Recent Posts

This is Beth from the meeting tonight.  I had such a good time and learned so many things tonight.  I am so glad that I came!

Hi! I'm 7 months post op and looking to meet people too. Welcome :)

Hello, and welcome!! You are right, there is a group that meets once a month. We meet at Ongwanda on porthsmouth the second Tuesday of the month at 6:30. It is a really great group of friendly people.  there is pre-op all the way to several year veterans there. Lots of support and encouragement, as well information and many laughs.  look forward to meeting you.

Barbie

As promised here are the articles that were written by the writer I was telling everyone about.

If anyone is interested in sharing their weight loss story with Alison send her an  email at [email protected]

to set up a telephone interview, as she is doing research for an article on bariatric surgery.  I did it and it was painless.

I invited Alison to join us at one of our meetings. I think she will be attending either in September or October so stay tuned.

Alison said, just so you know, writers don't have any say in the headlines. These aren't necessarily ones I would choose.

          Supersize me


*    30 October 2004 by Alison Motluk  
*    Magazine issue 2471 . Subscribe and save

WHETHER it is undertakers introducing a new range of extra-large coffins or airlines planning to charge passengers by the kilo, these days our expanding waistlines are rarely out of the news. It is hard to ignore the fact that body shape has changed dramatically over the past few decades.

In 1992 about 13 per cent of Americans were clinically obese. Only 10 years later that figure had rocketed to 22 per cent and in the three fattest states, Alabama, Mississippi and West Virginia, it was over 25 per cent. As the UK, Australia and many other western countries follow the US lead, the epidemic of obesity is now seen as one of the developed world's biggest public-health problems.

It is tempting to blame fat people for the state they're in. But health officials have recently begun to focus on a different culprit: the so-called "obesogenic" environment. In the US, goes the argument, the prevailing culture actually promotes obesity, making an unhealthy lifestyle the default option.

Take diet. "Calorie-dense foods are far more readily available than ever before," says Martin Binks, a psychologist at Duke University's Diet and Fitness Center in Durham, North Carolina. Thanks to widespread affluence and agricultural subsidies, food in the US is cheap and plentiful. Because fewer households have a stay-at-home parent to prepare meals from scratch, families increasingly turn to highly processed convenience foods, takeouts or fast-food restaurants. Half the average American food budget goes on food eaten outside the home, much of which is high-fat.

Another insidious influence on the American diet has been the gradual increase in portion sizes. "You eat more," says Judith Stern, a nutritionist and physician at the University of California at Davis, "even if you don't fini****" Restaurants and processed-food manufacturers can boost their profits by racheting up portion size and charging a little more because the price of food ingredients is so low relative to other costs such as packaging and transport. The original 1960s McDonald's meal of a hamburger, fries and a 12-ounce Coke contained about 590 calories. But today, a quarter-pounder with cheese, supersized fries and Coke - a meal that some kids consider an after-school snack - racks up a whopping 1550 calories. That's about three-quarters of the recommended daily calorie intake for an average woman.

The supersized diet is becoming the norm just as activity levels are dropping to an all-time low. "There's a great deal less access to physical activity than ever before in history," says Binks. The problem starts young. One-third of US secondary-school students fail to get enough physical activity and over a tenth get none at all, according to recent figures from the Centers for Disease Control in Atlanta, Georgia. "The average child doesn't have any physical activity in school any more," says Binks. Many schools no longer even have breaks, let alone structured physical education, he says. "Physical activity is put on the back burner in favour of test results."

And thanks to the way that most US towns and cities are designed, it is becoming increasingly difficult to get anywhere without driving. "We have suburbs without sidewalks," laments Stern.

Ironically, the US's obesogenic environment is one that societies through the ages have dreamed of: tasty cheap food in abundance, and barely a lick of hard work to be done. Who would have thought that it would one day hasten our demise?





          Life sentence


*    30 October 2004 by Alison Motluk  
*    Magazine issue 2471 . Subscribe and save

The nature-nurture debate is one of biology's oldest questions: is it genes or environment that shapes our bodies? But in recent years interest has grown in a third influence, which combines elements of both inheritance and environment - the environment in the womb.

It was David Barker, a physician and epidemiologist at the University of Southampton in the UK, who first showed that boys born small were more likely to develop heart disease in later life. In a further study, of Dutch women who had been pregnant during the second world war, Barker showed that malnutrition around the time of conception was linked with high blood-lipid levels, heart disease and diabetes in adulthood. Intriguingly, not only did the women who were pregnant through the war-induced famine give birth to smaller children, their daughters also tended to have smaller children. In an important addendum, Barker showed in 1999 that small babies who quickly caught up and eventually overtook their peers in weight tended to have even worse health later in life.

Barker made what seemed at the time a radical proposal: somehow the fetuses were being tipped off that life on the outside was going to be one of deprivation. "Babies set their metabolism according to the prevailing nutrition in the womb," says Barker. Their bodies were programmed to hoard energy as fat, particularly in stores around the waist. When the babies grew up in a world of unexpected plenty, that metabolism set them up for an increased risk of heart disease and diabetes. Having fat around the midriff is known to raise blood cholesterol levels.

This is not the only possible explanation for the so-called Barker hypothesis, or "fetal origins of adult disease", however. Perhaps the growing fetus is simply irrevocably damaged by malnutrition so early on in life. If nutrients are scarce, it would make sense for the fetus to preserve supply to the brain at the expense of other organs such as the heart, kidney and pancreas, Barker says. If it comes to choosing between brain damage from birth or ill-health in middle age, there is no contest. The two hypotheses are not mutually exclusive, however; Barker thinks both could be right.

A team of New Zealand researchers from the University of Auckland have been investigating an experimental model of the Barker hypothesis in rats. They subjected pregnant females to a low-calorie diet, and found they gave birth to unusually small pups which put on more weight as they grew up than control animals. And when the deprived pups were given a high-fat diet, they grew much fatter than control rats. "They were eating every time they saw food," says lead researcher Peter Gluckman. "They were big blobs of lard."

Just as a sedentary lifestyle is considered a factor in human obesity, the rats seemed lazier too. The researchers found that the prenatally starved rats were only about 70 per cent as active as the normal animals.

So how could events that go on in the womb have such long-lasting effects, even through to the next generation of offspring? Recent work has hinted that at least one mechanism operating could be a form of gene silencing known as methylation. This is a system for turning off genes by chemically modifying them, adding methyl groups to the DNA and surrounding histone proteins. Researchers such as Randy Jirtle, at Duke University in Durham, North Carolina, have now shown that in a certain strain of mice, a gene called agouti that affects coat colour can be turned off through methylation. And the extent of methylation is dependent on the mother's vitamin intake during pregnancy. The agouti gene is only found in mice, but Jirtle is confident that others like it will be found in humans. "We just don't know what they are," he says.





          The 10 roads to Fatsville


*    03 November 2006 by Alison Motluk  
*    Magazine issue 2576 . Subscribe and save

Ask anyone why there is an obesity epidemic and they will tell you that it's all down to eating too much and burning too few calories. That is undoubtedly true - you cannot get round the first law of thermodynamics. It's also true that we live in an "obesogenic environment": calorific food is plentiful and cheap and our lifestyles are increasingly sedentary. Most of us have to make an effort not to get fat.

That explanation appeals to common sense and has dominated efforts to get to the root of the obesity epidemic and reverse it. Yet obesity researchers are increasingly dissatisfied with it. Many now believe that something else must have changed in our environment to precipitate such dramatic rises in obesity over the past 40 years or so. Nobody is saying that the "big two" - reduced physical activity and increased availability of food - are not important contributors to the epidemic, but they cannot explain it all (see "Why the 'Big Two' just will not do", below) .

Earlier this year a review paper by 20 obesity experts set out the 10 most plausible alternative explanations for the epidemic (International Journal of Obesity, DOI: 10.1038/sj.ijo.0803326). Here they are.


1 Not enough sleep


It is widely believed that sleep is for the brain, not the body. Could a shortage of shut-eye also be helping to make us fat?

Several large epidemiological studies suggest there may be a link. People who sleep less than 7 hours a night tend to have a higher body mass index (BMI) than people who sleep more, according to data gathered by the US National Health and Nutrition Examination Survey. Similarly, the US Nurses' Health Study, which tracked 68,000 women for 16 years, found that those who slept an average of 5 hours a night gained more weight during the study period than women who slept 6 hours, who in turn gained more than those who slept 7. Two recent studies, one in Canada and the other in Germany, show that sleep duration and weight are linked in children too.

It's well known that obesity impairs sleep, so perhaps people get fat first and sleep less afterwards. But the nurses' study suggests that it can work in the other direction too: sleep loss may precipitate weight gain. One factor that could be at work here is the way sleep deprivation alters metabolism. Leptin, the hormone that signals satiety, falls while ghrelin, which signals hunger, rises - and this boosts appetite. Sleep-deprived rats eat about twice as much as rested ones. "They're voracious," says Carol Everson at the Medical College of Wisconsin in Milwaukee.

The same goes for people. In men allowed only 4 hours' sleep for two consecutive nights in a sleep lab, leptin levels dropped 18 per cent and ghrelin levels rose 28 per cent, and the volunteers reported they felt a lot hungrier. A big study recently confirmed these trends outside the lab. "Sleep loss seems to alter the ability of leptin and ghrelin to accurately signal caloric need," says Karine Spiegel at the Free University of Brussels (ULB), who ran the lab study, "and could lead to excessive caloric intake when food is freely available."

Although getting figures is difficult, it appears that we really are sleeping less. In 1960 people in the US slept an average of 8.5 hours per night. A 2002 poll by the National Sleep Foundation suggests that the average has fallen to under 7 hours. According to Spiegel, the decline in sleep is mirrored by the increase in obesity (see Diagram) .


2 Climate control


We humans, like all warm-blooded animals, can keep our core body temperatures pretty much constant regardless of what's going on in the world around us. We do this by altering our metabolic rate, shivering or sweating. Keeping warm and staying cool take energy unless we are in the "thermoneutral zone" - around 27 °C for a naked body - which is increasingly where we choose to live and work.

There's no denying that ambient temperatures have changed in the past few decades. Between 1970 and 2000, the average British home warmed from a chilly 13 °C to 18 °C. In the US, the changes have been at the other end of the thermometer as the proportion of homes with air conditioning rose from 23 to 47 per cent between 1978 and 1997. In the southern states - where obesity rates tend to be highest - the number of houses with air con has shot up to 70 per cent from 37 per cent in 1978.

Could air conditioning in summer and heating in winter really make a difference to our weight? Sadly, there is some evidence that it does - at least with regard to heating. Studies of people enclosed in respiration chambers for a few days show that in comfortable temperatures we use less energy. In one study of women exposed to 27 °C versus 22 °C, it amounted to a difference of about a megajoule (239 kilocalories) a day. That's the amount of energy in 27 grams of body fat.

Sweating burns up energy, however, and there's good evidence that high temperatures reduce the amount people eat, according to biostatistician David Allison of the University of Alabama, Birmingham. Whether these factors significantly alter energy balance is not clear, but it's got to be worth investigating.


3 Less smoking


Bad news: smokers really do tend to be thinner than the rest of us, and quitting really does pack on the pounds, though no one is sure why. It probably has something to do with the fact that nicotine is an appetite suppressant and appears to up your metabolic rate.

Katherine Flegal and colleagues at the US National Center for Health Statistics in Hyattsville, Maryland, have calculated that people kicking the habit have been responsible for a small but significant portion of the US epidemic of fatness. From data collected around 1991 by the US National Health and Nutrition Examination Survey, they worked out that people who had quit in the previous decade were much more likely to be overweight than smokers and people who had never smoked. Among men, for example, nearly half of quitters were overweight compared with 37 per cent of non-smokers and only 28 per cent of smokers.

Between 1978 and 1990, the prevalence of obesity in the US increased by about 9 per cent. Flegal reckons that about a fifth of this increase can be attributed to people giving up smoking (The New England Journal of Medicine, vol 333, p 1165). That's not to say that quitting smoking is a threat to public health - far from it. Smoking is so dangerous that you'd have to gain about 45 kilograms to justify continuing.


4 Prenatal effects


Your chances of becoming fat may be set, at least in part, before you are even born. Children of obese mothers - especially those who develop gestational diabetes - are much more likely to become obese themselves later in life. While this may be largely down to genetics, there is also evidence that some "intrauterine programming" goes on.

Offspring of mice fed a high-fat diet during pregnancy are much more likely to become fat than the offspring of identical mice fed a normal diet. Intriguingly, the effect persists for two or three generations. Grandchildren of mice fed a high-fat diet grow up fat even if their own mother is fed normally - so your fate may have been sealed even before you were conceived.

At the other end of the spectrum, we know from studying people born during the famine inflicted on the Netherlands during the second world war that energy restriction in the womb can lead to obesity later in life. This is especially likely if there is a period of rapid catch-up growth in the first two years of life. In the prosperous west, that might appear to be of little relevance, yet in the US the incidence of low birthweight has been rising since the mid-1980s and is now at its highest level for 30 years (National Vital Statistics Report, vol 53, p 1).


5 Fat equals fecund


Heavier people have more children. A study by Lee Ellis at Minot State University in North Dakota found "small but highly significant correlations" between BMI and reproductive rates. Women of normal weight or below had an average of 3.2 children, while overweight or obese women had an average of 3.5 children.

Does having more children make women gain weight, or does being overweight cause women to have more children? Probably both. Having lots of kids can increase the chances of getting fat - if for no other reason than poor sleep (see above). But Ellis also showed that people's BMI before they become parents is associated with the number of children they eventually have.

Explanations vary. Extreme thinness impairs fertility in both men and women. Extreme obesity does too, but Ellis thinks the effect is probably stronger at the thin end. Also, as David Allison of the University of Alabama at Birmingham points out, obesity can lead to lower socioeconomic status, which in turn is associated with having more children.

So why is this relevant to the epidemic? It's because obesity is heritable - twin studies indicate it's about 65 per cent genetic - so a tendency for this to be associated with having a large family will cause the proportion of overweight people to go up.



6 A little older...


Some groups of people just happen to be fatter than others. Surveys carried out by the US National Center for Health Statistics found that adults aged 40 to 79 were around three times as likely to be obese as younger people. Non-white females also tend to fall at the plumper end of the spectrum: Mexican-American women are 30 per cent more likely than white women to be obese, and black women have twice the risk (Journal of the American Medical Association, vol 295, p 1549).

In the US, these groups account for an increasing percentage of the population. Between 1970 and 2000 the chunk of the US population aged 35 to 44 grew by 43 per cent. The proportion of Hispanic-Americans also grew, from under 5 per cent to 12.5 per cent of the population, while the proportion of black Americans increased from 11 to 12.3 per cent. These demographic shifts may account in part for the increased prevalence of obesity.


7 More drugs


In the 1970s a new class of antipsychotic medication called neuroleptics came on the market, and millions of people worldwide now take these drugs. Alongside their undoubted success in treating psychosis, neuroleptics have a drawback: users typically gain 4 kilograms in the first 10 weeks, and another 4 or 5 kg in the year that follows.

Neuroleptics are not the only class of drugs to cause weight gain: anticonvulsants to treat epilepsy, antihypertensives for high blood pressure, protease inhibitors to treat HIV and diabetes medications, including insulin, have all been associated with packing on the pounds. Beta blockers add an average 1.2 kg to people using them, and taking contraceptive pills for two years will pad you out with an extra 5 kg. Even common, over-the-counter antihistamines can fatten you up.

So have pharmaceuticals contributed to the obesity epidemic? There is no firm evidence either way, but there is no doubt that the use of all these drugs has mirrored the rise in obesity over the past 30 years.


8 Pollution


In daily life, people are exposed to tens of thousands of industrial chemicals: pesticides, dyes, flavourings, perfumes, plastics, resins and solvents, to name but a few. We swallow them, inhale them and absorb them through our skin.

There is some evidence that low levels of some of these chemicals can lead to weight gain. Mice given small amounts of the pesticide dieldrin, for instance, more than doubled their body fat. Hexachlorobenzene, another pesticide, caused rats to gain significantly more than controls, despite eating half as much. Studies of humans exposed to PCBs by eating fish caught in North America's Great Lakes have found similar associations: the more the toxic load, the greater the body weight.

Some of these chemicals are endocrine disruptors that interfere with the functioning of hormones such as oestrogen. Numerous animal and human studies suggest that when oestrogen is not functioning properly, adiposity increases. Our exposure to such chemicals is on the rise: one Swedish study found that the concentration of PBDE (polybrominated diphenyl ether, a now-banned fire retardant) in breast milk doubled every five years between 1972 and 1998.


9 Mature mums


Mothers around the world are getting older. In the UK, the mean age for having a first child is 27.3, compared with 23.7 in 1970. Mean age at first birth in the US has also increased, rising from 21.4 in 1970 to 24.9 in 2000.

This would be neither here nor there if it weren't for the observation that having an older mother seems to be an independent risk factor for obesity. Results from the US National Heart, Lung and Blood Institute's growth and health study found that the odds of a child being obese increases about 14 per cent for every five extra years of their mother's age, though why this should be so is not entirely clear.

Could sheep hold a clue? Michael Symonds at the University of Nottingham, UK, has found that lambs born to older ewes lay down more adipose tissue in the first year of life. Symonds also found that first-born offspring have more fat than their younger siblings. As family size decreases, firstborns account for a greater share of the population. In 1964, the British woman gave birth to an average of 2.95 children; by 2005 that figure had fallen to 1.79. In the US in 1976, 9.6 per cent of women in their 40s had had only one child; in 2004 it was 17.4 per cent. This combination of older mothers and more single children could be contributing to the obesity epidemic. "It could skew the population to having fatter offspring," says Symonds.


10 Like marrying like


Just as people pair off according to looks, so they do for size. Lean people are more likely to marry lean and fat more likely to marry fat. In a study of 1341 Canadian families published in 1999, Peter Katzmarzyk at York University in Toronto found that there is a small but significant correlation between spouses of both BMI and "skinfold" measures of flabbiness that cannot be accounted for by the fact that they live together.

On its own, like marrying like cannot account for any increase in obesity. But combined with others - particularly the fact that obesity is partly genetic, and that heavier people have more children - it amplifies the increase from other causes.


Why the Big Two just will not do


Two prime suspects are in the frame when it comes to explaining the obesity epidemic: slothful western lifestyles, and the manufacturing and marketing practices of the food industry. It is not hard to think of examples of how these have changed for the worse: less physical education in schools, kids playing computer games rather than ball games, aggressive marketing of junk food, ever-bigger portions in restaurants, the increased use of high-fructose corn syrup in processed foods, and so on.

Yet any causal link between these changes and obesity is proving hard to pin down. A recent paper authored by 20 obesity experts from the US, Canada and Italy (International Journal of Obesity, DOI: 10.1038/sj.ijo.0803326) concluded that any evidence that they are the main cause of the epidemic - or that halting them would reverse it - is "largely cir****tantial".

For example, in 2000 Benjamin Caballero and colleagues at Pathways, a large obesity-prevention programme run through the Johns Hopkins School of Public Health in Baltimore, Maryland, recruited 1704 Native American children from 41 schools and randomly assigned them to experimental and control groups. The experimental group got a better diet, more physical activity and classes about healthy eating and lifestyle. The children were studied for three years. Astonishingly, they showed no significant reduction in body fat compared with the controls (The American Journal of Clinical Nutrition, vol 78, p 1030). "We threw tens of millions of dollars at the best investigators in the world - and they found absolutely no effect," says David Allison of the University of Alabama, Birmingham, one of the 20 authors of the review paper.

In a similar vein, attempts at linking children's obesity rates with how close they live to fast food outlets and parks have drawn a blank (Preventive Medicine, vol 38, p 57). The link between TV watching and obesity in young people has been shown to be statistically significant, though not large enough to make a clinical difference (International Journal of Obesity and Related Metabolic Disorders, vol 28, p 1238). And while obese people do eat bigger portions, there is no evidence to show that this is what causes their problem in the first place (Nutrition Today, vol 38, p 42).

Nobody is suggesting that these studies let the "big two" off the hook. But the case against them remains unproven, and many believe it is time to stop assuming that they are the only causes worth investigating.

Thank you everyone for a great meeting last night.  It is always so refreshing to be with a group of men and women who can relate to  everything I say, and I don't need to feel shy talking about anything.  I value these meetings so much, I hope everyone else does as well.

See everyone next month.

Mel