What You Need To Know News

Wolfing down your food and eating until your seams are straining could double your risk of becoming overweight, Japanese researchers have found.

A study published in the British Medical Journal this week reveals that men and women who eat rapidly or eat until they are full are twice as likely to be overweight compared to people who eat more sensibly.

People who both eat quickly and eat too much are around three times as likely to be overweight, the researchers found.

They also report that the link between the eating behaviour and overweight remains the same no matter what the actual calorie intake from the food itself.

Co-author of an accompanying editorial, Dr Elizabeth Denney-Wilson, says the study provides more evidence that eating behaviours themselves are a significant promoter of ‘positive energy balance’ - the situation where energy intake is higher than energy spent - and may be contributing to the current obesity epidemic.

Part of the problem is that humans are not very good at knowing when to stop eating, says Denney-Wilson, research fellow at the Centre for Primary Health Care and Equity, University of New South Wales in Sydney.

“Humans are not good at using the cues from their bodies to determine when they’re full,” she says.

“They’re much more likely to use visual cues so if they have a great big portion in front of them they’re likely to eat the lot.”

The researchers suggest these unhealthy eating habits are not necessarily there from birth but instead appear to be learned, or taught.

“It is possible to have children self-regulate their energy intake, and we certainly see that with breast-fed babies who are clearly regulating their own energy intake because they are able to determine when they are full.”

However the dramatic increase in portion sizes and unprecedented availability of food makes it harder to exercise restraint, the researchers say.

“Until recently there was just never more food than people needed, so it was impossible to eat beyond satiety,” says Denney-Wilson.

She says it is possible to overcome this urge to overeat by learning to recognise the cues of fullness, something that health professionals could work on with their patients.

While this is not the first study to suggest a link between fast eating and overweight, Denney-Wilson says the cultural context of the study is particularly surprising, as the Japanese are generally considered to be more ’social’ eaters compared to those in Western nations, where fast food is so readily available and eaten.

Source: http://www.abc.net.au/science/articles/2008/10/22/2398053.htm?site=science&topic=latest

Obesity may increase with each generation because overweight mothers give birth to offspring who have a tendency to become heavier, researchers have claimed.

A team of scientists believe that the genetic mechanisms that control the weight of a baby may be changed if the mother is obese before and during pregnancy.

This change could lead in turn to the baby becoming heavier than normal.

Scientists in Houston, America, made the claim after studying the eating habits of several generations of mice.

Dr Robert Waterland from Baylor College of Medicine, led the study.

He explained: “There is an obesity epidemic in the United States and it’s increasingly recognised as a worldwide phenomenon.

“Why is everyone getting heavier and heavier?

“One hypothesis is that maternal obesity before and during pregnancy affects the establishment of body weight regulatory mechanisms in her baby.

“Maternal obesity could promote obesity in the next generation.”

The team split the mice, all of which had a genetic tendency to overeat, into two groups.

One group was provided with a normal diet while the other was provided with nutrient-supplemented diet.

The nutrients in the supplemented diet encouraged the process of DNA methylation - a chemical reaction that silences genes with the hope that it would render the over-eating gene inactive.

The mice on the normal diet gained weight with each generation while the mice on the altered diet stayed roughly the same size.

Dr Waterland explained: “We wanted to know if, even among genetically identical mice, maternal obesity would promote obesity in her offspring, and if the methyl-supplemented diet would affect this process.

“Indeed those on the regular diet got fatter and fatter with each generation. Those in the supplemented group however, did not.”

Dr Waterland said the research had led the team to believe that the process of DNA methylation plays an important role in the development of the region of the brain that regulates appetite - the hypothalamus.
Source: http://www.redorbit.com/news/health/1567852/obesity_may_rise_with_generations/

Heart attacks are hitting the overweight more than a decade sooner than “normal” weight people, researchers are reporting.

A study of more than 111,000 people is one of the first to put real numbers to the risk of obesity and suggests “excess adiposity” - fat tissue - is more dangerous to the heart than smoking.

“The leading theory in cardiology right now is that the fat tissue is actually producing factors that precipitate heart attacks,” says lead author Dr. Peter McCullough, consultant cardiologist and chief of nutrition and prevention medicine at William Beaumont Hospital in Royal Oak, Michigan.

The theory is that cholesterol builds up in the coronary arteries and inflammatory or other chemicals produced by fat cells trigger the plaque to suddenly rupture, causing a blood clot to form and unleashing an acute heart attack.

But until now, earlier studies “simply just didn’t have enough patients of different body sizes having their first heart attack to really evaluate” whether obesity is associated with premature heart attacks, McCullough says.

His team analyzed data from a nationwide U.S. registry of people hospitalized for heart attack and unstable angina, or chest pain, from 2001 to 2007.

A total of 111,847 men and women who had experienced a first heart attack were included in the final analysis. They were grouped according to their body mass index, or BMI, a measure of body fat based on height and weight.

Researchers found that, the heavier the person, the younger the age of a first heart attack.

The most obese people had their heart attacks on average when they were 59.

That compares to about 75 for the leanest group (average body weight 47 kilograms, or about 103 pounds, meaning they were actually considered underweight), and 71 for people of “normal” weight, where the average weight is 65 kilograms, or about 142 pounds.

The most obese group had a BMI of 40 or more and weighed on average 127 kilograms, or 280 pounds.

“It’s not uncommon in daily life to see people at that size,” McCullough says. “I’m sure there are people in your office and people you see all the time at that body weight.”

The rate of diabetes was 17 per cent in the leanest group, and 49 per cent in the most obese. “You can get a feeling of how obesity-driven diabetes is,” McCullough says.

All the patients, regardless of body size, had about the same level of LDL cholesterol, the so-called bad cholesterol thought to be a major risk factor for heart attacks. That means the excess fat is causing heart disease in other ways, McCullough says.

In addition, rates of smoking were equal across the board. “We really can’t blame it on smoking.”

“Those patients at the highest body weight on average lost 12 years of life before their first heart attack.” The second most important factor was smoking, “where they lost just under 10 years of life before a first heart attack.

“This is really the first study that shows now that some factors are more powerful than smoking in terms of the prematurity of myocardial infarction (a heart attack),” McCullough says.

The study involved a type of heart attack called non-ST-segment elevation myocardial infarction. They always require hospitalization and have an in-hospital fatality rate of about 10 per cent, and about 20 per cent over the next six months, McCullough says. “They are not trivial events. They account for a leading cause of patients to lose time away from work and actually seek medical disability.”

The study clearly shows “that, contrary to some of the arguments out there about whether or not excess weight may be protective … there is a tremendous risk difference in terms of having your first heart attack if you are overweight or obese,” says Dr. Arya Sharma, chair of obesity research and management at the University of Alberta in Edmonton.

“You’re having a heart attack a decade before those who don’t have a weight problem,” Sharma says. “And 59 is actually a very young age. These are people who aren’t even close to retirement.”

McCullough says people could reduce their risk of cardiovascular disease by losing weight and body fat. According to the Canadian Community Health Survey, 23 per cent of Canadians aged 18 and older are obese.
Source: http://www.canada.com/topics/news/story.html?id=b172edd0-a4c2-41a3-bd89-a00f698871e1

Obesity significantly increases the risk of recurrent miscarriages, UK researchers have claimed.

When the body mass index (BMI) of almost 700 women who had experienced at least three unexplained miscarriages was investigated, 45% of the women were found to be overweight or obese.

All women had previously undergone comprehensive investigations, but no cause as to why they kept miscarrying was established.

In total, 1% of the women were underweight, 54% were of normal weight, 30% were overweight and 15% were obese.

In those who went on to have a subsequent pregnancy, 19% of those who miscarried again were obese, compared to 11% who had a successful pregnancy.

Mothers being over the age of 35 and high numbers of previous miscarriages were associated with poor pregnancy outcome.

When maternal age and number of previous miscarriages were adjusted, obese women were shown to have a significantly increased risk of a further miscarriage compared to those with a normal weight.

“Ours is the first study to look directly at the link between BMI and recurrent miscarriage. It shows that obese women who experience recurrent miscarriage are at greater risk of subsequent pregnancy loss,” said Winnie Lo of St Mary’s Hospital, London.

Ms Lo advised that all women with recurrent miscarriage should be weighed at their first consultation. Those who are found to be obese should be counselled regarding the benefits of weight loss in increasing their chances of a successful pregnancy, she said.

“Programmes should be in place to help with the weight loss progress,” Ms Lo concluded.

The research was released at the Royal College of Obstetricians and Gynaecologists 7th International Scientific Meeting in Montreal.
Source: http://www.irishhealth.com/?level=4&id=14281

Fat is not a feminist issue, despite what feminists used to say. It is a class issue. Well-to-do, well educated people are rarely fat, still less obese. You see few fat children in private schools. Fatness and obesity are directly related to low income and low education.

A fat map was published last week by Dr Foster Intelligence, showing the areas with the fattest populations, and sure enough the poorest industrial areas in the north of England and in Wales produce the most obese people. The problem seems to be getting worse, fast.

You hardly need expert medical data analysis to understand that. You need only to go to a few supermarkets. At a Tesco in western Scotland this summer I was astonished by the number of horribly obese shoppers waddling round the aisles with their elephantine children, who could not possibly have squashed themselves into an ordinary one-person chair. Young women, with eyes reduced to slits by the pressure of the fat on their faces, laughed grimly with each other as they scanned the shelves. And this is a rich country.

Even though the vast Oban Tesco is full of good food, the trolleys at the checkout were heaped with stuff that is either useless or positively bad to eat – crisps, snacks, swizzlers, twizzlers and guzzlers, cheesy dips and fatty whatsits, cakes puddings and pies, heavily dusted in additives. The obese seem to fill their carts regularly with several times their own weight in eatables that can make them only fatter, that they shouldn’t eat and that nobody should produce, as if they were determined to lay down yet more adipose tissue. Yet you rarely see such bloated people and trolleys in smart supermarkets in rich areas. These days you can easily tell people’s precise socioeconomic bracket and body weight by the contents of their trolleys.

Obesity seems to be the issue of the day, possibly because we are still in the silly season. Coincidentally last week, Andrew Lansley, the Tory health spokesman, spoke against obesity in a long speech to the Reform think tank. He was widely understood as saying that fatties have only themselves to blame; they must take responsibility for themselves and their weight because “we all have a choice”. And while that is a slightly unfair take on his speech, he does seem to mean something of the sort. Yet at the same time he offers what’s now called a whole raft of measures to stop people getting fat. This is awkward for Conservatives; either you interfere with people’s choices or you don’t. Empowerment, a word he used, is often just a weasel word for state intervention.

The question is why a Conservative government should interfere at all in people’s inalienable freedom to choke on deep-fried Mars bars if they choose to. The argument is that the fat and the obese (people with a body mass index over 30, which is something you could spot without a calculator) cost the country squillions in lost productivity and increased National Health Service costs. The obese tend to develop serious illness, particularly heart disease and diabetes, and are, generally speaking, crocked up and expensive to look after.

Somebody somewhere has come up with a figure for the cost of all this, which Lansley quotes – £7 billion a year, for what it’s worth. Last year’s Foresight report said this cost could go up by six times by 2050. And fat is getting fatter so fast. According to NHS figures, the proportion of obese men in the population rose during Labour’s time in office from 13.2% in 1993 to 23.1% in 2005. Among women it was even worse, from 16.4% to 24.8%. That is nearly a quarter of all women. If you consider people who are not obese but overweight (with a BMI of 25-30), 46% of men in England are overweight and 32% of women.

Fat is also an ethnic issue. According to NHS figures published in 2006, Irish and black Caribbean men had the highest incidence of obesity (25% each) and among women black Africans had 38%, black Caribbean 32% and Pakistani 28%. So, with migration trends and immigrant fertility, the costs of obesity are going to rise fast as well.

However, I wonder how much, if anyone knew the facts, the final cost of obesity would be to the taxpayer. For fat people die sooner and obese people die much sooner than others, thus relieving the NHS and the economy of their needs. It’s true that obese people need expensive treatment for diabetes and heart disease before they die, but that might easily be offset if they had significantly shorter lives – and they do. Current thinking seems to be that the obese die between five and seven years earlier than otherwise they would.

Few papers I’ve looked at on this subject discuss the possible cost-benefit of obesity, although one from an insurance company coyly mentioned the advantage to pension providers if a person died before he reached pensionable age. For years I used to argue that smokers were a net benefit, purely financially speaking, to the exchequer, because they died early. I still feel rather proud of being the first, I believe, to get a known expert (Professor Richard Peto in 1993) to agree publicly to this idea, now accepted. Might not the same be true of obesity? The real drain on the NHS is geriatric medicine; the obese might not reach old age.

If the only reason for interfering with what fat people eat is how much it costs the rest of us, perhaps we should leave them alone. It’s well known that obesity (and fatness) are associated with poor education, poor housing, poor employment or none, low expectations, low opportunities and all the rest. These are all social ills that this government has been trying to deal with for more than a decade. Yet little has improved and obesity – as an indicator of that fact – has swollen vastly while Labour has been in office. What prevents obesity is a good income, a good education, good opportunities and the kind of background that develops self-confidence. Prosperity, in short.

Obesity cannot be defeated by taskforces, better labelling on packets or investing in health accreditation schemes. This has all been tried and has failed. In the presence of a complex problem, and in the absence of a workable solution, perhaps it is better to leave people to their own devices. Nobody can pretend they don’t know what they’re doing. They should be left alone to do it.
Source: http://www.timesonline.co.uk/tol/comment/columnists/minette_marrin/article4641974.ece

Maternal obesity has been associated with diabetic complications in the resulting offspring, according to experiments in mice reported recently by researchers at the University of Louisville.

Obesity is presently a worldwide health issue, and it is commonly considered a risk factor for diabetes, cardiovascular disease, and stroke. When a pregnant woman is obese, her children can be affected by malformation, functional abnormalities, obesity, and type II diabetes. Since, presently, over 18% of American women are classified as obese, and between 18 and 38% of pregnant women meet this criteria, it is an important issue in maternal and child health in this country. However, very little is known about the mechanism of the link between maternal obesity and diabetic effects in offspring.

To investigate this association, Dr. Jianxiang Xu and Junying Han of the University of Louisville first established a viable animal model to function similarly to maternal diabetes might in humans. Female mice, genetically predisposed to obesity and further marked with a yellow coat color, were mated with normal mice, whose offspring could then be classified by coat color for this obesity gene. The obesity prone mice were obese between 6 and 8 weeks of age, but maintained normal blood glucose levels. Offspring from these and from normal crosses were then fed with normal food for up to 15 weeks, then fed with a high fat diet, and examined by sex, and the mother’s obesity status. In this first portion of the study, the birth weight of offspring from obese mothers was 14% higher than in the control group.

When the offspring, at 50 weeks of age, were administered 2 mg glucose per kg body weight. This resulted in similar glucose levels in each group, but major differences in the serum insulin levels. Namely, in female offspring from obese mothers, there was a significant increase in serum insulin levels, while females from obese mothers and males showed no significant differences. This indicates that β cell function was impaired in the female offspring of obese mothers.

To confirm this link, a second experiment was performed. Pancreatic cells were isolated from 50 week old offspring to be tested in vitro for insulin excretion. Cells from mice with a normal diet showed normal secretion, but in the high fat diet, insulin secretion was sharply reduced in offspring from an obese mother, especially when exposed to a high glucose concentration. The measure of other enzymes related to glucose metabolism such as transketolase, GAPDH, and PFK in the cells of the 50 week old mice indicated a decrease in production by the β cells ranging from 31% to 70% for those born to an obese mother.

According to the researchers, this shows that obesity in pregnancy is a factor by itself to impaired glucose tolerance in offspring, which could contribute to the development of gestational diabetes in the mother and type II diabetes in the offspring. Additionally, since there are many mothers who are obese without displaying gestational diabetes, this obesity might be a greater factor in the health of their children than previously expected.
Source: http://www.medicalnewstoday.com/articles/115691.php

Diabetic patients who join a short-term weight management program can maintain the resultant weight loss on a long term basis and that to on their own, reveals a new study.

The study by researchers from the Joslin Diabetes Center in Boston showed that diabetic patients, who enrolled in the Weight Achievement and Intensive Treatment (Why WAIT) program, successfully lost on average 24.6 pounds or 10.3 percent of their initial body weight during the 12-week program.

And after the one-year of follow-up period, the average weight loss was 18.2 pounds or 7.6 percent of initial body weight.

People have been waiting to see a longer term result of this novel program. Most people think that positive results of clinical trials around weight reduction in people with diabetes cannot be replicated in the real world and cannot give similar long-term results, said Osama Hamdy, M.D., Ph.D., director of the clinical obesity program at Joslin and the studys lead investigator.

This is going to change the way we treat diabetes and encourage us to move toward weight-based diabetes management rather than adding more medications.

The Why WAIT is a 12-week multidisciplinary diabetes weight management program designed for clinical practice and is mostly covered by insurance.

In the study, 85 participants were followed during the 12-week program and for a year afterwards when they managed their weight on their own.

The results indicated that 55 percent of participants continuously lost weight throughout the follow-up period and managed excellent diabetes and blood pressure control on less medications. Also, Hamdy said that patients saved average 561 dollars per year on diabetes medications alone.

The Why WAIT program included a change in diabetes medications to enhance weight reduction, structured dietary intervention with fewer than 40 percent of daily calories from carbohydrates and 30 percent of calories from protein and meal replacement drinks, an exercise program with an emphasis on strength training and weekly educational and support sessions.
Source: http://www.thaindian.com/newsportal/lifestyle/short-term-weight-loss-program-helps-diabetics-keep-off-the-pounds-long-term_10058063.html

Being obese can increase the risk of Alzheimer’s Disease by as much as 80 per cent, according to a study. But it’s not just weight gain that poses a risk. People who are underweight also have an elevated risk of dementia, unlike people who are normal weight or overweight.

US researchers carried out a detailed review of 10 international studies published since 1995, covering just over 37,000 people, including 2,534 with various forms of dementia. Subjects were aged between 40 and 80 years when the studies started, with follow-up periods ranging from three to 36 years.

The review, which included studies from the USA, France, Finland, Sweden and Japan, also included a sophisticated meta-analysis of seven of the studies, published between 2003 and 2007 with a follow-up period of at least five years.

All kinds of dementia were included, with specific reference to Alzheimer’s Disease and to vascular dementia - where areas of the brain stop functioning because the blood vessels that supply them are damaged by conditions such as high blood pressure or heart disease.

“Our meta-analysis showed that obesity increased the relative risk of dementia, for both sexes, by an average of 42 per cent when compared with normal weight” says Dr Youfa Wang, Associate Professor of International Health and Epidemiology at Johns Hopkins Bloomberg School of Public Health, Baltimore.

“And being underweight increased the risk by 36 per cent.

“But when we looked specifically at Alzheimer’s Disease, the increased risk posed by obesity was 80 per cent. The increased risk for people with vascular dementia was 73 per cent.

“The risks were greater in studies where sufferers developed Alzheimer’s Disease or vascular dementia before the age of 60 or in studies with follow-up periods of more than 10 years.

“We also found that obesity was more likely to be a risk factor for women when it came to developing Alzheimer’s Disease and for men when it came to vascular dementia.”

The authors estimate that 12 per cent of the dementia risk in the study population could be attributed to obesity, with this rising to just over 21 per cent in patients with Alzheimer’s Disease.

It’s estimated that up to 10 per cent of people aged 65 or more suffer from some form of dementia and two-thirds of those have Alzheimer’s Disease.

“There has been controversy about the links between obesity and dementia for a number of years, but previous findings have been mixed and inconclusive” says Dr Wang.

“The advantage of carrying out a meta-analysis is that it provides researchers with access to a large number of study subjects and it is possible to iron out the inconsistencies and come to overarching conclusions.

“Our detailed analysis clearly shows a U-shaped relationship between weight and dementia, with people who are obese or underweight facing a greater risk.

“We believe that our results show that reducing the prevalence of obesity is a promising strategy for preventing the progression of normal ageing into Alzheimer’s Disease.
Source: http://www.news-medical.net/?id=38144

Overeating disrupts entire networks of genes in the body, causing not only obesity, but diabetes and heart disease, in ways that may be possible to predict, researchers reported on Sunday.

The researchers developed a new method of analyzing DNA and used it to discover that obesity is not only complex — something already known — but complex in ways that had not been previously understood.
“Obesity is not a disease that is the result of a single change to a single gene. It changes entire networks,” said Eric Schadt, executive director of Genetics at Merck Research Laboratories.

His team identified networks of hundreds of genes that appear to be thrown out of kilter when mice are fed a high-fat diet.

“This network is completely rocked by exposure to a high-fat, Western-type diet,” Schadt said.
They then turned to a database of Icelandic people being studied by Decode Genetics Inc and found people have the same networks.

The joint teams did a detailed study of 1,000 blood samples and almost 700 samples of fat tissues from some of the Icelandic volunteers.

This showed that people who have a higher body mass index, a measurement of obesity, have characteristic patterns of gene activation in their fatty tissues not seen in DNA taken from blood.

“What it says it that the common forms of these diseases are very complex,” said Schadt.

“Simple genetic tests cannot detect these networks,” said Schadt, who also works at Merck subsidiary Rosetta Inpharmatics in Seattle.

Schadt said his team hoped to study these networks and identify the genes most key to causing disease. New drugs can be designed to target their activity, he said.
Source: http://www.canada.com/globaltv/national/health/story.html?id=e2427cc8-9b7d-499a-b67a-d324bddca53a

Sometimes the strongest longings for food happen when you are at your weakest point emotionally. Many people turn to food for comfort — consciously or unconsciously — when they are facing a difficult problem or looking to keep themselves occupied. But emotional eating — eating as a way to suppress or soothe negative emotions, such as stress, anger, anxiety, boredom, sadness and loneliness — can sabotage your weight-loss efforts.

Often, emotional eating leads to eating too much food, especially high-calorie, sweet, salty and fatty foods. The good news is that if you are prone to emotional eating, you can take steps to regain control of your eating habits and get back on track with your weight-loss goals.

The connection between mood and food

Major life events — such as unemployment, health problems and divorce — and daily life hassles — such as a stressful work commute, bad weather and changes in your normal routine — can trigger emotions that lead to overeating.

But why do negative emotions lead to overeating? Some foods may have seemingly addictive qualities. For example, when you eat enticing foods, such as chocolate, your body releases trace amounts of mood- and satisfaction-elevating hormones. That “reward” may reinforce a preference for foods that are most closely associated with specific feelings. Related to this is the simple fact that the pleasure of eating offsets negative emotions.

Food can also be a distraction. If you are worried about an upcoming event or rethinking an earlier conflict, eating comfort foods may distract you. But the distraction is only temporary. While you are eating, your thoughts focus on the pleasant taste of your comfort food. Unfortunately, when you are done overeating, your attention returns to your worries, and you may now bear the additional burden of guilt about overeating. How to regain control of your eating habits

Though strong emotions can trigger cravings for food, you can take steps to control those cravings. To help stop emotional eating, try these suggestions:

* Learn to recognise true hunger. Is your hunger physical or emotional? If you ate just a few hours ago and don’t have a rumbling stomach, you are probably not really hungry. Give the craving a few minutes to pass.

* Know your triggers. For the next several days, write down what you eat, how much you eat, when you eat, how you are feeling when you eat and how hungry you are. Over time, you may see patterns emerge that reveal negative eating patterns and triggers to avoid.

* Look elsewhere for comfort. Instead of unwrapping a candy bar, take a walk, treat yourself to a movie, listen to music, read or call a friend. If you think that stress relating to a particular event is nudging you toward the refrigerator, try talking to someone about it to distract yourself. Plan enjoyable events for yourself.

* Don’t keep unhealthy foods around. Avoid having an abundance of high-calorie comfort foods in the house. If you feel hungry or blue, postpone the shopping trip for a few hours so that these feelings don’t influence your decisions at the store.

* Snack healthy. If you feel the urge to eat between meals, choose a low-fat, low-calorie food, such as fresh fruit, vegetables with fat-free dip or unbuttered popcorn. Or test low-fat, lower calorie versions of your favorite foods to see if they satisfy your craving.

* Eat a balanced diet. If you are not getting enough calories to meet your energy needs, you may be more likely to give in to emotional eating. Try to eat at fairly regular times and don’t skip breakfast. Include foods from the basic groups in your meals. Emphasize whole grains, vegetables and fruits, as well as low-fat dairy products and lean protein sources. When you fill up on the basics, you are more likely to feel fuller, longer.

* Exercise regularly and get adequate rest. Your mood is more manageable and your body can more effectively fight stress when it is fit and well rested.

If you give in to emotional eating, forgive yourself and start fresh the next day. Try to learn from the experience, and make a plan for how you can prevent it in the future. Focus on the positive changes you are making in your eating habits and give yourself credit for making changes that ensure better health.

Source: http://www.thedailystar.net/story.php?nid=27711