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GraceGirl
10-17-2007, 03:23 PM
I saw this today:

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Genes Might Help Drive Overeating By Kathleen Doheny
HealthDay Reporter
1 hour, 19 minutes ago



WEDNESDAY, Oct. 17 (HealthDay News) -- Chronic overeaters may have their DNA to blame, research suggests.


Scientists from the University at Buffalo say people with genetically lower levels of dopamine, a brain chemical that helps make eating and other behaviors more rewarding, may be driven to consume more food.


"We weren't studying obesity, per se, but motivation to eat. We wanted to understand how the brain regulates motivation to eat," explained study co-author Jennifer Temple, a research assistant professor of pediatrics.


Reporting in the October issue of Behavioral Neuroscience, Temple's team looked at genes associated with differences in brain activity, in particular the influence of a genetic variation linked to a lower number of dopamine D2 receptors on cells. About half the population has this variation, called the Taq1A1 allele.


According to the researchers, people with fewer of the dopamine receptors need to take in more of a rewarding substance -- such as food or drugs -- to get an effect that other people get with less.


Investigating further, the Buffalo team studied 29 obese and 45 non-obese men and women, aged 18 to 40. The researchers took DNA samples from inside each person's cheek to see if they carried the Taq1A1 variation.


"They came to the lab twice," Temple said. "The first visit, we gave them a large portion of six snack foods and told them it was a taste test. They rated the food on taste characteristics. We left the food in the room while they were completing the rating." Participants were told they could eat as much as they wanted, and the researchers took note of their intake.


On the second visit, the researchers evaluated each participant's motivation to eat. To earn a food reward, each person had to click a computer mouse 20 times. "To get more food, they had to click 40 times," Temple said. "We were looking to see how hard they were willing to work for food." The participants could choose food or the chance to read a newspaper as a reward.


"The combination of being very motivated to get food and having the genotype made people eat the most," Temple said. "We had people very high in motivation to get food who didn't have the genotype," she added, but those people still "ate less than people who were both motivated and had the [Taq1A1] genotype."


The bottom line: "A combination of [having] this genotype with being very motivated to consume food or with being obese seems to make people more prone to overeat," Temple said.


The study results do not imply that your genes doom you to obesity, however. "People who had the genotype were heavier, but there were certainly people who had the genotype who were not obese," Temple stressed.


While other research has turned up similar findings, Temple said her team looked at behaviors associated with the genotype. "Others have found that differences in the density of dopamine are associated with obesity," she noted.


In their future work, the team will use brain scans to reveal more about the relationship between the genotype and the drive toward eating.


Eventually, Temple said, the dopamine system may become a target for weight-loss therapies. For instance, drugs that affect the dopamine system, such as drugs now used for attention deficit hyperactivity disorder (ADHD), might help with weight-loss efforts, she theorized.


Another expert, Dr. Samuel Klein, director of the Center for Human Nutrition at Washington University School of Medicine in St. Louis, said the study "addresses an important and relatively overlooked area in obesity -- the contribution of reward addiction in the regulation of food intake."


Dr. Julio Licinio, professor and chairman of psychiatry and behavioral sciences at the University of Miami Miller School of Medicine, agreed. "This really is like another piece of the puzzle, showing there is a genetic component and that those with this genotype are likely to have different weights because of the food reinforcement."


Licinio published similar research last year, in which he found that people with a particular genotype for a receptor for the brain chemical serotonin were more likely to eat red meat than those who lacked it.

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Thoughts, comments...??

Erik
10-17-2007, 03:31 PM
Ties into this post which was made in the Food Addiction thread ...


Ok, so there was a post that said food addiction is not about the food at all, and that comparing an addiction to any food to other addictions like alcohol or drugs, is wrong and dangerous (or something like that). That it's not physiological per se. That the idea of abstaining is bad.

There's lots of new research coming out in this area and even people on this thread have reported experiences that support some of the things said early on in the thread. They do better when they abstain. Have a little of that 'food' (whatever is is)? All hell breaks loose. For SOME people that is the best course of action.

It's a popularly held belief that food addiction is an emotional problem, which while probably partly true, really doesn't make much sense to me. And, there's now research that actually supports the fact that it is a physiological or medical condition which adversely affects all areas of life, including emotional and mental stability. There's a physiological, biochemical condition of the body which creates a craving for refined carbohydrates. The craving and its biochemistry is the same as the alcoholic's craving for alcohol.

Research is calling this a biogenetic disease now. One that can be inherited, yes inherited. They have found a particilar gene that is linked to addiction. StrongChick, are you up on this at all?

Addictions specialists from the University of California at Los Angeles have focused their research on a dopamine receptor gene that is responsible for the sensations of pleasure or reward. A form of the pleasure gene is called A1, previously linked to alcohol and cocaine abuse, may be the cause of carbohydrate craving and compulsive eating is what the researchers are saying.

They did a study on 70 people who were obese, and the researchers found that twice as many of them as expected carried the rare, dopamine receptor pleasure gene A1. The 'normal' gene is called A2.

In previous studies they say that the brains of people carrying the rarer A1 gene had fewer dopamine receptors than those with the more common A2 gene.

What's that suggest? Thta people with fewer dopamine receptors may use substances to satisfy the deficit. Just as alcohol and cocaine increase the level of brain dopamine, so do carbs.

People eat carbs to 'feel good' by bringing the brain into a temporary balance. Such foods increase the level of brain chemicals. Addiction is a process of self medicating a distressed brain in chemical imbalance. People take prescribed drugs to medicate a distressed brain in chemical imbalance in depressive states.

When a person eats a trigger food (some kind of refined carbohydrate probably), the brain is flooded with dopamine, serotonin and norepinephrine (chemicals!). Flooded brain = feel good.

So therefore there ARE people with food issues for whom it IS the food itself, just like it is the alcohol itself that is a problem for alcoholics. All? Of course not. Some? Definitely. At least according to the research that is happening now. In cases like this, where there is a physiological link abstaining IS good. Look at how many people do awesome when they abstain and then fall off the cliff when they introduce some kind of trigger that they know is a trigger.

I would imagine the diagnostic updates in the future will reflect these findings. There are many sub classifications of eating issues and one size obviously doesn't fit all. Not in classification or in treatment.

GraceGirl
10-17-2007, 03:43 PM
So once again, everyone else is starting to catch on to what you've said all along. Is there a Nobel Health & Fitness Prize? :p

Erik
10-17-2007, 03:51 PM
:lol:

I wish I could take credit, but I came across the stuff I wrote about in my own research of other people's writings.

But interestingly, as I said, there's just going to be more and more support for a physiological basis to food issues, whether old school thinkers wish to accept it or not. At least in my opinion.

Espi
10-26-2007, 01:09 PM
Like many of us who started doing a low-carb diet and suddenly could manage their food intake much bettter , had discovered all along. It's also very much blood sugar driven, but even moreso hormonally driven.

Would this also explain why for some people exercising makes them undereat , since exercising causes the formation of endorphins. And others start overeating because of ... perhaps too low blood sugar?

In any case it's extremely interesting.
Here's that article as discussed in Lyle's recent news letter.


King NA et. al. Individual variability following 12 weeks of supervised exercise: identification and characterization of compensation for exercise-induced weight loss. Int J Obes (Lond). 2007 Sep 11; [Epub ahead of print] Links

Objective:To identify and characterize the individual variability in compensation for exercise-induced changes in energy expenditure (EE).Design:Twelve-week exercise intervention.Subjects:Thirty-five overweight and obese sedentary men and women (body mass index, 31.8+/-4.1 kg m(-2); age, 39.6+/-11.0 years) were prescribed exercise five times per week for 12 weeks under supervised conditions.
Measurements:Body weight, body composition, resting metabolic rate (RMR), total daily energy intake (EI) and subjective appetite sensations were measured at weeks 0 and 12.
Results:When all subjects' data were pooled, the mean reduction in body weight (3.7+/-3.6 kg) was significant (P<0.0001) and as predicted, which suggested no compensation for the increase in EE. However, further examination revealed a large individual variability in weight change (-14.7 to +1.7 kg). Subjects were identified as compensators (C) or noncompensators (NC) based on their actual weight loss (mean NC =6.3+/-3.2 kg and C=1.5+/- 2.5 kg) relative to their predicted weight loss. C and NC were characterized by their different metabolic and behavioural compensatory responses. Moderate changes in RMR occurred in C (-69.2+/-268.7 kcal day(-1)) and NC (14.2+/-242.7 kcal day(-1)). EI and average daily subjective hunger increased by 268.2+/-455.4 kcal day(-1) and 6.9+/-11.4 mm day(-1) in C, whereas EI decreased by 130+/-485 kcal day(-1) and there was no change in subjective appetite (0.4+/-9.6 mm day(-1)) in NC.
Conclusion:These results demonstrate that expressing the exercise-induced change in body weight as a group mean conceals the large inter-individual variability in body weight and compensatory responses. Individuals who experience a lower than predicted weight loss are compensating for the increase in EE.