Scientists find how 'obesity gene' makes people fat

[alp227]

Source: Reuters

Scientists have unraveled how a gene long associated with obesity makes people fat by triggering increased hunger, opening up potential new ways to fight a growing global health problem.

A common variation in the FTO gene affects one in six of the population, making them 70 percent more likely to become obese - but until now experts did not know why.

Using a series of tests, a British-led research team said they had found that people with the variation not only had higher levels of the "hunger hormone" ghrelin in their blood but also increased sensitivity to the chemical in their brains.

"It's a double hit," said Rachel Batterham from University College London, who led the study, which was published in the Journal of Clinical Investigation on Monday.

Read more: http://www.reuters.com/article/2013/07/15/us-obesity-gene-idUSBRE96E0KB20130715

[Jessy169]

1. I call B.S. on the "obesity gene"

Looking back at my high school yearbooks -- talking 1969 to 1970 -- out of a few thousands students in my Houston-area high school there were approximately 5 - 10 "fat" kids.

Obesity genes?! Give me a break. Try processed foods, laziness, fast food restaurants all over the place, lack of exercise, eating instead of smoking (or other crutches) to handle stress. Did I say processed foods?

Maybe people who are overweight are relieved to learn about the "obesity gene", because that takes the spotlight off them -- as in, "hey, I've got the obesity gene, nothing I can do about it".

Both of my brothers became obese, and they both managed to slim back down to "normal". It was a mental effort, not a removal of the hated "obesity gene" from their genetic make-up.

[Marrah_G]

2. There are a bunch of reason for obesity, genetics is one of them

When you mix all the problems together it becomes a great big problem.

I was raised in a slim, athletic family. No junk food, very little TV. My parents were teachers and very health oriented. I have two brothers, the biological children of my parents, I was adopted at birth.

I've been heavy all my life, nothing my parents did helped for very long. What did happen was I grew to despise myself as bring broken, damaged, no willpower a failure.... etc.

I found my birth family 10 years ago. To my surprise my mother and two sibling all struggle every day with weight. My mother has had lap band surgery and is doing much better. I am still on the yo-yo thing. Every year I lose a bunch of weight and then I fall off the wagon and gain it all back and then some. Hopefully someday I will find a solution that works for me.

[JDPriestly]

8. 1 out of 6 they think have the obesity gene.

Some in my family just gain a lot of weight. Some stay thin no matter what.

But in the U.S. a lot of people eat the wrong food and are overweight for that reason. I nibble a lot, so i try to nibble on vegetables and fruit, not on starchy or fatty things.

Just now, I ate a bunch of radishes.

Eating fruits and vegetables is good for your skin and other health as well as for your weight. One other reason for obesity is people's social lives.

I notice that those in my family who are most active in their churches are obese. I think it is because they eat in a social situation.

But some people have a genetic propensity for obesity and some have it for thinness.

I have a friend who has been very thin all her life. She has to eat things like peanut butter, etc. to keep her weight up. She is not that active. I would not dare eat peanut butter, but I don't have a really bad weight problem. There are genetic differences, differences in metabolisms.

So, you are right. But a lot of obesity in the U.S. is due to poor diet.

[Marrah_G]

10. Combine poor diet, lack of excessive and genetics and its a bad mix

Also mental health issues like depression can have a big impact. For alot of people... it is a vicious circle of these things. People like to say it is just simple calories in, calories out. If that were the case then there would not be such a small percentage of people able to loose it and keep it off.


I think one of the biggest issues is poor diet and a food system controlled by people who want us to continue eating more mixed with ever lowering wages.

I know for myself, I can do great, feel great and step off the wagon in one momentary lapse and it all goes to shit. It's like a drug you can never really quit.

[Hekate]

13. I understand.

It's a complicated problem, with many many pieces to the puzzle. I always find it shocking how many DUers are eager to jump on the fat-shaming bandwagon because for them this has never been a problem. I find the self-righteousness depressing.

When someone like you, separated at birth from their biological family, discovers that the characteristics they share go far beyond eye color, one would think it would cause others to be curious and sympathetic, not shaming and blaming.

Best of luck in your search for health, Marrah. For me, it was stopping a medication I was on for 20 years. I could literally feel a switch in my brain turn off once it cleared my system. I am left with a number of health issues, and now am past menopause, so it's not like my troubles are over yet. But the cravings that made no sense are gone. For a friend of mine, Overeaters Anonymous has been the key -- 12-step program, sponsor, daily phone calls, and everything. She says I am the only person outside OA that understands.

Hekate

[Marrah_G]

15. I'll look into that

[KansDem]

3. Brutal, but fair assessment...

The Official US Obesity Rates Timeline .

Also, check out this comparison of the percentage of soft drinks consumed vs. the rate of diabetes:

Adult diabetes rate:


Gallons of per capita soft drinks:


Those two maps look almost identical!

Source:
http://www.ediblegeography.com/united-states-of-food/

[lupine25]

4. I (respectfully) call BS on your calling BS

...and I do mean this respectfully, plus I realize this is not necissarily the same thing as a obesity "gene." But I'm a personal case of this. I was born of a severely gestationally diabetic mother and weighed in at time of birth at 12.1 pounds. Yikes! I've also been diabetic my entire life as a result of this and I've always had some "flab" to me. As an adult (I'm 28 years old now), I've tried diets, excercise (running, mountain biking, hiking) regularly and even spent 3 years in Paraguay running around in the sub-tropical heat, eating pretty much hardly anything but rice and beans and at my "skinniest" I weighed in at 205 pounds.

This has also caused other health problems with me such as not only the diabetes, but my skin tends to "redden" quicker than most people, which I've been told by my doctor has to do with damage I sustained while "in utero." So, by no choice of my own, I have all of these problems including my flab that never goes away.

The difference is, I try not to think of it as "well I'll never be skinny so...why bother???" But, you have a good point in that many people have and will think that. It's a sad fact and wish I would help others change their attitude about obesity. In my case, I know I will never be skinny as a rod, but I have to keep eating well to manage my diabetes and keep myself at a healthy weight. Which thankfully is easy for me to keep up the exercise part since I take the bus to and from everywhere, which means I have to walk a lot (1.5 miles to work on the weekends each direction..... anybody want to call me lazy? Haha!)

The key here is attitude and willingness to work with doctors to help manage weight -- which is why I'm excited about this news about the "obesity gene" simply because this may lead to a way to help people in the same boat as me. Rest assured, I'm going to be watching this story closely.

[Bernardo de La Paz]

5. Just because temptation is one factor, it does not affect the reality of the obesity gene.

If you want to look back, look back to photos of 1930s farm families or urban street scenes.

Yes, bad food choices increase obesity.

And Yes, obesity genes increase obesity too. They make it harder to avoid temptation because the person is more hungry more often. However, too many people use the excuse of "bad genes" to avoid doing what they need to do to get to a healthy weight.

People (like me) who seem to not have the obesity gene(s) need to be a little more understanding of those who are obese, though ultimately not buying into the excuse-making. In the final analysis, excess food in means excess pounds on. At the same time, there are ranges of challenges that people face when handling weight. For some people saying no to excess food is much harder than for other people.

But ultimately, everyone can say no to excess food, especially if they have health care that includes preventative assistance. Investment in preventative medicine is the best medical investment a person can make and a state or country can make.

The obesity gene(s) is real and needs to be taken into consideration as a factor, but it is not the only factor.

[lolly]

6. Why is this seen as "excuse-making?"

More evidence suggests that obesity is a mix of environmental, genetic, and personal factors.

No one wants to be fat--people who have serious weight issues are not looking for an "excuse" not to do anything. It isn't a crime, and people don't need an alibi or excuse.

The point of the research is to find ways to combat obesity. If one of the factors involved--genetics--can be studied, then perhaps one of the causes can be helped. Why would that bother people?

[ReRe]

7. I DO believe that some obesity issues are genetic.

This has happened in my family. Have a couple cousins (from both paternal and maternal sides of family); niece who WAS overweight but changed her life by becoming a vegan, exercising incessantly and never wavered or backslid. Mother was overweight and I have a son who is overweight also. More prevalent on my Mother's side of the family. All the rest of the family is tall and thin. It sticks out like a sore thumb when people are raised in the same household and have the same activity level and same diet as everyone else, but end up overweight.

Allot of obesity is caused from poverty. They have to survive on starchy cheap foods, boxed dinners, hot dogs & hamburger, junk food from McDonald's, etc. The problem in this group is extreme poverty/ economic issues.

If this country was really the "greatest country on earth", we wouldn't have an obesity problem. Our citizens would have jobs making livable wages, enabling them to afford healthier diets. And we wouldn't have junk food restaurants on every corner. We wouldn't have grocery store shelves loaded with foods that are loaded with high fructose corn syrup, SALT and SUGAR, and now God only effing knows how many GMOs.

One thing that really gets under my skin are those who look down their noses at those with weight issues. Just remember, "There but for the Grace of God go you." Don't blame the people, blame the corrupt practices of our food industry and a government which allows such junk to end up on our tables. DON'T BLAME THE VICTIMS.

[DreamGypsy]

9. "Scientists find how 'obesity gene' makes people fat" is a popular media translation...

of the title of the research paper "A link between FTO, ghrelin, and impaired brain food-cue responsivity" in media language of dumbed-down, half-truth, popular pablum.

I will give Reuters credit for two things in their presentation of the reseach:

1). The words obesity gene appear in single quotes, suggesting it is something like a so-called obesity gene.
2). In the introductory line of the article (as quoted in the post) the description is of "a gene long associated with obesity" and there is no use anywhere in the article of any form of the word "cause".

Association is not causation.

These are the results as presented in the introduction in the research paper in the Journal of Clinical Investigation (emphasis mine):

FTO is an AlkB-like 2-oxoglutarate–dependent nucleic acid demethylase of uncertain cellular function (1). Genome-wide association studies (GWAS) have reliably established that SNPs within the first intron of FTO are robustly associated with increased BMI and adiposity across different ages and populations (2–6). Subjects homozygous for the “obesity-risk” A allele of FTO rs9939609 have a 1.7-fold increased risk for obesity compared with subjects homozygous for the low-risk T allele (2). Evidence to date suggests that the association between SNPs in FTO and BMI is predominantly driven by increased energy intake. Subjects homozygous for the obesity-risk A allele of rs9939609 exhibit overall increased ad libitum food-intake (7–9), particularly fat consumption (7, 9–11), and impaired satiety (12, 13). Furthermore, preschool AA children (AA denotes homozygosity for the A obesity-risk allele in the rs9939609 FTO variant) exhibit obesity-prone eating behaviors, including increased food responsiveness and a tendency to eat in response to external cues, prior to the development of an association between FTO rs9939609 and BMI (14). FTO rs9939609 also has per-allele effects on feeding behavior (10) and BMI (2).

Several lines of evidence from rodent studies are consistent with FTO playing a key role in regulating energy homeostasis. First, Fto is highly expressed in brain regions controlling feeding and energy expenditure, such as the hypothalamus (1, 15). Second, hypothalamic Fto expression is modulated by fasting (1, 16–20) and restricted access to food (21), although both upregulation (17, 18) and downregulation (1, 16, 19) have been reported, apparently depending on the severity of caloric restriction. Exposure to a high-fat diet also modulates hypothalamic Fto expression, with downregulation reported with short-term exposure (20) and upregulation with more prolonged exposure (22). Further evidence suggesting that Fto is nutritionally regulated comes from in vitro studies in mouse and human cell lines in which glucose and total amino acid deprivation decreases FTO expression (23, 24). Finally, phenotypic analyses of transgenic mice in which FTO function is either eliminated or enhanced further implicate a role for FTO in regulating energy homeostasis. Mice with constitutive Fto deletion exhibit a tendency toward leanness (25–27), and similarly, mice generated with a dominant missense mutation in the C-terminal of FTO, leading to a partial loss of function, also display a lean phenotype (28). In contrast, mice with global Fto overexpression have increased food intake, body weight, and fat mass (29).

<snip>

Gut hormones are released from the gastrointestinal tract in response to nutrient ingestion and regulate appetite and body weight (33). Circulating levels of the orexigenic hormone, acyl-ghrelin, and the satiety hormone, peptide YY3-36 (PYY3-36), alter appetite, food intake (34–36), and modulate brain activity within both homeostatic and reward-related brain regions (33, 37–39). Thus, we hypothesized that the FTO rs9939609 genotype impacts circulating PYY3-36 and/or acyl-ghrelin levels and the neural responses to food cues, thereby resulting in the reduced satiety (12, 13), increased energy intake (7–9), preference for energy-dense foods (7, 9–11), and increased food-cue responsivity (14) seen with the AA genotype.

To test this hypothesis, we assessed appetite and circulating ghrelin and PYY3-36 levels in AA and TT (TT denotes homozygosity for the T low obesity-risk allele for the rs9939609 FTO variant) adiposity-matched male subjects in response to a standard test meal. We found that AA subjects exhibited attenuated postprandial suppression of both hunger and circulating acyl-ghrelin levels. In parallel, we used blood oxygen level–dependent (BOLD) functional MRI (fMRI) scanning to assess the effect of the FTO genotype on neural responsiveness to food cues and endogenous changes in acyl-ghrelin concentrations. Next, we undertook a series of studies to explore the mechanistic link between FTO and ghrelin. We measured ghrelin levels in Fto KO mice (25) and examined the effect of FTO overexpression on ghrelin mRNA abundance and m6A methylation and total ghrelin and acyl-ghrelin concentrations in both MGN3-1 cells, a ghrelin-producing mouse cell line (40), and in HEK293T human cells. Finally, we analyzed FTO expression, ghrelin mRNA m6A methylation, and ghrelin expression in peripheral blood cells from AA and TT subjects.

The results of the research are present in detail in the report, including discussions of MRI results that show response to food cues.

[thenooch]

11. Here

Here's how the fat gene works;

Caloric Intake > Calories Burned = People get fat (it's really that simple)

[alp227]

12. Evidence? Or PIDOOMA? n/t

[Scout]

17. it's really that simple, for the simple minded.

you really think the human metabolism is no more complex than that? snort.

[Hekate]

18. Simple minds, simple answers. nt

[thenooch]

19. Hmmnnnn...

Yawl sound fat!

[Hekate]

20. Simple minds, simple insults.

You'll fit right in.

[Kablooie]

14. So it's not my fault I'm fat. It's Gene's fault. He's in big trouble now.

[Hekate]

16. Processed food companies spend millions of dollars to manipulate desires

If it didn't work, they wouldn't do it, and it is done in laboratories that would do B.F. Skinner proud. Every sense is engaged -- what you see, taste, smell, touch, and hear -- precisely calibrated and all heading for a feedback loop in the brain.

If there is a genetic/psychological weakness in the armor, they will gleefully exploit it without a moment's hesitation. Diabetes in little kids? Pfft -- that's mommy's fault.

Add to that a sedentary lifestyle and additives no one can pronounce (what I call "poisoning our food chain&quot and you have trouble.

There are many pieces to this puzzle. Many. But shaming people is not the answer, because individuals are up against forces they can't even see.

This, however, is the Land of the Free and the Home of the Brave, where corporations are people, my friend, and regulations are a Really Bad Thing.