Pathogen from gut of obese human causes obesity in germfree mice
nature.com
nature.com
It works kind of like this:
You eat too much refined/processed food, that is high in sugars of any kind, especially complex polysaccharides and the food is not fully digested by your stomach + small intestine, and ends up in your large intestine. This surplus of sugars provides abundant food to your billions of gut bacteria, and they start to grow out of control, and mutate. Those mutated bacteria now dump their toxic waste by-products into your body.
Following restricted diets that are intended to reduce the food supply to your gut bacteria colonies is a valid and often the only successful way to treat the conditions caused by this influx of bacteria and toxins.
Antibiotics of any kind are simply too broad a weapon - they will attempt to eliminate everything which will result in other imbalances. The food we eat every day is the most important factor for intestinal and therefore overall health...
[1] This book is helpful: http://www.breakingtheviciouscycle.info
This is why weed reduces one's risk of diabetes and also often helps obese people lose weight.[1] For what it's worth, you can now actually (supposedly) buy CBD (supposedly) legally online:
CBD is one of the more common non-psychoactive cannabinoids in marijuana, and it is responsible for many of the anti-inflammatory benefits. While more research is needed, lots of people are reporting the same sorts of benefits that this research is reporting, but without the obvious negative side effects of taking anti-biotics. (Whether there are negative effects of longterm CBD use is anyone's guess, but as far as I know nothing has been discovered so far.)
[1] http://blog.norml.org/2012/12/12/study-cannabis-associated-w...
Cannabidiol is most definitely illegal in the US, too. That DixieX site you link to is just hemp oil products -- no psychoactives.
Also the amount of cannabinoids DixieX is citing is actually the minimum CBD content. They show their lab results on their Facebook page. The reason the don't cite the CBD content is because CBD is illegal, but hemp products are legal if the THC content is below a certain level. They're trying to play it off as a legal grey area and are taking a calculated risk.
And I don't mean 25-50% of the plant mass, I mean CBD will often make up 25-50% of an extract. (Wikipedia has my back with a 40% figure: http://en.wikipedia.org/wiki/Cannabidiol)
Fiat non-psychoactive, not fiat legal. It's definitely still illegal. But it's included on all the lists of non-psychoactive cannabinoids.
As for that journal article, it's behind a paywall even though it's from 1940 so I can't comment on it. But if you look at the menus for any dispensary that tests for both THC and CBD, you'll see that CBD is rarely a significant percentage of the cannabinoids, e.g.
Or am I missing something here? Someone with a bit more knowledge of organic chemistry and biology can feel free to chime in here.
I'm not disputing that fibers help "push things along" by absorbing water, adding bulk, etc. But are we overeating them? Do we really need to be making a conscious effort to add or supplement them in our diets?
FWIW: I'm not pushing some sort of anti-fiber claim or agenda here. I'm neutral on the subject. I'm simply inquiring.
My exhusband is part Viking, basically. They ate a lot of meat, in part because they lived so far north that you couldn't grow enough plantbased foods. My ex ate a very high meat diet. Our sons eat less meat than he did, but they are 1/4 Norwegian whereas he is 1/2. Still, they tolerate more meat in their diet than I do. I am convinced there is a genetic component here.
(Yes I know: Anecdotal and all that.)
Even the site you link to talks about lamb and other meat being a regular part of the Viking diet. In Europe, the children's rhyme "peas porridge hot, peas porridge cold" refers to the common practice of serving some sort of hot meal at lunch and cold leftovers at dinner. Peas porridge was likely either vegetarian or had very little meat in it. When I had some poetry class in college, it pointed out that "Greasy Jane stirs the pot" suggested a servant in an upper class household preparing a dish containing meat, which was something of a luxury item. The "greasy" imagery indicates it contained meat. Peasants could not afford meat on a routine basis. Further back in history, Romans ate far more eggs than meat.
My ex was a history buff. We talked a fair amount about things like that.
Sorry for the sloppy wording earlier.
Eskimos' diet is not a parameter to anyone other than Eskimos. Those populations have adapted to survive on those diets, and even then, with drawbacks to health and life expectancy. Also, Eskimos are certainly the exception, saying a lot of cultures live on meat only is a stretch.
> I'm not disputing that fibers help "push things along" by absorbing water, adding bulk, etc. But are we overeating them? Do we really need to be making a conscious effort to add or supplement them in our diets?
Fibers are integral part of a diet with minimal amounts of fruits, vegetables or grains. You don't need to add fibers unless all you eat is processed food.
"Created?" This is definitely the wrong concept to refer to here. The correct sentence is (correct because it takes mountains of scientific evidence into account):
"We were not evolved to evacuate bricks."
Essentially my question is this: A fresh vegetarian diet is going to be high in the complex polysaccharides that you mention. So why are vegetarians statistically thinner than the average population, if these complex polysaccharides are wreaking havoc on their digestive systems?
This whole question breaks down if I'm mistaken about the definition of complex polysaccharide. Thanks.
But at least your questions are in an area where I can maybe help out. Carbohydrates are just what the name says: carbon molecules with hydrogen and oxygen attached to them. Complexity of carbohydrates is a spectrum, with formaldehyde being at one end and ultra-complex molecules such as huge amino-saccharides or polymers on the other. Saccharides are sugars, who all belong to the carbohydrate family. As far as nutrition is concerned, most sugars are based on the glucose molecule, that's a unit with 6 carbon atoms typically wound into a ring with six or five edges. Chaining those rings together makes polysaccharides.
Overly long saccharide chains only fit into our sweetness taste detectors at one point, that's one ping each from a huge number of saccharide rings. Smaller sugars (like dextrose) cause a lot more signal by fitting better into the detectors, that's why they tend to taste sweeter. Polysaccharide disassembly starts with enzymes in the saliva of the mouth, that's why some things get sweeter when you chew on them for a while. For people who don't gobble down their food to quickly, that means only small sugar molecules even arrive in the small intestine, where they are further split into monosaccharides which can finally be resorbed through the intestinal wall. The small intestine is ill-equipped to handle longer chains, though, that's why they pass into the large intestine. In itself that's not a problem, but if there is a _regular and large_ amount of this stuff in the large intestine, it will attract microbes that live off it.
So if a lot of sugars regularly make it into the large intestine, chances are there will be a population of bacteria (or worse: funghi) taking advantage of that. It's not like the bacteria cause obesity as some articles suggest, their presence is itself a symptom of a nutritional problem (such as too much intake). Of course sometimes these colonies cause other problems like inflammatory reactions that eventually necessitate flushing them out. But saying those bacteria cause obesity is just the new "I'm not fat, I'm big boned", a mechanism designed to deflect the responsibility for obesity away from a person's behavior.
The digestive system is designed to survive and thrive on a variety of food, but there is also a lot that can go wrong. It's not "evil complex polysaccharides" wreaking havoc and producing energy out of thin air to make people fat, it's (as always) people eating too much who are bringing this upon themselves.
One good thing food cults such as the different "nutrition plans" and "strategies" can do, however, is making people reflect on their habits and generally lower their energy consumption. To make it extra clear: I don't think vegetarianism is one of these cults, but it too causes people to eat more carefully.
this article suggests the bacteria are causing obesity, and explores it by having a flora transplant into a regularly non-obese mouse that causes obesity in that mouse.
...It's not like the bacteria cause obesity as some articles suggest, their presence is itself a symptom of a nutritional problem (such as too much intake)....
How do you square this with the claim from the original article that giving mice a toxin produced by gut bacteria (Lipopolysaccharide endotoxin) causes obesity and insulin resistance, and that "[m]ono-association of germfree C57BL/6J mice with strain Enterobacter cloacae B29 isolated from the volunteer’s gut induced fully developed obesity and insulin resistance on a high-fat diet but not on normal chow diet, whereas the germfree control mice on a high-fat diet did not exhibit the same disease phenotypes"?
It's not "evil complex polysaccharides" wreaking havoc and producing energy out of thin air to make people fat, it's (as always) people eating too much who are bringing this upon themselves.
Why, then, do some people become obese when they eat as their instincts tell them, and others do not? For example, I eat whenever I'm hungry, stop when I'm full (or even overfilled), snack frequently while working (mostly nuts, dried fruits, and sometimes Fritos), and yet remain thin, while others eat carefully and remain obese. What's the difference?
I think the article makes some dubious claims, mostly centered around a single human volunteer (!), using a mice experiment to back that up - I'll remain skeptical until it can be reproduced by another team. The inclusion of Traditional Chinese Medicine alone as playing a key role to curing the condition is a huge tipoff that something is amiss.
But even taking all those doubts into consideration, let's entertain the hypothesis that this bacterium does produce signals that make a person eat more. It's possible. But you still acquire the bacterium by eating too much in the first place. It simply couldn't colonize you if you didn't.
> Why, then, do some people become obese when they eat as their instincts tell them, and others do not?
My personal opinion is there are two big factors. First, lifestyle. People eat too much because that's simply how they live their lives. It may be because they only have access to high-calorie food, or because everybody around them eats too much, or because they have made a habit of eating too much. The second group (which I'm a part of) is worse: for them, food is an addiction. Many of them may already eat "healthy", high-quality stuff - so moving away from fast food does nothing for them. Eating simply has the same effect on them as drugs do on other people.
I invite you to do the following experiment at home. Get yourself a petri dish and fill it with sterile Agar. Then wash your hands. After that, make some fingerprints in the Agar. Incubate for a few days. You'll be surprised.
I really don't know how to discuss this with you. You blame everything on "behavior" then claim to have a food addiction. Your view strikes me as rather handwavy, while dismissing a possible specific cause for some individuals: exposure to a pathogen. This is not the first time I have heard this, so I doubt that there is only one study.
No, I likely cannot convince you of anything. But you are equally failing to convince me.
> You blame everything on "behavior" then claim to have a food addiction.
This is certainly a gross mischaracterization, and I can only assume you're using it to aggravate me somehow? I invite you to read again what I actually wrote regarding this and several other different issues. I'm not sure if you're just trying to troll me or if you actually want to have a discussion, but I'll just assume you're not trying to behave like an asshole on purpose and move on.
You misunderstood my point about how gut bacteria take hold in the first place. Mostly, enterobacter strains are something which lives inside people's guts anyway. There are several pathogenic strains but this is not what the article is talking about. We're talking about an organism that lives off what you feed it. There is nothing hand-wavy about that. It's just a fact. Just as food intake determines individual weight-gain, the availability of nutrients in combination with its environment determines the amount present of a given gut bacterium. It's also a fact that our daily environment is rich in gut (and other) bacteria.
> It didn't just magically pop into existence from the ether because "you ate too much".
I failed to explain this properly then. People have a certain mixture of different gut bacteria inside them, they also tend to acquire them in the "hand-wavy" manner described above. Now, a bacterium needs to eat in order to survive and reproduce. Different bacteria are optimized to eat different things in different environmental conditions. If E.c. colony size is indeed statistically larger in obese people (a point that still needs to be shown conclusively), the reason for that will be that they get a lot of nutrients under favorable conditions. There is nothing magical about it, just basic biology.
> No, I likely cannot convince you of anything. But you are equally failing to convince me.
It depends where you're coming from. I'm not even sure we're speaking the same language, otherwise I can't explain how some of my points could have come across in such a distorted fashion (even taking into account my infamous inability to communicate). In some sentences you portray my views as exactly the opposite of what I actually said. I really mean it when I say I'm sorry we're at this point, but I'm also unsure what I could have done better.
Also, a meta point: have we done this before? I'm not sure.
There are a lot of people who are either obese and have tried everything and can't lose weight or are thin and have tried everything and can't gain weight. But your opinion is "some people just eat too much", apparently with no real cause. Equally, you are comfortable with "bacteria are everywhere -- if you eat too much you can grow them". You really aren't willing to admit that different people carry different bacteria due to exposure of some sort and this might be a factor in why some people "just eat too much". In your view, the eating too much has to precede the bacterial overgrowth. Seems awfully convenient. But people don't get AIDS or anything else because "well, germs are everywhere". They get AIDS from an infected lover or contaminated needles or due to exposure to some other specific vector. You can "eat too much" all day long and if you weren't exposed to a specific pathogen, you won't grow it.
I have lost enormous amounts of weight in recent years. I never counted calories. I had zero goal of losing weight. My only goal was to kill off the overgrowth of germs which were killing me. Last year, I lost so much weight, so rapidly that total strangers began stopping me in public places and asking me how I did it. I did not feel like getting into my medical situation, so I made vague noises about dietary changes and walking a lot. However, I am a sample of one, so that will also be dismissed by most members of this forum as "not scientific".
I really doubt this discussion will do much for either of us. I regret making my initial post. I really should know better by now, but my recollection was that you are a very reasonable member of the forum. So I chanced it.
Please have a good evening.
Having discussions with smart people who disagree with me is one of the reasons I enjoy HN so much. But it is no fun if key points are misunderstood, ignored, or repeated out of context. So I really wanted to find out why this was happening.
I won't repeat things I said earlier, but as a summary: I really don't think there can be any contention about the growth mechanism of bacteria. As a point of personal opinion, I have voiced doubts about the study and its methodology. I also expressed a personal theory on two major factors that make people fat, one of which I (somewhat regretfully) tied myself to.
> There are a lot of people who are either obese and have tried everything and can't lose weight or are thin and have tried everything and can't gain weight.
Those two are very different. There is absolutely no doubt that obesity comes from excess intake of energy. None. Some diseases cause the body to grow excess tissue or to store water excessively, but that's not obesity. Failing to gain weight, however, can be down to a lot of factors both behavioral and biochemical.
> But your opinion is "some people just eat too much", apparently with no real cause.
I did not say that or anything even resembling that.
> Equally, you are comfortable with "bacteria are everywhere -- if you eat too much you can grow them".
It's a simplified summary, but it's fair.
> In your view, the eating too much has to precede the bacterial overgrowth. Seems awfully convenient.
I don't think that's convenient for anybody. It's just the only way you can multiply microorganisms to any significant numbers.
> But people don't get AIDS or anything else because "well, germs are everywhere".
That one leaves me a little speechless. HIV is a virus, it doesn't have a metabolism of its own. It's a rogue piece of software that hijacks the human runtime, so to speak. That's an exceedingly bad example, but there are bacteria out there that would be much better suited for the point you are trying to make: Take MRSA for example, because it grows and lives off living human tissue. Contrast that to the enterobacteria we were talking about originally, they live off our waste products. So it's clear why, for example, E. cloacae is directly related to the food you eat, but MRSA is not. MRSA attacks the body and provokes an immune response, E.c. does not. That's also the reason why MRSA is something you contract, whereas E.c. is something which in all likelihood you already have. It's worth repeating that enterobacteria actually lend essential assistance to our digestive system.
> My only goal was to kill off the overgrowth of germs which were killing me.
Now I understand so much better where you're coming from. We could have saved a lot of time... Whatever works for you is fine, I didn't want to sabotage that - nor did I have any idea why my dry descriptions provoked such a visceral response, but now I see why.
> I really should know better by now, by my recollection was that you are a very reasonable member of the forum.
Well, I do think this exchange was worth pursuing in retrospect. I do try to be reasonable, though of course I often fail. I'll just have to try harder :)
I really don't wish to discuss this further in this thread. Again: Please have a good evening.
Also, it's actually morning here in Europe. In the spirit of a new day: don't ever shut up, but do lighten up.
How did strangers know that you'd lost weight?
I am tall with naturally curly hair and apparently striking features. It isn't terribly uncommon for people to notice me whom I never noticed. That sort of experience goes back at least to high school, where people recognize me and I have no clue who they are. (Edit: This is probably compounded by my crappy eyesight. I sometimes don't recognize people whom I do know until I am practically on top of them.)
I really really want to see good quality food diaries for people who claim to eat little but not lose weight. I'd also want to see how much exercise they do. (And not even actual exercise, just how much they move around during the day.)
This trend correlates well with the above idea, since smaller meals means that the sugars should be absorbed before the large intestine, thereby further robbing the bacteria of their food.
It would also explain the opposite effect - that eating larger meals makes losing weight harder, since the larger quantity of food has a better chance to get to your large intestine.
Refined/processed food should be eaten in minimal quantities because it spikes blood sugar and causes insulin fatigue, which in the long run causes Type II diabetes.
And I'm in medical school, so yes, I do know what I'm talking about.
What precisely does refined/processed food mean, from a chemistry standpoint? Is there a particular common process that transforms my homegrown lettuce into "refined lettuce"?
You realize those bacteria are living off the fat, sugar and protein you consume right? They are essential to our ability to utilize the chemicals we get from these macro nutrients.
>Refined/processed food should be eaten in minimal quantities because it spikes blood sugar and causes insulin fatigue, which in the long run causes Type II diabetes. True, but this also an increasingly old school and one dimensional way of thinking about how type II develops. There are a host of genetic and environmental factors that effect an individual's response and eventual tolerance to insulin.
Sadly, being in med school does not guarantee you "know what you're talking about", in fact, even after you get to wear that white coat you'll probably realize you know way less than you could ever imagine. The perception that kind of attitude creates only narrows our minds and hurts our patients.
I'm done with med school.. and I realize on a daily basis I still have no clue what I'm talking about :)
They also disallow milk, but allow cheese. My ancestors didn't spend thousands of years evolving lactose-tolerance for nothing, you know.
Strong claims require strong evidence.
1. Two independent facts from the experiment: A pathogen that causes obesity (in mice) seems to be active in some obese humans.
2. Severely restricted diet seems to powerfully reduce the population of this organism.
I doubt that these facts are unrelated. It's classic host-parasite behavior. The pathogen depends on high calorie intake in its host, and therefore engineers that behavior (somehow).
Further there is no reason to make the leap that the only or best way to counter this pathogen is through diet. It's not impossible that a targeted antibiotic that eliminates this pathogen would have an effect on the body composition of the host.
they have done studies though to see if doing a guy bacteria transplant from a healthy person to an obese person would change their weight, I believe there wasn't any difference found for weight loss but that there was some hope in using it as a treatment for diabetes. I'd have to look it up.
This particular study though I wonder if it was the calorie restriction, the weight loss or the content of the diet that caused the changes to happen.
"After 9 weeks on the WTP diet, this Enterobacter population in the volunteer's gut reduced to 1.8%, and became undetectable by the end of the 23-week trial"
So the thesis is that this bacteria lives in obese people's gut, and it makes them more obese. But once they diet to a point where they are not obese, the bacteria dies off? I wonder if they are going to try a diet + anti-biotic treatment, diet + placebo trial on two obese patients to see if it improves their chances to get back into a regular balance.
But before you think the researchers left a big hole in their research, remember that the addition of bacteria makes mice obese. Now if we could just try that on humans...
edit: As pdx points out below, not antibiotics, pre-biotics. Big difference.
Could be just the caloric deficit, could be the bacteria. It's an interesting correlation and should be explored further.
I believe the theory is the reverse - by killing off the bacteria, the person becomes less obese.
Anti-biotics probably won't work as well as you hope because they kill all the bacteria in the gut - good and bad - which will just create more digestive problems.
Dietary intervention and sampling. This volunteer was given a diet composed of whole grains, traditional Chinese medicine and prebiotics (WTP diet) for intervention. He was given 4 cans of gruel per day as staple food contract prepared in the form of cooked porridge (370 g wet weight per can) then canned by a food manufacturer (Shanghai Meilin Meida Food Co., Ltd.) for 23 weeks. Each can contained 100 g dry ingredients (59 g of carbohydrate, 15 g of protein, 5 g of fat, and 6 g of fiber) providing 336 kcal energy (70 % of carbohydrate, 17 % of protein, 13 % of fat). Fresh fecal samples were collected with 4 or 5 weeks intervals. Whole blood and serum samples were collected with 0, 9 and 23 week (0d, 9w, 23w). All samples were immediately frozen on collection and stored at -80 °C for subsequent analysis.
A magic bullet in this case would be something that allowed weight reduction with no restriction of calories. From experience, restricting calories long-term is very difficult.
But hey, perhaps they can get a study going on it to determine the causal relationship between the endotoxin, human obesity, and intestinal flora.
"Tank: Here you go, buddy; 'Breakfast of Champions.' Mouse: If you close your eyes, it almost feels like you're eating runny eggs. Apoc: Yeah, or a bowl of snot. Mouse: Do you know what it really reminds me of? Tasty Wheat. Did you ever eat Tasty Wheat? Switch: No, but technically, neither did you. Mouse: That's exactly my point. Exactly. Because you have to wonder: how do the machines know what Tasty Wheat tasted like? Maybe they got it wrong. Maybe what I think Tasty Wheat tasted like actually tasted like oatmeal, or tuna fish. That makes you wonder about a lot of things. You take chicken, for example: maybe they couldn't figure out what to make chicken taste like, which is why chicken tastes like everything. Apoc: Shut up, Mouse."
It's a strange notion, that bacteria still own the earth, but we are host to more bacteria than we are our own cells. It's such an interesting yet scary thing to think about - does higher order life exist solely as vessels for bacteria propagation?
It's not too scary a though though -- taking the evolutionists point of view, there is no "underlying" reason that higher order life exists. It exists because the processes of natural selection have enabled it to exist and reproduce.
If bacteria contribute to the survival and reproduction of our species (they do), then they are simply part of the process. It goes both ways. We exist and reproduce because they help us do so, and they exist because we provide a nice host. One hand washes the other...
"The endotoxin-producing Enterobacter decreased in relative abundance from 35% of the volunteer’s gut bacteria to non-detectable, during which time the volunteer lost 51.4 kg of 174.8 kg initial weight and recovered from hyperglycemia and hypertension after 23 weeks on a diet of whole grains, traditional Chinese medicinal foods and prebiotics."
"The obesity-inducing capacity of this human-derived endotoxin producer in gnotobiotic mice suggests that it may causatively contribute to the development of obesity in its human host."
If even some cases of metabolic syndrome can be linked to a simple bacterium -- and cured simply by killing that bug -- this will have the economic and medicinal effects of, well, not the eradication of smallpox, but pretty close.
Scientifically it's the equal of marshal and warren finding the bacterial cause of peptic ulcers -- and they got the Nobel for medicine for that.
Heart disease kills far more people than smallpox ever did. You have a 20% higher chance of heart disease if overweight.
Ergo, bacteria may be driving obesity.
> The volunteer lost 30.1 kg after 9 weeks, and 51.4 kg after 23 weeks, on a diet composed of whole grains, traditional Chinese medicinal foods and prebiotics (WTP diet, Supplementary Information; Supplementary Figure 1), with continued amelioration of hyperinsulinemia, hyperglycemia and hypertension until most metabolic parameters improved to normal ranges (Table 1). After 9 weeks on the WTP diet, this Enterobacter population in the volunteer's gut reduced to 1.8%, and became undetectable by the end of the 23-week trial, as shown in the clone library analysis (Table 1; Supplementary Figures 2 and 3).
"Gut bacteria are the cause, I can do nothing"
"It's genetics"
No, it's calories in vs calories out. Maybe these bacteria make you want to eat more, maybe they somehow pull more energy out of food than normal gut flora somehow, in the end it doesn't really matter. Eat less, lose weight; eat more, gain weight; the definition of 'more' and 'less' are individual.
Finally, I get tired of arm chair nutritionists going off and telling people that it is all about eat less and exercise more. Obesity isn't a one solution fits all problem and it is only arrogance to think otherwise.
This article points out that there is yet another possibility to look into. Yet again, something that works against the old mantra eat less exercise more. We simply still don't know enough about the human body. There are going to be many more surprises for the obese population. In the mean time we have to combat our weight and jerks who think they know everything.
1. increase iodine intake in some fashion
2. cut out all wheat products including whole grain
3. Atkins-style diet with restricted carbs in general
4. increased use of ginger as a spice or in tea (some believe it helps increase metabolic rate).
5. high intensity interval training (you mention exercise).
Everyone I've ever known or read about has gained weight by eating more and lost weight by eating less, again less and more vary from individual to individual but the fact that calories in = calories out for maintenance is a law of physics.
But this article doesn't appear to be saying that. So your attack in this thread is uncalled for. Generally, people trying to find a solution to obesity (like these people seem to be) are not in the obesity is a healthy lifestyle camp. They appear to be in the obesity is a problem we should look into camp.
Until you brought it up, nobody had said that this article means fat is a-okay. In fact, the article treats obesity as a disease, so it's the reverse.
If you ever find yourself getting mad at people for what they might say, you are definitely dealing with your own issues.
Doubly so if you take the time to rebut these imaginary enemies in a public forum.
That isn't to say that there are no genetic differences that influence body weight, there certainly are! It's just that the mechanism isn't energy efficiency, it's genetic factors that influence how much a person eats and how active a person is.
Being morbidly obese and healthy? Very unlikely to be true. Morbidly obese and ok with? That's 100% legit, it's your body and you are free to do as you please.
> No, it's calories in vs calories out. Maybe these bacteria make you want to eat more, maybe they somehow pull more energy out of food than normal gut flora somehow, in the end it doesn't really matter. Eat less, lose weight; eat more, gain weight; the definition of 'more' and 'less' are individual.
Except we already have strong evidence to suggest that calorie deficit diets do not have a causal relationship with weight loss and that those diets are hard to maintain over a long period of time, leading people to have yo-yo issues with their weight.
> I don't care if someone is fat.
When you call fat acceptance folks loons, I don't think you can say that with a straight face.
When obese people fly they rarely buy two seats. They can pretend that their state of health doesn't affect the people around them, but they are deceiving themselves.
I fit in a standard airline seat without hanging over the armrest into the next seat, so why should I pay for it? So yeah, my state of health isn't particularly good right now, but it actually isn't affecting anyone I fly with.
Blanket generalizations don't do anyone any good.
Of course there will always be those who insist on missing the forest for a tree or two -- the forest in this case being my attempt to keep in mind a wholly unoriginal thought: we are not isolated, and the state of our bodies and minds redounds not only to ourselves.
I don't know if you meant something else here, but of course eating less causes weight loss.
This article could shed more light on the obesity problem and solutions to it. For example, it could very well be that our intestinal flora influences our own decision making. There is at least one known case of a micro-organism that does: the toxoplasma gondii.
It is also apparent that people become addict to sugar and that definitely would influence decision making.
On top of that, our behavior is in great extent influenced, if not determined, by the chemistry of our bodies. It may very well be that chemical imbalances caused by a combination of diet, intestinal flora and hormones, causes obesity.
In short, saying that it is simply a problem of calories in and calories out is a gross over-simplification of the problem. Science is way beyond that point.
Stop leaving out the fucking calorie absorption efficiency factor if you don't want to sound like just as much of an idiot as the people you are complaining about.
Gasoline has a shitload of calories in it. You will definitely not get fat drinking it.
There is literally no one in the field who thinks this is true or ever did. There is certainly an argument about how widely the absorption efficiency varies from person to person, but that's not the same thing as the assertion that it is simply 100% all the time for everyone.
There is a fair amount of evidence indicating both genetic and epigenetic contributions to obesity.
http://www.ncbi.nlm.nih.gov/pubmed/12574619
http://www.ncbi.nlm.nih.gov/pubmed?cmd=Search&db=pubmed&...
http://www.ncbi.nlm.nih.gov/pubmed?term=obesity%20epigenetic...