Bacteria in the Intestines May Help Tip the Bathroom Scale, Studies Show
nytimes.com
nytimes.com
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.
http://www.abc.net.au/science/articles/2011/05/10/3212802.ht...
Edit: Here's another link I found in one of my old comments from a week or two ago:
The GP was entirely correct in stating that nutrition research has been "screwed up".
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).
That is possible if it's a small reduction of calories and you're not very far off your ideal weight.
Otherwise is a thermodynamical impossibility.
And yes, losing weight is one problem, keeping it off is a different matter.
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".
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.
1. This is a review of 31 studies that comes to the same conclusion: http://mann.bol.ucla.edu/files/Diets_don%27t_work.pdf
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!).
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.
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.
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.
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.
Not a single one of them defined low carbs as 5%, in them low carb was like 30%.
30% carbs will make anyone fat with enough calories (exactly what you said was demonstrated.
I'll wait for the 5% carbs version.
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!
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?
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.
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).
Unfortunately, it is hard to get researchers and patients to agree to get an enema of someone else's poo.
Money does wonders. And since we spend untold billions a year trying to lose weight or to mitigate it's side effects, the money is there.
Even if we lost half an ounce a day, it would be roughly 10lbs a year. More than enough for most people.
http://www.nytimes.com/2013/01/17/health/disgusting-maybe-bu...
Human fecal transplants already exist
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.
Net caloric balance is an important predictor, but not the sole predictor. That's why it "drives people nuts" - because it is not true.
For example:
http://www.newscientist.com/article/dn23127-abnormal-gut-bac...
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.
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.
People WILL pay for this shit (literally).
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:
http://www.nytimes.com/2013/01/31/health/antibiotics-can-sav...
http://www.freakonomics.com/2011/03/04/freakonomics-radio-th...
Memorably, they called a fecal transplant a "transpoosion".
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.
"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.