I think this is a great example (well, counter-example) of how screwed up nutritional research has been. We spent the last 30 years trying to shoe-horn the low-fat-low-cholesterol-is-everything, when we had no idea how the body works.
It is great to see research like this happening. I've followed nutrition for a long time as I've dealt with chronic weight problems, and things have gotten much more interesting (read: less parroting of the "party line" and more new research) in the last 5-8 years.
It's unfortunate that so much time was lost, because it takes 10-15 years to go from mice to people. Now if we could only get some experiments with decent controls, so we can actually learn something.
This research has been around for 30 years. There was one case in the 70's where obese adults were given controlled calculated diets in a hospital and one of them gained weight anyway as her gut flora was so good at extracting nutrients.
It isn't screwed up. In broad strokes, we understand very well. Calories in - calories out = weight gain. This has been demonstrated in thousands of lab studies.
That's about 85%. Now we are just figuring out details and special cases.
Someone with a (big enough) caloric deficit will lose weight, sooner or later
Someone with a (big enough) caloric surplus will gain weight.
Big enough is because the body will adapt its metabolism to small (and one shot) caloric surpluses/deficits.
But what happens beyond that is very interesting. And so beyond the 'food pyramid' and "conventional knowledge" it's not funny.
Oh and by the way, protein diets (usually) work. Why? Caloric deficit (of course) promoted by modified hunger sensation (that's another piece of the puzzle).
Losing weight is immaterial. Keeping weight off is what matters, and pretty much every study for the last 100 years has shown reducing calories does not keep weight off. Just the opposite: reducing calories invariably leads to a gain of 5-7%.
In a lab with controlled portions people lose weight.
Outside the lab where they are free to revert to gluttony they also typically revert to their original weight (exactly as harris/benedict predicts).
Cals in/cals out works fine. But only if you actually work it. I've successfully used it myself to modulate my weight in both bulking and cutting cycles, as well as reducing my weight from obese to healthy back in the day.
It is not thermodynamicly impossible because your body is not a fixed system. It can (and does) regulate energy usage based on how much energy it is receiving, what kind of energy it is receiving, what the environment is (primarily reflected through cortisol and stress), etc. all of these intertwine, making it nearly impossible to look at calories alone to measure, well, much of anything.
Reducing calories causes the body to reduce its calorie usage and starts pumping hormones that cause fat to be retained and your desire to eat to increase, until the hormonal system forces an "override" where you have to eat more. Sure, there are some people who manage to overcome the hormonal override, but they are by far the exception and not the rule, and any weight loss program that tries to override the body's built-in protections against starvation (which go back who knows how long and exist in pretty much any animal) is a recipe for failure.
The keys to the whole hormone cycle are insulin and leptin. Any successful weight loss regimine will have to address those hormones, which calorie reduction "inflames" rather than "pacifies".
Yes, you are right (and explained it quite nicely)
But there's an absolute minimum of calories the body need to operate, even at 'low gear' (I'm not sure, but this is around 1000kcal per day), so if you're really limiting the calories below a certain point you will lose weight.
Apart from that, if you're trying to lose weight, but not actually consuming less calories, of course you may have a weight gain.
Fair enough, but I would say that's only useful if you are wanting to lose a little weight before a cruise or want to get into a lower weight class for a wrestling match. Weight loss that doesn't "stick" is probably more dangerous than not losing, because it tends to focus as visceral fat instead of subcutaneous fat; and, unfortunately, study after study[1] show that dieting does not result in long-term weight loss[2].
2. My anecdotal story, I tried restricting calories for 15 years with the result of hitting 350+ pounds. Seven years after a gastric bypass, I've found low-carb to be the only way I can maintain my weight. Even with the gastric bypass, I can't limit myself to the 1200 calories or less a day I would need to maintain (and I feel like crap). Low carb, I never have to even think about the number of calories (I trade one number for another :) and my energy goes up.
I was experimenting with this and, when the results were positive, it really drove me to understand why the results are positive. I'm (slowly) starting to get an understanding of the biochemistry involved (that is a lay understanding, for sure!).
The fact that you say calories in == calories out is typical of my complaint. Follow the metabolic pathway of glucose versus fructose in the liver and you quickly see a calorie is not a calorie, and many types of calories are much worse for you than others. Look at how ketones impact cell efficacy (admittedly, early results in rats hearts) and contrast that with conventional wisdom of "ketones are poison" and you can see the study of nutrition and obesity has not followed the study of biochemistry and endocrinology at all.
I think the obesity epidemic demonstrates quite clearly how incorrect our understanding of nutrition has been.
The relatively recent acknowledgement of the role of the insulin response to refined carbohydrates is a major example of how "calories in - calories out = weight gain" is far too simplistic a view.
> I think the obesity epidemic demonstrates quite clearly how incorrect our understanding of nutrition has been.
No, I think it's an excellent demonstration that for most people 'calories in' is the primary driver of weight gain.
There's not an epidemic of people getting fat from eating 2,500 kcal per day but which is mostly refined carbs.
Most people who are overweight are eating far more calories than that, usually as sugar or fat. They have problems with portion control, and recognising just how much they are eating.
I'm being careful to say 'most' because as this research shows there's a small number of people who might be affected by other things.
As another poster points out elsewhere in this thread - that's like saying that fuel consumption is the primary cause of auto accidents.
They have problems with portion control, and recognising just how much they are eating.
Nutrition is about far more than calories in. Controlling cravings through controlling the insulin response is enormously important. The types of foods that make up calories is enormously important.
The body isn't a closed thermodynamic system. You have to take into account metabolism, the human waste that is eliminated, the satiety of the foods consumed, etc. Not to mention the make up of bacteria as evidenced in the article.
I disagree. There are ways of dieting in which your fat composition declines, but your muscle composition stays the same. Most diets, where you simply reduce the number of calories going in, results in a weight loss of 50% fat and 50% muscle (ie: if you lose 2 pounds, 1 pound is fat and 1 pound is muscle).
You're also making the assumption that less fat results in a healthier human being. that is also something that depends entirely on the nutrient content of your food. You can lose weight by eating nothing but small portions of white rice, but it's not going to result in a healthy individual.
I think most of medicine is like this. We really haven't advanced much beyond witch-doctory in a lot of therapies... we've found things that seem to help, by experimentation, but in a lot of cases we really don't understand why.
I've been digging deep into to biochemistry of the energy cycle this year and I'm actually impressed at how much we know. What I'm disappointed by is how little of that knowledge has worked it's way into the 60s and 70s diet dogma that "nutritionists" blanketed our country with.
The mouse studies, the C.fid studies, fascinating stuff. Would be a hell of a project to do flora studies. Perhaps we could blend it with Gate's new toilet initiative, press this button if you're you willing to enter a survey of gut flora and a chance to win an Amazon Gift card! Now please don't move while the swab extends ...
The whole gut bacteria thing is quite fascinating. It evolves depending on our diet. The intestinal flora of a fetus is boootstrapped with bacteria from his mother. Gut bacterias can get genes from ingested bacterias:
http://phenomena.nationalgeographic.com/2010/04/07/gut-bacte...
And this kind of symbiosis with bacterias is not limited to humans (the rumen of cows is filled with bacterias that break down normally undigestible components of grass such as cellulose.)
I bet research on this symbiosis will produce lots of interesting results!
For as logical a group as I perceive HN to be, any nutrition related article reminds me of the simple fact that most people can't assimilate new information when it conflicts with previously held mental models. For whatever reason, diet is something we get drilled into our head from the time we're very young. Even though most of it has been thoroughly debunked by scientific studies (cholesterol, the food pyramid, excessive cardio, saturated fat, wheat) people refuse to believe it. Every time, I see people trot out the same arguments (calories in/calories out seems an especially stubborn one).
So, my question is this - How do we communicate new science in a way that will change people's minds? Or should I just be content that the next generation might stumble on this stuff through a web search before what they are taught in school firmly takes hold?
I really don't understand arguments like this - the problem is that some people have digestive systems that are "too" efficient, and so the "solution" is to cripple their ability to properly absorb nutrients. It seems rather wasteful.
I don't know if you're thin or overweight. I'm fat, always have been. I'll admit to a past of bad eating habits that put me where I am. But the point is that we live with an excess of calories around us. If I have a certain kind of over-efficient gut bacteria helping me out, the survival mechanism in my situation supports the less-efficient variety. Too many calories, whatever their source, has a huge negative effect on my life.
Not quite. More like some people have "hoarding" digestive systems that refuse to let excess nutrients be expelled. I do agree that having people waste food is bad, but having unhealthy obese people is even worse.
Honestly who cares? It's not like the food saved will go to feed a starving kid in Africa or something. Food is rotting in warehouses already, so it' more of a logistics /distribution thing. That takes time to solve and is a totally separate issue from the medical one..of people dying and suffering from fat /obesity. Different groups can work on separate issues.
> That takes time to solve and is a totally separate issue from the medical one..of people dying and suffering from fat /obesity.
AFAIK, studies about deaths correlated or caused by being fat have been totally debunked and had nothing to do with body weight in the first place. To that end, one does not die from being fat and being fat doesn't mean you are suffering (except for how people and society treats you as a fat person).
Mouse studies always turn out to be a tease when it comes to weightloss. I say we skip all the probiotic piddling and go straight for human fecal transplants.
Unfortunately, it is hard to get researchers and patients to agree to get an enema of someone else's poo.
It's not that hard when patients are suffering and the treatment works. Fecal transplants are already being done for other disorders, and patients are demanding it:
Before people get too excited, remember, correlation isn't causality (aside: I never thought I'd get to be that guy on HN who says that).
It's just as possible that different microbial populations follow from obesity.
Actually, it seems more likely that this is the case, given that the populations change after band surgery.
And, as always, there is no biological mechanism so far discovered that transcends the conservation of energy and matter.
Given how hilariously silly any thread on diet becomes on HN (because for some reason saying "net caloric balance is the sole predictor of long term average body mass" drives people nuts), I believe I will sit this out to avoid getting a severe case of XKCD386.
> saying "net caloric balance is the sole predictor of long term average body mass" drives people nuts
Because it is like saying that fuel combustion causes car crashes. And then smugly congratulating yourself about how you have solved a major public health problem by prescribing a fuel shortage.
> It's just as possible that different microbial populations follow from obesity.
In which case transplanting the skinny microbes to a stout animal would make no difference. The research in question shows it does.
Does this suggest that maybe we should be sharing each other's poo to prevent our gut being dominated by a single bacteria?
And does that suggest, maybe, that obesity is in some way partly caused by modern hygiene and hand-washing preventing this from happening 'naturally'?
It seems ironic that, after decades of bleach and bacterial hand-wash, I might be 'cured' of my obesity by eating a capsule someone else's fecal matter.
Here's how to get rich quick: Open a Fecal Transplant Clinic. Let your clients choose from a pamphlet of slim & trim fecal source (I want that one), and for a modest fee they get the shape they want.
Could we see a legit probiotic capsule that is sold over the counter that has fat burning capabilities? so we identify the bacteria common in thin people and let fat people spend $$$ to acquire it?
I'd guess that the balance of bacteria depends more on whole-system factors, especially diet and personal chemistry/digestive-tract-structure. Unless a strain is completely missing, adding a few more of one kind might be unlikely alone to change the equilibrium.
Now, if you knocked out the old strains with antiobiotics, the repopulation might be more sensitive to the small amounts first reintroduced. These studies of a wasting disease in Africe offer more hints of the interplay of gut microbiome, diet, and antibiotics:
They say this explains why gastric bypass works, but from what I've seen, people who get gastric bypass can only physically eat a few calories per day in the beginning without terrible consequences. Eventually you can eat more, and I've seen the weight go back, so I'm confused why it would be bacteria.
They say it probably accounts for 20% of the weight loss.
Outline of the experiment:
Take a mouse model of human obesity. Divide your sample in three groups:
* Gastric bypass
* Sham surgery (fake bypass, the surgical equivalent of a placebo)
* Sham surgery + caloric restriction.
Observe gut flora change in the first group only.
"Graft" some of the gut bacteria of the three groups in obese mice who didn't undergo surgery.
Observe a moderate weight loss, only in the mice who received a stool sample of the first group.
Here's the abstract:
Roux-en-Y gastric bypass (RYGB) results in rapid weight loss,
reduced adiposity, and improved glucose metabolism. These effects
are not simply attributable to decreased caloric intake or absorption,
but the mechanisms linking rearrangement of the gastrointestinal tract
to these metabolic outcomes are largely unknown. Studies in humans and
rats have shown that RYGB restructures the gut microbiota, prompting the
hypothesis that some of the effects of RYGB are caused by altered host-microbial
interactions. To test this hypothesis, we used a mouse model of RYGB that
recapitulates many of the metabolic outcomes in humans. 16S ribosomal RNA
gene sequencing of murine fecal samples collected after RYGB surgery, sham
surgery, or sham surgery coupled to caloric restriction revealed that
alterations to the gut microbiota after RYGB are conserved among humans, rats,
and mice, resulting in a rapid and sustained increase in the relative abundance
of Gammaproteobacteria (Escherichia) and Verrucomicrobia (Akkermansia). These
changes were independent of weight change and caloric restriction, were
detectable throughout the length of the gastrointestinal tract, and were most
evident in the distal gut, downstream of the surgical manipulation site.
Transfer of the gut microbiota from RYGB-treated mice to nonoperated, germ-free
mice resulted in weight loss and decreased fat mass in the recipient animals
relative to recipients of microbiota induced by sham surgery, potentially due
to altered microbial production of short-chain fatty acids. These findings
provide the first empirical support for the claim that changes in the gut
microbiota contribute to reduced host weight and adiposity after RYGB surgery.
It is great to see research like this happening. I've followed nutrition for a long time as I've dealt with chronic weight problems, and things have gotten much more interesting (read: less parroting of the "party line" and more new research) in the last 5-8 years.
It's unfortunate that so much time was lost, because it takes 10-15 years to go from mice to people. Now if we could only get some experiments with decent controls, so we can actually learn something.