REVIEW RSS FEED
NON-FOOD CAUSES OF WEIGHT GAIN
Sharon Begley of Newsweek reported: "Evidence has been steadily accumulating that certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge."
Since studying obesity in adults is tricky due to the high number of factors, the most compelling research on the subject has come from a study from the Harvard School of Public Health in 2006 that looked at medical records of more that 120,000 kids over a 22-year period.
What the researchers found was that "the prevalence of overweight children less than 6 years old jumped 59 percent, from 6.3 to 10 percent." And even more shocking, "The results show surprising increases in the number of overweight children up to 6 months old. From 1980 to 2001, the increase in overweight infants ballooned 74 percent."
This is bad news for these kids later in life because "accelerated weight gain in the first few months after birth is associated with obesity later in life," said Matthew Gillman, an associate professor at Harvard Medical School
In 2002, an unknown Scottish academic published a paper about the link between obesity and synthetic chemicals, the Newsweek article explains. This eventually triggered some interest from others in the field.
Already in Japan, scientists were finding that bisphenol A (a chemical compound used to make plastic drinking bottles and baby bottles, among other things) pushed certain cells to become fat cells in experiments performed in the lab and also acelerated the growth of existing fat cells. If their results held true outside the lab in people, it would mean that BPA, and potentially other synthetic chemicals, were in fact contributing to obesity.
The next break came from a study done in the U.S on mice that were given low doses of estrogen-micking chemicals, and they were found to gain weight even when given the same amount of food and exercise as other mice.
Then in 2006, Bruce Bloomberg at the University of California , Irvine
As later tests would show, tributyltin is not the only obesogen that acts on the PPAR pathway, leading to more fat cells. So do some phthalates (used to make vinyl plastics, such as those used in shower curtains and, until the 1990s, plastic food wrap), bisphenol A and perfluoroalkyl compounds (used in stain repellents and nonstick-cooking surfaces).
6 Comments:
It doesn't matter. They will continue to demonize fat people and make them feel like sub-human monsters.
It doesn't matter. Some people are genetically sensitive to alcohol, and become addicted easily. They still have the responsibility to stay away from alcohol. Others get an adrenaline high, which also seems to be at least partly heritable. They have the obligation to not engage in impulsive actions that may harm others.
I had an interesting conversation with a woman so morbidly obese that she could not touch one hand to another. She spoke of eating a donut while driving. She lost control of her car, couldn't steer with just one hand, and knew that if she didn't drop the donut and use two hands on the steering wheel that she would hit a truck. She said that she just could not drop the donut.
There is significant recent research into the biochemistry of compulsive disorders. It appears that there is a common reward pathway for all of them that has become pathological. There are some drugs to assist in controlling some of these disease expressions, but ultimately it is the patient who must come to grips with their problem. One's genetics, gestation and early upbringing may play a part, but they are not an excuse.
m,
Just because you talked to one person who has a serious eating disorder, doesn't mean that her situation is true for every person who carries a few extra pounds. Your one person example is meaningless.
If what this article says is true then people afflicted with synthetic chemical contamination may start out 20% fatter then a non contaminated person. Trying to not express the 20% fat that comes with the contamination could mean starving to death just to try to be thin, and starving to death to become thin is yet another eating disorder.
The conversation with the obese person is not the argument here, merely as a demonstration that food disorders can effect others. The argument here is that there is a common pathway to the same reward system.
Fat tissue is a storage mechanism. Eat more or exercise less, calories are stored. Eat less, exercise more, then calories are utilized and stored fat is reduced.
I am not saying that it is easier to eat less, but rather that it still the responsibility of the individual person to do so. Just as it is for alcoholics, drug addicts, work addicts, compulsive gamblers, etc. Just because something makes it more difficult doesn't relieve the individual of the burden.
Much work has been done on the perceptions of the obese in terms of exercised performed and food eaten. All that I have seen have shown that the obese eat much more than they report, and exercise much less.
People who are moving 400lbs around are going to use a lot more energy than those who are closer to ideal body weight. Their homeostatic calorie base is typically two or more times that of someone at prime weight.
This post has been removed by the author.
I have a lot of empathy for overweight folks in a society that constantly barrages everyone with food ads for unhealthy food and eating. I think the main culprits are fat and empty carbs - white bread, white pasta, potatoes, white rice, and too much sugar. Oh and cars - lack of exercise
Post a Comment
<< Home