Deep brain stimulation of the so-called “feeding centre” (the lateral hypothalamic area) was associated with weight loss via increased metabolism in morbidly obese patients

http://www.sciencedaily.com/releases/2013/06/130613092007.htm

After nine months, one patient who had experienced a 9 percent increase in resting metabolic rate reduced his weight by 16.4 percent. Another patient, whose metabolic chamber metabolic rate change was indeterminate due to motion during the selected stimulation approach, lost 12.3 percent of her weight after 11 months at the optimal setting. The final patient had a 0.9 percent decrease after 16 months at optimal settings, but also commented that this was the first time in her life that she did not have to fight constant hunger, and her binge eating score reduced from severe to within normal range.

The team believes expanded research studies might show that optimal settings would reduce appetite and food cravings, as well… In order for survival during lean times, humans have evolved to automatically lower metabolic rate when food intake goes down -- an innate "set point" that can add challenge to weight-loss efforts. This work by Oh and colleagues suggests that the "set point" can be adjusted like a thermostat.

Dietary fructose causes liver damage in animal models:

no suprises here really!:

http://www.sciencedaily.com/releases/2013/06/130619164437.htm

Fructose rapidly caused liver damage even without weight gain. The researchers found that over the six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group.

Kavanagh's team studied monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period. Not surprisingly, the animals allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group. They developed diabetes at three times the rate of the control group and also developed hepatic steatosis, or non-alcoholic fatty liver disease.

Ten middle-aged, normal weight monkeys who had never eaten fructose were divided into two groups based on comparable body shapes and waist circumference [surely 10 is too small a number to draw great conclusions from though!]. Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.

Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein. [which if you ask me adds way to many confounding variables to the study to conclude much!!]

In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there. It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate, Kavanagh said.

One of the limitations of the study was that it only tested for fructose and not dextrose. Fructose and dextrose are simple sugars found naturally in plants.

"We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can't say conclusively that fructose caused the liver damage," Kavanagh said. "What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.

"The liver damage began even in the absence of weight gain. This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems."

If you think diet is more important than exercise, you have a lower BMI

http://www.sciencedaily.com/releases/2013/06/130618113858.htm

From an initial online survey, they discovered that people seem to subscribe to one of two major beliefs about the primary cause of obesity:"Some people overwhelmingly implicated poor diet, and a roughly equal number implicated lack of exercise. Genetics, to our surprise, was a far distant third."

Not only did people tend to implicate diet or exercise as the leading cause of obesity, people who implicated diet as the primary cause of obesity actually had lower BMIs than those who implicated lack of exercise.

"What surprised me the most was the fact that we found lay theories to have an effect on BMI over and above other known factors, such as socio-economic status, age, education, various medical conditions, and sleep habits," says McFerran.

The researchers hypothesized that the link between people's beliefs and their BMI might have to do with how much they eat.

A study with Canadian participants revealed that participants who linked obesity to lack of exercise ate significantly more chocolates than those who linked obesity to diet. And a study with participants in Hong Kong showed that participants who were primed to think about the importance of exercise ate more chocolate than those primed to contemplate diet.

Believing diet to be major cause of obesity, does better for you BMI, than believing exercise is the major factor… I wonder what believing genetics was paramount would do!?!?!

racial/ethnic differences in obesity can be explained by behavioral risk factors

http://www.sciencedaily.com/releases/2013/06/130603163759.htm

We know that, already by the age of 2, black and Hispanic children have close to double the rate of obesity of white children in the U.S. Our finding that most of these racial/ethnic differences can be explained by behavioral risk factors indicates that designing and implementing interventions to reduce those risk factors during pregnancy, infancy and early childhood could help eliminate racial and ethnic disparities in childhood obesity."

almost all known early-life risk factors for childhood obesity -- including low rates of breastfeeding, lack of sleep, and high consumption of fast foods and sugar-sweetened beverages -- are more common among black and Hispanic children.

• rapid infant weight gain
• non-exclusive breastfeeding
• introduction of solid foods before 4 months
• sleeping less than 12 hours per day
• drinking sugar-sweetened beverages
• eating fast food frequently
• the presence of a television in the bedroom
 

Mind you, lets not forget this seems to be happening everywhere, to everyone, albeit it at a faster rate to those ethnic/racial subgroups:
http://www.sciencedaily.com/releases/2013/06/130612173238.htm
The number of children admitted to hospital for problems related to obesity in England and Wales quadrupled between 2000 and 2009, a study has found.

"It's clear that rising obesity levels are causing more medical problems in children, but the rise we observed probably also reflects increasing awareness among clinicians, who have become better at recognising obesity."

Better at recognising obesity?! What do these guys want?! A fucking medal?! You're either obese or your not, its a simple matter of weight (kg) over height (m)squared and the end number being over 30. Its as clinical as you can possibly get. A machine can get it right EVERY time, so why can't we? *Sigh*, one day where going to look back at our own kind in history and say "what the hell was wrong with us? These are supposedly some of the most highly trained professionals within society and they can't weigh a patient and calculate a BMI (which, lets be honest, is a shity indicator anyway, with bodyfat% being just as valid, if not a more important consideration - but still better than not diagnosing at all!).