says the study results should apply to kids in the U.S. as well.

The United Kingdom began a government-led campaign to cut salt consumption in 1996 and researchers say more recent studies show that salt intake has already decreased.

In the United States, the Food and Drug Administration is taking public comment until March 28 on a consumer group’s proposal to restrict the amount of salt in processed foods, among other options. And the American Medical Association has urged the government to require strong labeling of high-salt foods because if salt’s connection to high blood pressure and heart problems.

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Being obese or even overweight may increase a person’s risk of developing up to a dozen different types of cancer, European researchers report in a new study.

Doctors have long suspected a link between weight gain and certain cancers, including colon and breast cancers. But the new study, published Friday in the journal Lancet, suggests it could also increase chances for cancer of the esophagus, thyroid, kidney, uterus and gall bladder, among others.

While the study suggests a link, there is no definitive proof that being fat in itself causes cancer.

“To make the link between cause and effect, we need to tick several boxes,” said Dr. Andrew Renehan, the study’s lead author and senior lecturer at the School of Cancer Studies at the University of Manchester. “This study begins to tick the first two or three boxes, but more research is needed to confirm it.”

The researchers compiled data from 141 studies and considered more types of cancers and more diverse populations than had been done previously. The research covered more than 280,000 cases from North America, Europe, Australia and Asia.

The subjects, both overweight and normal weight, were followed for about nine to 15 years, with researchers tracking their body mass index, or BMI — a calculation based on weight and height — and correlating it with incidents of cancer.

In men, an average weight gain of 33 pounds increased the risk of esophageal cancer by 52 percent, thyroid cancer by 33 percent, and colon and kidney cancers each by 24 percent, the research found.

In women, a weight gain of 29 pounds increased the risk of cancer in the uterus and gall bladder by nearly 60 percent, esophagus by 51 percent and kidney by 34 percent, the study said.

The link was weaker for bone and blood cancers, for both men and women.

In Asian populations, there appeared to be a stronger link between increased BMI and breast cancer, the study said.

“This study provides a lot of circumstantial evidence about the dangers of obesity,” said Dr. David Robbins, a gastroenterologist at Beth Israel Medical Center in New York, who was not involved in the study. “It also highlights the cancer crisis we face as obesity rates increase worldwide.”

Scientists are unsure how being overweight could make people more susceptible to cancer.

“One of the hypotheses is that the presence of excess fat cells could affect the levels of hormones in your body,” Renehan said. “At a cellular level, that may favor the development of tumors in humans.”

Because many studies have found that fatter people are more likely to get cancer, experts often recommend losing weight to reduce cancer risk.

“The simple message is that, if you manage to keep a healthy body weight, you will have a lower risk of developing cancer,” said Ed Yong, of Cancer Research United Kingdom.

The Lancet study was paid for by British Medical Association, the University of Manchester and the University of Bern, Switzerland. Renehan has consulted for several pharmaceutical companies that make hormone replacements.

Obesity Raises Cancer Risk

The more weight you carry on your body, the greater your odds of developing cancer, British researchers report.

This is true not only of fairly common cancers such as colon and breast, but also of lesser known varieties, including gallbladder. Moreover, the degree of risk differs between men and women and among different ethnic groups, report the authors of a comprehensive new paper appearing in this week’s issue of The Lancet.

“This is a profoundly important issue. Obviously, the obesity epidemic is a huge problem itself, and the relationship to cancer is only one of the many adverse health effects of being overweight and obese,” said Dr. Michael Thun, head of epidemiological research at the American Cancer Society. “The evidence has been accumulating now for over 10 years. . . This study tries to provide a quantitative measure of how much the relative risk goes up with each increment, basically jumping from one BMI [body-mass index] category to another.”

Although extra fat has already been identified by research as a risk factor for several different types of cancer, Thun said, “the problem of obesity is so large and so difficult to solve that there’s a very sound reason for ongoing studies of things that have become increasingly well-known, just because it helps the momentum in stimulating approaches that will actually help people maintain a healthy weight.”

Last year, a report issued by the American Institute of Cancer Research and the U.K.-based World Cancer Research Fund concluded that body fat is associated with an increased risk for several different types of cancer including esophageal adenocarcinoma, as well as cancers of the pancreas, colon and rectum, breast (postmenopausal), endometrium and kidney.

Although that report was one of the most comprehensive to date, it did leave some questions unanswered. For instance, are there associations between less common cancers and body weight, and do the associations differ between the sexes and people of different ethnic backgrounds?

The issue is a pressing one, with about two-thirds of adult men and women in the United States overweight or obese. That number is only expected to increase as people continue to eat more and exercise less.

This study, from scientists at the University of Manchester, analyzed 141 articles involving 282,137 cancer cases and 20 different types of malignancies to determine the cancer risk associated with a 5 kilogram-per-meter-squared increase in BMI, roughly the increase that would bump a person from middle-normal weight into overweight.

In men, such an increase in BMI raised the risk of esophageal adenocarcinoma by 52 percent, thyroid cancer by 33 percent, and colon and kidney cancer by 24 percent each.

In women, the same increase in BMI increased the risk of endometrial and gallbladder cancer by 59 percent each, esophageal adenocarcinoma by 51 percent, and kidney cancer by 34 percent.

In men, there were weaker associations between increased BMI and rectal cancer and melanoma. In women, there were weaker associations between increased BMI and postmenopausal breast, pancreatic, thyroid and colon cancers.

In both genders, there were associations between increased BMI and leukemia, multiple myeloma and non-Hodgkin’s lymphoma.

For colon cancer, the associations were stronger in men than in women (24 percent vs. 9 percent).

There were stronger associations in Asia-Pacific populations between greater BMI and both premenopausal and postmenopausal breast cancers.

Although the main message is still to maintain a healthy weight, this research might indicate earlier screening for certain cancers, said Dr. Greg Cooper, interim chief of the gastroenterology division at Ireland Cancer Center of University Hospitals and Case Comprehensive Cancer Center in Cleveland. “If someone is obese, then lower the threshold for screening,” he said. “One of the cancers they identified is esophageal adenocarcinoma, which is not as common as colon cancer, but it is increasing in incidence. It is thought to be related to reflux, so as a gastroenterologist, if I have a patient who has reflux and is obese, I might lower the threshold for doing an endoscopy. For other cancers like colon cancer, those guidelines are pretty well-established, and this probably wouldn’t change practice.”

Experts aren’t sure why extra fat can lead to malignancies, but changes in the circulating levels of various hormones (insulin, insulin-like growth factors and sex steroids) might explain the link.

Here’s more bad news as the world heads for a smoke-free future: An accompanying commentary from Swedish researchers notes that as people quit smoking (the biggest cause of cancer in developed countries), weight gain may become the main lifestyle factor contributing to new cancers.

British researchers link obesity to more cancers

Obesity can double the risk of several cancers, according to a study published on Friday that for the first time also links being overweight with a number of less common forms of the disease.

The analysis of 144 published studies incorporating some 282,000 men and women also showed that gender can make a difference in the relationship between obesity and some cancers, the researchers reported in the Lancet medical journal.

The findings come after a major report from the World Research Cancer Fund in October showed that excess body fat was likely to cause some cancers, said Andrew Renehan, a cancer specialist at the University of Manchester, who led the study.

“This study has extended that further and reported specifically on 20 different types of cancer,” he said in a telephone interview. “We showed an association with less common cancers that had not been shown before.”

These included blood cancers such as adult leukemia, multiple myeloma and non-Hodgkin’s lymphoma for both men and women, he said.

Obesity is a major issue worldwide and also raises the risk of diseases such as type 2 diabetes and heart problems. The World Health Organisation classifies around 400 million people as obese.

Renehan and his colleagues looked at what happened to people whose body mass index (BMI) increased from the normal range to overweight or from overweight to obese.

BMI is a calculation of height to weight, and the normal range is usually considered to be 18 to 25, with more than 25 overweight and above 30 obese.

For men, the risk of thyroid cancer rose by a third and went up 24 percent for colon and kidney cancers, the researchers said. In women who went from normal to overweight, the risk of gall bladder cancer rose 59 percent and kidney cancer went up 34 percent.

“Increased BMI is associated with increased risk of common and less common malignancies,” the researchers wrote. “For some cancer types, associations differed between sexes and populations of different ethnic origins.”

The association of cancer and obesity was largely similar across Asia, Europe and North America, though the link between higher body mass index and breast cancer was higher in Asia, the researchers said.

There were also strong differences between men and women for cancers like bowel and kidney cancers. Knowing this kind of information could help scientists focus research on what is exactly causing some of these cancers, Renehan said.

“We suspect there are differences in changes in hormones due to the amount of fat cells in our body, and whether a person is a man or a woman,” he said.

Children lacking enough shut-eye face a greater risk of becoming obese than kids who get a good night’s sleep, according to a study released Thursday.

Each extra hour of sleep cuts a child’s risk of becoming overweight or obese by nine percent, according to an analysis of epidiomogical studies by researchers from Johns Hopkins Bloomberg School of Public Health.

By contrast, children who got the least sleep had a 92 percent higher change of being overweight or obese than children who slept enough, said the study published in the journal Obesity.

“Our analysis of the data shows a clear association between sleep duration and the risk for overweight or obesity in children. The risk declined with more sleep,” said Youfa Wang, a senior author of the study.

“Desirable sleep behavior may be an important low cost means for preventing childhood obesity and should be considered in future intervention studies,” Wang said in a news release.

“Our findings may also have important implications in societies where children do not have adequate sleep due to the pressure for academic excellence and where the prevalence of obesity is rising, such as in many East Asian countries.”

The researchers reviewed 17 published studies on sleep duration and childhood obesity.

Some research recommends that children under five years old sleep 11 hours or more a day, while children age five to 10 should get 10 or more hours of sleep, and children older than 10 should sleep at least nine hours.

Want to lose weight? Try sleeping more

If you want to lose weight, get more sleep. In a new article appearing in the current issue of Obesity Reviews, University of Michigan researcher Michael Sivak presents calculations showing that replacing one hour of inactive wakefulness—such as watching television—with sleep can result in a 6 percent reduction in caloric intake.
“Caloric consumption in a society with readily available food is likely to be approximately proportional to the number of hours of being awake,” said Sivak, head of the Human Factors Division at the U-M Transportation Research Institute. “By replacing one hour of being awake with sleeping, we forgo a significant consumption of food because of the resulting reduction in the opportunity to eat.”

Sivak says that a person who sleeps seven hours a night and consumes 2,500 calories during the remaining 17 hours of the day can cut 147 calories by simply sleeping an extra hour instead of watching TV. He calculated that such a decrease in caloric intake would result in a body-weight reduction of about 14 pounds per year.

“Recent research has suggested that the levels of the hormones leptin and ghrelin mediate an association between lack of sleep and weight gain. But this may turn out to be only part of the story,” he said. “The behavioral, non-hormonal relationship between sleep and weight is another possible connection.

“To the extent that a large proportion of the population is both overweight and voluntarily sleep-deprived, replacing some sedentary activity with sleeping might offer a practical behavioral solution for a large segment of the overweight population.”

The brain circuitry that controls appetite might be wired differently in some people, and that could predispose them to obesity, California researchers suggest.

The study was conducted in rats, not humans, and yet it could ultimately lead to novel obesity treatments, said Philip Smith, director of the Office of Obesity Research at the National Institute of Diabetes and Digestive and Kidney Diseases.

“It is not just about drugs that modify short-term appetite,” he said, “there may be drugs that stimulate development of the appropriate neural pathways. So, it is an exciting, but very early, time in this field.”

Sebastien Bouret, an assistant professor of neuroscience at the University of Southern California, and his colleagues examined neural circuits emanating from the appetite, hunger and body-weight control center of the brain — the so-called arcuate nucleus of the hypothalamus (ARH) — in a series of rats bred to be either prone to, or resistant to, obesity.

The team found fewer neural connections projecting from the ARH in obesity-prone animals than in their leaner counterparts. Surprisingly, Bouret said, this deficiency developed very early in life, before the animals became obese, and appeared to extend into adulthood.

“Somehow, these animals are programmed to become obese,” Bouret said. “The obesity is hard-wired into the brain.”

When the researchers then looked at why the brains of obese rats differed from their normal-weight counterparts, they found that the neurons from obesity-prone animals were less responsive to leptin, a hormone that controls the development of these circuits, and which also signals the body’s energy status and controls metabolic rate.

“This paper presumes to say, these animals must be leptin-resistant, and that is why the pathways are not developing,” said Smith.

But that doesn’t mean they are doomed to a life of severe obesity, said Dr. Barbara Kahn, chief of the Division of Endocrinology, Diabetes and Metabolism at Beth Israel Deaconess Medical Center, in Boston. How they live their lives also matters.

“It is important not to ‘blame’ the obese person or imply that he/she is responsible for being obese,” Kahn noted. “Having said that, reasonable, healthy caloric restriction and a safe and sustainable program of physical activity can help limit weight gain and often bring about some degree of weight loss. In addition, healthy eating and regular exercise can reduce the complications of obesity such as type 2 diabetes and cardiovascular disease.”

At the same time, she added, not everyone can wear a size 4.

“There is a certain aspect of genetics that sets somebody in a certain range of possible body weights, and then how that person lives his or her life will determine whether they are at the bottom or top of the range,” she explained.

Human obesity has both genetic and environmental roots. The rats used in this study, like most humans, developed obesity when fed a high-energy diet. On a normal diet, they were heavier than normal rats, but not yet obese.

“This is quite an exciting paper,” said Smith, “because it links more closely to human behavior than most rodent models we have seen.”

The findings also suggest a possible therapeutic approach to combating human obesity. If drugs could be designed to influence the formation of neural circuits during development and targeted to at-risk pregnancies, Smith said, “there is a good likelihood we could have successful interventions that improve the health of the mother, and which have a major impact on disease risk for the infant, during pregnancy.”

A related study from Boston University researchers in the same journal found that bulking up muscle mass can lead to a general metabolic improvement in obese individuals. “Interventions designed to increase skeletal muscle mass in at-risk human populations may prove to be critical weapons in the fight against obesity and obesity-related comorbidities, including diabetes, heart disease, stroke, hypertension and cancer,” an accompanying editorial stated.

Obesity may be hard-wired in the brain

Obesity may be hard-wired into the brain from birth, according to a new animal study released Tuesday that appears to bolster the notion that some people are more prone to pile on the pounds than others.

The study showed that obese rats had faulty brain wiring that impaired their response to the hunger-suppressing hormone leptin.

In obesity-prone rats, “it seems that appetite and obesity are built into the brain,” said Sebastien Bouret, an assistant professor of neuroscience at the University of Southern California, Los Angeles.

“The neurodevelopmental differences in these animals can be seen as early as the first week,” he said.

“The results show that obesity can be wired into the brain from early life. The three-million-dollar question now is how to get around the problem.”

Leptin plays a central role in fat metabolism. Produced by fat tissue, it acts as a signal to the brain about the body’s energy status.

Its role in weight regulation is still unclear, but what scientists do know is that the brain calibrates the need for food intake based in part on leptin levels.

Previous research had shown that the brains of obesity-prone rats were insensitive to these leptin signals, so the researchers looked for brain abnormalities that could explain this.

They found defects in the brain circuits that relay leptin signals throughout the hypothalamus — the brain’s central switchboard for regulating conditions in the body.

While the rats’ condition might be improved by exercising and eating right, the findings suggest that the propensity to gain weight can’t be reversed, Bouret said.

If the findings are replicated in humans, then those individuals who are genetically predisposed to obesity because of the way their brains are configured would have to be very careful about “diet and energy balance,” said Richard Simerly, another researcher who worked on the study.

The findings also fly in the face of the one-size-fits-all approach that characterizes much of the discussion about weight management and weight loss in the media, said Simerly, who is director of the neuroscience program at the Saban Research Institute at the University of Southern California.

“The message in the media that weight regulation is all a matter of nutrition or lifestyle choices does a disservice to people whose biology predisposes them to obesity,” he said.

The study appears in the February issue of Cell Metabolism.