I just keep wondering what happened to the concept of personal accountability? Genetic predisposition or not, it's still a CHOICE! Does a person with a genetic predisposition towards alcoholism have to become an alcoholic? Of course not! It's ridiculous!
Hmmm...sounds like a get rich scheme to me. Someone needs to revoke his license or something...That's not right to say we're pre-determined to be obese then "but I have identified the gene and for only $99.99 per pill, YOU too can kill the gene!!" Bah!!!
(Not his exact words..but I can see this scenario in one of those 30-minute annoying infoo-mercials.)
Of course it's the gene pools fault, the genes are wallowing in a pool of fat that is McD's, Burger King, and all the other fat food joints in North America... When all these junk joints were not around people where not obese! Of course an obese person can use the gene pool as an excuse, but that's all it is, an "excuse"... Genes may make loosing weight not easy, but it's not impossible... He's definitely looking to make a few buckaroos this Friedman...
Well, that's it, I guess I'll head on over to the Chinese buffet and then to Baskin Robins for dessert since I'm obvioulsly doomed! Whatever! This guy is so full of crap. I know he has the right to say whatever he wants, but good grief! I'm so glad I didn't see this before I started trying to lose because who knows where I'd be now. I may not have even bothered trying. Now that is a scary thought. I wonder how many others' chances he's ruined with his so called "expertise". This truely makes me sad.
He left clinical medicine in 1980 after discovering that his true passion was the laboratory. By 1981, he had begun his scientific career, and within a few years he was taking on what seemed like an impossibly onerous task, finding a gene whose absence made mice grow massively obese.
He keeps mementos from those days. He still has the purchase order, from December 1986, for the first batch of mice he used for the experiment.
Maybe this is the heart of the problem -- all he's dealt with is MICE in a LABORATORY. And despite what some scientists may want to think, there's a world of difference between mice in cages and people in the real world, like you and me. Just because certain genetically engineered mice in a lab will gorge themselves until they're obese doesn't mean that we're doomed to mindlessly eat our way to obesity. As so many of you pointed out, we have free will. We decide when to eat, how much to eat, whether we exercise etc. We've got brains and like StarPrincess said, that means we can make choices. We're not unthinking mice at the mercy of our genes and hormones.
I just keep wondering what happened to the concept of personal accountability? Genetic predisposition or not, it's still a CHOICE! Does a person with a genetic predisposition towards alcoholism have to become an alcoholic? Of course not! It's ridiculous!
Exactement ma chère, it's true, yes, none of us are those people who can eat all they want and not gain a pound (yes there are a few people in the world like that, but they probably fall into a tiny percentage of the population). For us it takes work. I know someone who has alcoholism in his family so he's made some strong conscious decisions NOT to have alcohol in his house, to never drink alone and to only ever drink with other people etc (and he doesn;'t drink often, he's not an alcoholic BTW, but does have to be careful). We have to assess our conditions and learn what works for us to help us not fall into our genetic predispositions. It can take work, I can't have too much food in my house (well junk food), I have to know my binge triggers, I have to exercise (which is a great cure-all for many things).
Overall I knew that eating junk food wasn't healthy. I learned what proper portion sizes were. I learned how to eat well, it wasn't natural for me at first, but I adapted (it was hard at first, I started by banning fried foods at lunch, now fried food is a rare treat for me and I don't mind. I preferred grilled stuff overall).
My wish for the next tens years? The "statistic" of 95% of all people who lose weight gain it back and then some will be abolished.
This is a good thread. I just happened on it by accident and you can add me to the list of people who have, indeed, successfully taken off substantial weight and kept it off ... more or less, though I'm having a few setbacks here and there. I do think it's close to inevitable that in most cases (especially mine), some regain does occur, but I also think there are a lot of studies showing people successfully maintaining over the long haul, e.g., the successful "losers" do regain but they handle it before it gets to the point of going back into obesity.
The National Weight Loss Registry comes to mind in showing how many people do successfully maintain a weight loss.
One person's opinion, scientist or not, does not constitute any kind of proof in my book. However, I've heard this drivel repeated (not the drivel of the posters on this thread, the drivel of how it's impossible to lose substantial weight and keep it off) again and again and it infuriates me as well.
I guess I should just give up, lie on the couch all day eating and gain 100 pounds, since according to the good doctor, I'm going to do it anyway.
And for the record regarding the gene pool, I had an overweight but not obese mother, an underweight father and an overweight brother (all deceased) as well as a very much alive, tall, thin brother who is putting on too much around-the-middle weight due to midlife stress.
I reached the 247-pound mark posted in my sig line by binge eating and a few other eating disorders, absorbing too many calories and eating too much junk and not exercising. I took it off by doing the opposite. When I eat too much (like tonight) over time, my weight goes up, when I do the opposite, it goes down.
I know exactly what I am doing and am not genetically mesmerized to do diddlysquat.
I respectfully disagree with the good doctor's conclusions!
here's an excerpt from a CME activity put out by a generally reliable source. and a link to the rest of it. it's a state-of-the-science review of obesity: epidemiology, risk factors, pathogenesis, and treatment. the key points for this discussion [especially of friedman's work on leptin and other genetic issues] are these:
Here's the excerpt:
Pathophysiology: The pathogenesis of obesity is far more complex than the simple paradigm of an imbalance between energy intake and energy output. Although this concept allows easy conceptualization of the various mechanisms involved in the development of obesity, obesity obviously is far more than the mere result of excess eating and/or too little exercise. However, the prevalence of inactivity in developed countries is significant and relevant. In the United States, only approximately 22% of adults and 25% of adolescents report significant regular physical activity. Approximately 25% of adults in the United States report no significant physical activity during leisure, while approximately 14% of adolescents have similar reports of inactivity.
Two major groups of factors with a balance that variably intertwines in the development of obesity are genetics, which is presumed to explain 40-70% of the variability in obesity variance, and environmental factors. While the high prevalence of obesity in the children of parents who are obese and the high concordance of obesity in identical twins suggest a significant genetic component to the pathogenesis of obesity, the secular trends of the last few decades, which are coincident with recent changes in dietary habits and activity, also suggest a significant role for environmental factors.
Leptin
Leptin was discovered in 1994 by Friedman et al and ushered in an explosion of research and a great increase in knowledge about regulation of the human feeding and eating cycle. Since this discovery, the neuromodulation of satiety and hunger with feeding clearly is far more complex than the simplistic older model of the ventromedial hypothalamic nucleus and limbic centers of satiety and the feeding centers of the lateral hypothalamus. Leptin is a 16 kd protein produced predominantly in white adipose tissue and, to a lesser extent, in the placenta, skeletal muscle, and stomach fundus in rats. Leptin has a myriad of functions in carbohydrate, bone, and reproductive metabolism that are still being unraveled, but its role in body weight regulation forms the major claim to fame (leptin from the Greek word leptos, meaning thin).
The major role of leptin in body weight regulation is to signal satiety to the hypothalamus and, thus, reduce dietary intake and fat storage while modulating energy expenditure and carbohydrate metabolism to prevent further weight gain. Unfortunately, unlike the Ob/Ob mouse model in which this peptide was first characterized, most humans who are obese are not leptin-deficient but rather leptin-resistant and, thus, have elevated circulating leptin levels. While most human obesity is polygenic (>90% of cases), the recognition of monogenic variants has greatly enhanced our knowledge about the etiopathogenesis of obesity.
Monogenic models for obesity in humans and experimental animals
The various available monogenic models have greatly increased our knowledge about mechanisms for the development of obesity, and they also have provided multiple potential targets for future antiobesity medications.
Proopiomelanocortin (POMC) and alpha–melanocyte-stimulating hormone (alpha-MSH) both act centrally on the melanocortin receptor 4 (MC 4) to reduce dietary intake. Genetic defects in POMC production and mutations in the MC4 gene both have been described as monogenic causes of obesity in humans. Of particular interest is the fact that patients with POMC mutations, because of the deficiency in MSH production that results, tend to have red-colored hair. Also, because of their diminished adrenocorticotropic hormone (ACTH) levels, they tend to have central adrenal insufficiency. Some recent data suggest that as many as 5% of children who are obese have MC4 or POMC mutations. If confirmed, these would be the most common identifiable genetic defects associated with obesity in humans (band 2p23 for POMC and band 18q21.3 for MC4).
The Ob/Ob mice are the prototypical mice that set the stage for the discovery of leptin. These mice lack the leptin gene and are overweight and hyperphagic. A few humans have been identified who have a similar genetic defect with similar phenotypic consequences. This variant of obesity, although minor in the grand scheme of human obesity, is exquisitely sensitive to leptin injection, with reduced dietary intake and profound weight loss (band 7q31).
The Db/Db mice have mutations of the leptin receptor in the hypothalamus. Fa/Fa mice also have leptin-receptor mutations. These mice have early-onset obesity and hyperphagia like the Ob/Ob mice, but they also have normal or elevated leptin levels. Human counterparts of this model are very rare and are associated with hyperphagia, hypogonadotrophic hypogonadism, and defective thyrotropin secretion, but they are not associated with hypercortisolism, hyperglycemia, and hypothermia as occurs in Db/Db mice (band 1p31). The leptin receptor is one of the cytokine receptor families of receptors and is activated through the Janus kinases/signal transducers and activators of transcription (JAK/STAT) mechanisms.
Prohormone convertase is an enzyme that is critical in protein processing, and it appears to be involved in the conversion of POMC to alpha-MSH. Patients identified to have this, although rare, have significant obesity, hypogonadotrophic hypogonadism, and central adrenal insufficiency. It is one of the few obesity models not associated with insulin resistance (band 5q15-21).
PPAR-gamma is a transcription factor that is involved in adipocyte differentiation. All humans with mutations of the receptor described so far have severe obesity (band 3p25).
In addition to the above monogenic models of obesity, genome-wide linkage analyses and microarray technology have revealed a rapidly growing list of potential susceptibility obesity genes. Among those identified that are being actively studied are genes on chromosome arms 2p, 10p, 5p, 11q, and 20q.
In the same line as the evidence that proved Helicobacter pylori as the cause for peptic ulcer disease, some evolving data suggest that a significant inflammatory and possibly infective etiology may exist for obesity. Adipose tissue is known to be a repository of various cytokines, especially interleukin-6 and tumor necrosis factor-alpha.
Some data have shown that adenovirus 36 infection is associated with obesity in chickens and mice. Other data also suggest that while humans who are not obese have a 5% prevalence rate of adenovirus 36 infection, humans who are obese have a prevalence rate of 20-30%.
and here's the link to the entire article, including references:
Tar and feather Jiffypop? Unthinkable! How about a spa day instead?
And I'm not sure we're really in radical disagreement, anyway. What I object to in Dr. Friedman's comments is not the idea that there is a genetic component to obesity, but the notion that obese people are "doomed" to gain weight no matter what they do. That's a distortion, and it doesn't help.
The fact is, a lot of people have genes for one disorder or another. I've got PCOS, and it very nearly got out of control, until I consciously decided to take the matter in hand and do everything I could to get healthy. A person with diabetes or hypothyroid is in a similar situation. In fact, now that I think of it, most diseases and conditions have some sort of genetic component-- including cancer, arthritis, MS, etc. etc.
Does that mean the patient with any such disease is a helpless victim? I think not. You and I may have various genetic predispositions, but we also have the power to affect our health outcomes to a profound degree, sometimes with diet and exercise alone.
What Dr. Friedman is saying, it seems to me, suggests we are all helpless in the face of our genetic destiny. Here's his statement again:
Quote:
"body weight is genetically determined, as tightly regulated as height. Genes control not only how much you eat but also the metabolic rate at which you burn food. When it comes to eating, free will is an illusion.
That kind of statement is totally irresponsible and unscientific, IMO. It's a radical overgeneralization from the data available. Particularly the one about genes controlling your metabolic rate. I can change that rate very fast, I assure you, just by hitting the gym hard for a couple of weeks. I'd have to eat more just to keep from losing weight too fast. And that goes for a lot of people, especially athletes.
In fact, it would be terribly interesting to know how many athletes have "defective genes" that predispose them to obesity. Or hypothyroid, or diabetes, or any number of other metabolic disorders. Or cancer. Hey, if I'm going to believe in any man, I'll take the courage and determination of Lance Armstrong over the fatalism of Dr. Friedman any time.
hmmmm... i'm not so sure i'd go so far as to say that his statement was 'irresponsible.'
i think his statement that "Genes control not only how much you eat but also the metabolic rate at which you burn food" is VERY accurate. IN THE ABSENCE OF ANY INTERVENTION such as exercise. it goes a long way to explain that point that we all discuss: if i'm doing ALL THIS EXERCISE and EATING SO FEW CALORIES, why am i not losing? maybe your genes let you burn more calories with exercise than mine do. and maybe my genes let me burn more calories than someone else's at the same weight and exercise level.
let's face it: if we all had metabolisms that balanced intake/output [like those people who can stay thin even without exercise and careful diet], we wouldn't have this battle.
as for free will being an illusion when it comes to eating, again, i'm looking at this as the situation in the absence of any intervention, in this case, a conscious decision to make significant changes. how many of us are often fighting TRIGGER foods? BINGE urges? are these battles because of a lack of 'will power' [whatever that is]? i don't think so. do they come from deep-seated pyschological issues? maybe. are they a learned response to a stressor? maybe. but what in our genes - which determine to one extent or another how we react and what we react to - sends out these signals that we have to battle?
we have all proven that we can WIN this, by hook or by crook- or even by surgery!, but in the battle to maintain, we ARE up against our genes, to one extent or another.
and that's an area that we really know nothing about.
and thanks for not tarring and feathering me....i really appreciate it!!!!
i think his statement that "Genes control not only how much you eat but also the metabolic rate at which you burn food" is VERY accurate. IN THE ABSENCE OF ANY INTERVENTION such as exercise. it goes a long way to explain that point that we all discuss: if i'm doing ALL THIS EXERCISE and EATING SO FEW CALORIES, why am i not losing? maybe your genes let you burn more calories with exercise than mine do. and maybe my genes let me burn more calories than someone else's at the same weight and exercise level.
Every single biology student on this planet will tell you that many, many factors go into the "metabolic rate at which you burn food." And it's not a number that's cast in stone, it changes from day to day, as a constant adaptation to the environment. Put a person in a freezing environment, and she starts to shiver, which burns calories. But her in a hot environment, she starts to sweat. It even changes according to mood, because if I get really pissed off, my heart rate goes up, I start sweating, flexing, and I get ready to "fight or flight!" My metabolism adapts to my needs immediately.
But an overweight person, especially one who has been overweight for a very long time, has a "feedback loop" effect that makes weight loss that much harder. Being overweight makes it harder to move, so you move less, and move more slowly. I'm talking about the activities of daily living, here, not necessarily planned exercise. Less movement over many years translates to a lower metabolic rate overall, which tends to make you store food as fat rather than burning it. Eventually you get to the point where you can't move well and you're not burning much, either. So you get fat on few calories.
Repairing that situation takes YEARS, --really-- years, because the whole body almost has to be rebuilt, along with any tissue damage related to being overweight, such as kidneys, liver, etc. So you may very well not see any weight loss when starting an exercise program. I lost 30 pounds in my first 2 years, but that's 1.25 pounds a MONTH! Not much at all. But I accepted it because I wanted my whole system to be functioning in a normal, healthy way, so I had to let the healing process happen cell by cell by cell. Once my body had rebuilt a more normal metabolism, it "allowed" me to lose faster. So it's true, I have a faster metabolism than many obese people. But that wasn't always the case. I helped my body BUILD a faster metabolism over 2 years of conscious, steady effort. And if I had not made that effort, I would surely have laid the groundwork for a slower and slower metabolism every single year, with more and more weight gain.
It's going to be harder still for a person who has been overweight for decades, because the body's metabolism is that much more damaged. But that doesn't mean the body can't heal, to a remarkable degree. It might take a person 5 years or more to repair the metabolism, but that effort is not wasted, even if it doesn't "show" for years.
And as far as the psychological issues go, there may very well be a genetic factor there, too. But what of it? I may have the genetic disposition to homicidal psychosis, but I don't "have" to express that genetic tendency by murdering my fellow man. I may have a genetic tendency to depression or binging, but I can get myself to a shrink, I can take meds, I can act. Day by day. I may still have a disorder, heck, I do have a disorder, I'll always have PCOS with it's tendency to obesity. But I don't have to give in to it.
But I don't have to give in to it because I believe I have free will. It's the fundamental belief in free will that drives positive action, in the weight loss arena as well as in many other areas of life. The belief in free will over fatalism and determinism gave us both the scientific method and modern democracy itself. So a scientist, of all people, who tells me that "free will is an illusion" is being very, very irresponsible indeed.
And here's the ultimate evil place where this type of nasty Social Darwinism leads: if all these overweight people have bad genes, and they can't be fixed, then maybe we just shouldn't have them in the gene pool at all. After all, fat people cost taxpayer dollars and they're lazy and don't work, so why should they be around mucking up the efficiency of the State? You see where I'm going with this: this doctor is just another nasty outbreak of Social Darwinism-- the very basis of Fascism in our time.
There are always forces who will tell us we are "fated to fail" because of our genes, our sins, our neuroses, or our class. There are people who say we're no good, it's no use, give up, give in. But that's not true! It will never be true.
It was a group of democracies with the "illusion of free will" who led the fight against Fascism the last time around. Millions of ordinary, genetically flawed mere humans, making mistakes every day, beat back that horror. They died. They won. You can win.
OMG!!!!! you are TRULY fabulous... and taking that social darwinism to its logical conclusion: we will ALL be encouraged to die off because we ALL have something wrong with our genes. oh yes. that's it... DUH... we're ALL programmed to die!!!
All I can say is that I am in awe of this dialogue and I'd much rather have coffee with the two of you than tar and feathers. Thank you both for the thought-provoking article and insights. Much to think about here. It's not a simple issue, is it? Of course, since we LIVE it every day, we know there's no easy answers.
BTW, Jiff, I just went and looked at the Chicago pictures and pink is your color, dahling.
