Revelations from Gedankenexperiments vs. Wirklichenlebenexperiment

Traffic Bump!

Occasionally I see traffic to old posts whilst perusing stats.  I saw this was getting a few hits and decided to bump it.  Especially since the fervor for finding the single bogeyman dietary agent of all doom seems to be hitting a fever pitch lately.  Even Dr Oz is getting on board, and as the Judith Mazel of the low carb world tells us:
Dr Oz is one of the most well respected conventional doctors—and he has major influence because he is educating millions of people every single day on his show.
{you can stop laughing now ...}

Original post date:  11/29/12

In my last post I discussed one of the "thought experiments" Gary Taubes wrote about recently.  In his latest quest to convince people it's not the calories but the type of calories, he proposed an experiment on male twins.  In a nutshell, confine them to a metabolic ward for 20 years, feed them the same 3000 cal/day throughout, with the only difference being one gets 300 cal of sugar while the other 300 cal of starch.  This amounts to a difference of 37.5 g/day of fructose vs. glucose.   Gary posits that the fructose fed twin becomes insulin resistant leading to hyperinsulinemia that starts to tuck small amounts of calories away as fat.  As this twin gets fatter, he's not allowed to eat more so he wastes muscle mass and/or his energy expenditure is reduced to allow all of this fat accumulation.  Said twin kicks the bucket before his glucose fed brother. OK, I took some liberties with that last statement, but it's not far off from the scenario his gedankenexperiment led him too.  He writes:
If you believe this scenario is a possibility, even a likely possibility, as I do, you still believe in the laws of thermodynamics. You’re still thinking like a scientist (as my friend might say). But now, I hope, you can see what I mean by calories being the wrong paradigm. If we believe in calories, as my friend put it, then we believe that the twins end up identical, just as they started, because the quantity of calories consumed in the two diets was identical and it’s quantity that matters, not quality. What do you believe?
Gotta love Gary because he makes you feel all smart and all by complimenting you for thinking like a scientist for following his logic.  Oh wait, scientists are idiots, and this could also read that you're still thinking like one.  Grin.

But I can't help but think there's something missing from this experiment.  Where's the fat and protein gluttony?  With this experiment, Gary is doubling down on the quality of your carbohydrate calories making you fat!   But while he suggests the sugar come in a rapid delivery form like a drink, he makes no mention really of how the glucose should be delivered.

He no doubt had the Havel studies in mind, but the more I think of it, what an odd interpretation indeed.  Those studies are evidence that when the average overweight person takes 25% of his/her usual intake in liquid sugar form, they do not spontaneously compensate for the calories by reducing solid foods ... rather they overeat to the tune of around 8%.  This is either a crucial flaw in Havel's studies, or unanticipated genius as they demonstrated quite well how our nation's obsession with caloric drinks has almost certainly contributed to our obesity.  Taubes waters down this study in his gedankenexperiment by:
  • Starting with 20 year old lean men
  • Varying 150 calories of fructose v. glucose instead of over 600 calories
  • Capping total calories
So convinced is Gary that sugar is now the real cause of obesity, he seems to believe his scenario whereby these men will get fat anyway without overeating!  We're back to the nonsense he first put forth in his NYT article.  We're back to this notion that the obese do not eat more than the lean.  The hypothesis has morphed to focus on this so-called lipophilia and reverse arrow of causation between intake and obesity -- that is we get fat (accumulating) and then we overeat because the rest of our cells are starving and crying out for food.  But in this experiment he won't even allow the men to overeat, yet he still envisions one getting fat and one not.  

But ... If the glucose-fed twin does not get fat, or sick, and lives longer, doesn't this fly in the face of everything we've heard from Gary Taubes?  That carbs drive insulin drive fat accumulation.  Is there going to be a promotional blurb from Gary Taubes on the back cover of the new Perfect Health Diet?!  Note to Paul, it sure sounds like Gary is on board with safe starches!  :-)  

The route by which fructose would do this has nothing directly to do with insulin, but rather later on your insulin levels go up to compensate for IR.  Sigh.  But this is also light years away from the notion that fat doesn't impact body weight because fat doesn't stimulate insulin.  Or maybe Gary's right, insulin resistance is the precursor to obesity that drives the overeating because IR leads to basal hyperinsulinemia leads to fat accumulation leads to overeating and/or undermoving to compensate for the internal energy deficit.  I don't think so.  The literature is mountainous demonstrating that overnutrition is the primary cause of insulin resistance.  Cells in the obese and insulin resistant are anything but starving for nutrition that is supposedly "locked away" in the fat cells.

The Havel studies even counter this in a way, because only the fructose group became IR, while both groups overate and both groups gained weight.  Indeed the glucose group gained (statistically insignificant) more total weight than the fructose group.   Between the two, it was glucose that seemed to cause slightly more "internal starvation".

Meanwhile, since Gary Taubes now tells us it's just sugar that makes us fat and sick, some changes are in order!  Mark Sisson better cut out that teaspoon of the stuff in his morning coffee, and Jimmy Moore best be switching back to the sugar free chocolate.  Crack out the pasta and potatoes!  Rice, beans, and bread, oh my!!  These will not make you insulin resistant (true!!).  Gary Taubes has acknowledged this, Havel's study confirms this.  I consider this a key revelation of the tiefegedankenexperiment.

However, THE prime revelation is the missing thought, the fehlendegedanken.  We've been told by Gary for a decade now that it was low fat that made us fat.  That as we dutifully heeded government advice to cut the fat, we started eating more carbs.   What carbs?  Well, the advice was whole grains ... the base of the food pyramid. Sugar may have been given a bit of a pass compared to fat, but it was right up in the teensy peak along with added fats on the pyramid.  So we were replacing lard with linguine, and butter with baguettes, not replacing potatoes with pixie stix or rice with raisins.  Why wasn't his first thought for an experiment to replace carbs with fat, or fat with carbs?  Even if he's convinced we replaced fat with fructose, why not that experiment?  

Perhaps Gary has more respect for the intelligence of his audience than he lets on after all.  Or perhaps even he couldn't write with a straight face about how fructose → IR → hyperinsulinemia → fat accumulation, but fat → IR but not → hyperinsulinema and → no fat accumulation.  Perhaps he is aware of the diversity of ways fat has been implicated in producing the IR state.  Perhaps he's read some of the many papers showing chronic overnutrition -- almost always involving a high fat diet -- is what creates IR.  I don't know.  

What I do know, is that the biggest revelation to come out of his thought experiments on calories is that he doesn't think about fat vs. carb calories any more and yet, his denial of the role of calories in all of this is as strong as ever.  Perhaps he can't think about it or his head would explode.

He summed up his post with:
You can see how thought experiments can lead us to all kinds of conclusions and (at least hypothetical) observations that might not be intuitively obvious otherwise.
I'd say it's more like "imagination experiments", or as an homage to his German terms, we're talking  einbildungexperiments!  Such experiments IGNORE observations and require ventures into the land of glauben machen (I'll save you the trip to babelfish, it means "make believe").  Or perhaps we can call these "wishful thinking experiments", or wunschdenkenexperiments (← I like that one!).   

He finishes his blog post out with full blown wunschdenken:
Yes, I believe that calories are a useful measure of the energy contained in the foods we consume and a useful measure of the energy our bodies expend. (Just as I believe miles are a useful measure of how far I have to travel to get, say, from Oakland to Los Angeles.) Yes, I believe in the laws of thermodynamics and I believe, as I say in both my books, they always hold true. That’s why we call them laws. But, no,
I do not believe that we can learn anything useful about why people get fat or why they get the diseases that associate with getting fat, by focusing on the calories they consume and expend. It’s not about the calories.
OK Gary.  Only back to reality.  You can hem and haw all you want about how experiments haven't been done.  How they aren't long enough, not good enough, etc.etc.  But for the most part they have been done.  Let's start with the fact that however flawed, NHANES or USDA data or whatever else.  Americans eat some 300-600 cals/day more on average now than we did in the 70's.  If there's a scientific question to be answered here, it is why that might be, but Havel's studies as a jumping off gedankenexperiment aren't helpful (fructose consumers overate less than glucose ones).

Certainly disease and health can be impacted by what you eat, not just how much.  BUT ... where obesity is concerned, calories clearly matter.  When we're talking obesity and disease it is harmful to the discourse to treat "simple obesity" -- the stuff of the epidemic, not rare genetic conditions  -- as a disease that is caused by a macronutrient or subclass of macronutrient concurrently with disease.  The only way obesity is induced via the food supply is to provide the animal with a more readily available energy source (e.g. one that is more easily converted to body fat).  We see it with grain in ruminants.  We see it with fat in rodents.  We see it with processed/refined fat+sugar+starch vs. whole foods in humans.

Some get sick without getting fat.  Some get fat without getting sick.  Some get fat and sick.  The CAF rat study may involve rodents, but that real life experiment -- henceforth the wirklichenlebenexperiment -- tells us more about what makes us fat than all the gedankenexperiments ever could.  We humans in industrialized countries are in one giant wirklichenlebenexperiment, it would seem.  The nice thing about rats is that we can cage them and control what they eat day in nad day out for their entire lives if we want.   Regular (low fat) rat diet?  Normal rats.  High fat diet?  They actually consumed fewer calories but became fatter. High sugar/low fat diet?  Surprisingly they consumed about the same calories, but became fatter rats.  Human junk foods?  Overeat by 35%, get really fat and sick.  QED :-)

As I mentioned in that blog post, that study also addressed Gary's forgotten experiment -- fat vs. sucrose.  A very high sugar diet did cause a bit of liver damage and result in heavier rats.  Unfortunately we don't have body composition data here.  But the high fat chow resulted in similarly heavy rats (again no composition, slightly but insignificantly heavier) with consumption of less food.  These rats had some liver and adipose tissue "sickness".  But who took the cake?  Well, the rats fed cake -- and pepperoni, and jelly beans, and pork rinds, and Doritos, and .... -- see:  Why We Get (Sick) Fat - Lessons from a Cafeteria Rat.  How about that insulin resistance?  I thought you'd never ask!  In our wirklichenlebenexperiment, they did on IP glucose tolerance test (glucose injected into abdomen).

Moral of the story?  Don't eat a 35% sucrose diet, it will induce a modicum of insulin resistance.  But the high fat (45%) diet led to greater IR ... and the CAF diet even moreso.  Mr. Taubes, you ignore this at your peril because sooner or later someone is going to wonder why you've abandoned the fat golden cow.

To me, Good Calories Bad Calories was misguided.  To look at what makes us Americans (and our counterparts in other industrialized nations) fat we don't need to go hunting around the planet for examples of populations that may appear to be obese despite apparent high activity and/or undernutrition.  You just have to look in front of your nose at the data -- take your pick of source, they all point in the same direction though numbers differ slightly -- we have on Americans.  It's a no-brainer we ARE eating more than we did before this epidemic.  Why?  Because we're no better than CAF rats, who when offered the option of an appropriate rat diet and human processed foods, chose the human crap hands down (they only ate about 15% cals as chow).  And despite being offered sweets and savories and fat+sugar bombs, the diet was ultimately higher in fat and lower in carb -- which is, actually, what the SAD is.  

But worry not folks!  NuSI is on it!! 

Gotta comment on some of the comments on Gary's post.  I mean really folks, when you eat sugar, do you turn to a sloth?  You'd think so reading Emily H.:
Hypothetically, the sugar-eating twin’s body might find ways to expend less energy performing the “same” motions. If a person can eat all the calories they need, their body is more likely to waste energy on excess motion or heat. That person (Twin B, the glucose eater) might walk or run with a more energetic stride, or stay warmer in cold weather. Alternately, Twin A could make up for the missing calories by shrinking his organs and muscle tissue. This is what happens to people in real life who are underfed and don’t have the option of being less active, as documented in Todd Tucker’s book “The Great Starvation Experiment.”

You could think of this as metabolic efficiency, but it’s really just a starving body’s way of coping with unsufficient energy. It’s similar to how a person making less than living wage will be forced to be more fiscally efficient.
Twisted logic!  Ahh, and someone who will be familiar to most, Gallier2 chimes in:
The clearing of the blood glucose is the difference in that case. Only glucose will stimulate insulin, glucose will be shuttled to the adipose tissue, fall back to normal and lipolysis resumes quickly. The other case, a little less insulin → insulin resistance → less clearing of glucose → more insulin → clearing of glucose, but slower than normal → lipolysis inhibited longer → starvation at cellular level → stuffing its face with snacks.  The mechanism is in fact a bit more complex than that. The effects of insulin resistance are quite different depending on which tissues are resistant, liver, muscle or adipose tissue, in what state the body is in, ketotic, starving, hyperglycamiae whatever. To disentangle all that and have a better view of the whole is what NuSI is all about.
OK.  So insulin spikes lead to faster glucose clearing so lipolysis can begin anew more quickly.  Meanwhile not spiking insulin leads to insulin resistance.  I'm so confused!!  A Paul weighs in with:
Of course, you don’t have to restrict calories to lose weight because it is all about insulin. (Though you might slow your weight loss down, the availability of ketones from food would slow the rate at which your fat stores become depleted.) Carb-restriction is effective because it works with the body’s fat regulatory mechanisms, not against them.
Seriously?  Anyone believes this crap anymore?  Should I laugh or cry?  There are so many more I want to comment on, but I'm kinda bored with it already ;-)  


Diana said…
Oh dear, you read Taubes so I don't have to. I can't get beyond his mendacious writing style. I tried "The Inanity of Overeating" and all I could think was: "The Inanity of Gary Taubes."

His method hasn't changed. Say a lot of things that are true but not to the point, then bait and switch and claim, voila!, you've made your point. Add some snotty snark about anyone who disagrees with him and finish with a flourish.

Like his Pima arguments, none of it stands up to scrutiny.

blogblog said…
I'll take taubes side on this one.

Nutrients 2011, 3(3), 341-369; doi:10.3390/nu3030341
Starches, Sugars and Obesity

"...From the literature reviewed in this paper, potential beneficial effects of intake of starchy foods, especially those containing slowly-digestible and resistant starches, and potential detrimental effects of high intakes of fructose become apparent..."
CarbSane said…
Dang -- had a whole reply that got zapped and didn't respond to ctrl-Z :(:(

This review mostly compares low GI starch to SSB's. I looked for references to fruit, and the only one to whole fruit is positive (in the context of improving metabolic parameters). One "hit" on fruit landed me at cite 106:

"To determine the association between surrogate markers of insulin resistance (fasting insulin, fasting glucose, homeostatic model assessment of insulin resistance (HOMA-IR), and the insulin sensitivity index (ISI0.120)) and SSB consumption, Yoshida et al. [106] used data from 2500 subjects with an average age of 54 years from the Framingham Offspring Study. 53% of the study population consumed SSB’s and did this with an average of two servings per week. After adjustment for potential confounding variables, the frequency of SSB intake was positively associated with fasting insulin. The associations between the frequency of SSB consumption and fasting plasma insulin and HOMA-IR remained statistically significant after further adjustment for dietary glycemic index, fruit intake, or vegetable intake. No significant associations were found between SSB intake and fasting glucose or ISI0.120. In this study, the HOMA-IR largely reflected fasting insulin concentrations. Both insulin resistance and β-cell dysfunction precede type 2 DM, and thus increased consumption of calorically sweetened beverages containing rapidly absorbable simple sugars may contribute to an increased risk of type 2 DM [106]."

Well from that study:

"Sugar-sweetened drink consumption was positively associated with fasting insulin (none vs. ≥2 servings/d, 188 vs. 206 pmol/L, P-trend <0.001) after adjusting for potential confounders. Sugar-sweetened drink consumption was not associated with fasting glucose or ISI0,120. Fruit juice consumption was inversely associated with fasting glucose (none vs. ≥2 servings/d, 5.28 vs. 5.18 mmol/L, P-trend = 0.006), but not with fasting insulin (none vs. ≥2 servings/d, 200 vs. 188 pmol/L, P-trend = 0.37) or ISI0,120 (none vs. ≥2 servings/d, 26.0 vs. 27.0, P-trend = 0.19) in multivariate models."

So SSB's associated with slightly increased fasting insulin but not glucose, while fruit juice associated with slightly decreased blucose but not fasting insulin. This is the table for SSB's. I note the reporting of the SSB consumption of the population in your review is misleading -- 53% consumed more than 2/week, but the associations are for 2 or more SSB's per day. Of 2500, only 125 (5%) consumed 1-2/day and only 96 (4%) consumed 2+/day.

Such negligible differences seem hardly worthy of mention.
Diana said…
blogblog: "potential beneficial effects of intake of starchy foods...." is not something I associate with Gary Taubes.

I admit that I've gotten behind the curve knowledgewise in what is going on in the LC world. Have they now come to "Good Carbs, Bad Carbs"?
Lerner said…
So after whining for years that the correct studies haven't been done to test his looney toon theories once and for all, Taubes gets a gullible billionaire to give him the money to finally do the studies. After months, Taubes instead comes up with a 'thought experiment', which means he can continue bamboozling the gullible segment of the public into believing his arguments about pathways and mechanisms.

After years of Taubes-worshippers fanning across the internet saying 'Taubes teaches us that calories don't matter, only carbs make you fat', Taubes now says, "of course calories matter, except they don't".

Also, "only carbs-->insulin make you fat, but I really meant sugar-->IR... but wait, maybe I really meant both".

Also, "exercise makes you fatter, except I exercise and I'm not getting fatter".

His whole epic tome GCBC is all about insulin, yet he apparently never even mentioned the seminal study "An insulin index of foods" by Holt, Brand-Miller, Petocz

He still claims that it's the 'processed' carbs that spike insulin, so he never has even yet seemed to have looked at the study.

Insulin scores:
whole meal bread 96
white pasta 40

Underneath it all is the assumption that fat is made out of thin air, just as with the insulin injection site photo.

Meanwhile, his sidekick Attia is all about gluconeogenic proteins but Taubes never mentioned that in GCBC, either.

What a zoo.
Adam Noel said…
This comment has been removed by the author.
blogblog said…
"His whole epic tome GCBC is all about insulin, yet he apparently never even mentioned the seminal study "An insulin index of foods" by Holt, Brand-Miller, Petocz'

Nutrition science has progressed a great deal since the paper was published in 1996. The Glycemic Index concept has now largely been discredited as it seems to have very little real world influence on health outcomes.

Current nutrition science (post 2005) is firmly focused on the interaction between foodstuffs and the gut microbiota in individuals. Free sugars, especially in liquid form, appear to be extremly unhealthy while cellular starches are generally highly beneficial.
Lerner said…
I'm talking about the insulin index, why are you bringing up glycemic index>
blogblog said…
"why are you bringing up glycemic index?"

Because in the real world the GI and insulin index are meaningless concepts. They do not reflect what happens to the individual over the long term.The reality is that people can eat vast quantities (2-4kg/per day) of potatoes and not develop diabetes or obesity.

The problem with the LC crowd (and the LC critics) is a fixation with ancient history. Studies from 10, 20, 50 or even 150 years ago are little more than footnotes from history.

Current nutrition research is focused on the microbiome and inflammation processes - not metabolic studies or basic physiology. Obesity, diabetes etc are now known to be caused by the interaction of the microbiota and immune system in certain genetically predisposed people. eg most Caucasions will not get fat from eating large amounts of starchy foods but they will from eating a high sugar diet.
CarbSane said…
Umm, blogblog, I post about a lot of current nutrition research, and I think your description of it being focused on the microbiome and inflammation vs. metabolic/physiologic processes is off base. Sure the gut flora and inflammation studies are "in" these days, but I wouldn't say it's a central focus.

That said, countering Taubes requires meeting him at his level. That is he focuses solely on what happens the few hours after you eat carbs and this is where the Holt satiety and insulin index data are applicable. I don't think Taubes knew protein stimulated insulin when he wrote GCBC -- or someone told him it wasn't much or it didn't matter b/c of glucagon stimulation, or whatever and he didn't investigate further.
Lesley Scott said…
" I don't think Taubes knew protein stimulated insulin when he wrote GCBC" ...hmmm, I guess even though amazing antique research from the dawn of time was lost in the anti-German War Bias divide until Superwriter (I forget GT's Asylum Superhero character name & whether or not he bravely fights fructose with a Pool Noodle) liberated it. Or, wait, maybe our biology changed in a short amount of time or he would have had to do a "fourth PhD" worth of research. Or, i dunno, maybe it would help if he were an actual scientist rather than just playing one on the NYT Bestseller list.

Craig said…
The literature on nutrition, health, and weight is vast, and I have neither the time nor the interest to study this vast literature sufficiently to develop an informed opinion regarding who is right or wrong on a particular issue. So when someone comes along with a claim that they have reviewed the literature and come to an understanding of it, I'm going to at least give them a hearing. But I also understand how easy it is to cherry pick studies to support a particular conclusion, if that is your agenda.

In the case of Taubes, I did read GCBC, and WWGF, and found them interesting, to the point that I tried carb restriction as part of my dieting strategy. Like many people, I found that carb restriction worked fabulously well for a while.... and then seemed to lose much of it's effectiveness. I still cannot eat to appetite and lose weight or maintain a desireable weight, even with a low carb approach. I have to make some effort to limit calories. It is also clear that lots of other people have the same result. LC can be a useful dieting strategy under some circumstances, but is not a full solution to the obesity epidemic.

So even without reviewing the underlying science, that kind of real world experience is enough to tell me that Taubes theories are just too simplistic, if not flat out wrong.
Diana said…
"Nutrition science has progressed a great deal since the paper was published in 1996."

Not according to Taubes. He thinks everybody is full of shit except him.
blogblog said…

I really meant to say inflammation and the nicribiome are at the cutting edge of nutrion research rather than teh current focus.

@ Craig:

LC certainly works for a year or so. However this probably has nothing to do with a "metabolic advantage". A more likely explanation it is that the diet temporarily changes the microbiome to a less inflammatory profile.
Unknown said…
"A more likely explanation it is that the diet temporarily changes the microbiome to a less inflammatory profile." - Blogblog

I can see how that might be the case. Also, these high-fat, and even high-meat diets tend to be less bulky and pose less of a physical burden on the digestive system.
blogblog said…
Saturated fat is strongly anti-microbial. I noticed an almost immediate 80-90% reduction in stool volume when I started drinking coconut cream. This is despite a moderately high fibre diet.

Coconut can be used as dietary supplement in ruminants to reduce pathogens in the gut.
Sanjeev said…
Highly speculative.

"likely?" bollocks.

Bloody hellish bollocks.
Josh said…
Whilst short and medium chain saturated fats have anti-microbial properties, long chain saturated fats are the most probacterial and proinflammatory of fats -
blogblog said…
there have been thousands of peer reviewed papers published since the 1980s indicating that inflamamtory processes involving the gut microbiota are involved in the development of hundreds of diseases including obesity, diabetes and autism.

Unknown said…

How much fibre are we talking about when you were consuming coconut cream?
Sanjeev said…
> A more likely explanation it is that the diet temporarily changes the microbiome to a less inflammatory profile

PROOF please. GOOD proof. - you followed a chain of logic there and you need to prove that

1. gut microbiome changed because of the diet
2. to a less inflammatory profile
3. and this specific reduction in inflammatory microbiota was the LIKELY (your word)
4. this change in microbiota is temporary
5. this temporary microbiota reverses back to the regular WITH NO CHANGE OF THE DIETARY RATIOS
6. this reversal re-introduces inflammation
6. this re-introduciton of inflammatory microbiota is the LIKELY cause of weight re-gain.

and what about people that do not change the dietary ratios at all but simply reduce calories. Do their microbiota change to a less inflammatory profile?

I find your explanation HIGHLY SPECULATIVE,

please avoid logical fallacies
Sanjeev said…
especially the "likely" part - speculative
Sanjeev said…
having written all of the above, I apologize if I mis-read what you wrote.

"more likely than metabolic advantage" is a really, REALLY low bar.

but more likely than any other explanation I would find highly speculative.
CarbSane said…
blogblog: The gut microflora studies in humans are mostly observational, which as we all know tells us nothing about cause/effect. The only experimental intervention I'm aware of was the small study of fecal transplants to obese diabetics. As I recall, it improved glucose tolerance but didn't alter weight. Given as incretins are involved in glucose homeostasis, I'm not surprised. Are you aware if there's been a follow-up on that? Did the new flora "stick" and the effect remain?

Are there any studies where diet is changed and changes in microflora demonstrated in humans?

I don't know. Perhaps I'll be proven wrong, but my gut (pun!) just tells me that the microflora, to the degree that diet contributes, is the effect, not the cause of obesity for starters. Certainly having the wrong kind and amount of bacteria in the gut can cause permeability issues that could precipitate any manner of issues.

I just see too much chasing mechanisms by which obesity "spontaneously" has been caused that can be fixed by just changing that one mechanism -- if not by diet, then by pill. Not going to happen!
blogblog said…
with respect all nutrition bloggers need to read the current literature. A Medline search using the terms "intestinal microbiota disease" gives 1063 results. One quarter (271) of these papers were published in 2012. Only ONE paper was published before 2001.

The gut microbiota is currently implicated in the development of virtually every medical condition including autism, allergic rhinitis, NAFLD, obesity, diabtes schizophrenia and Parkinson's disease.

Unfortunately the whole nutrition blogosphere seems to be arguing about ancient history. Virtually all the literature published prior to 2000 has been updated or discredited. Yet we still have people quoting 50-100 year old research to support their arguments.
Jane said…
It's well established that the 'right' bacteria ferment things and produce organic acids which improve mineral absorption. Look up 'resistant starch mineral absorption' or 'bifidobacteria mineral absorption'.
CarbSane said…
I don't know what your point is that only one paper was published before 2001, other than that it's a scientific line of inquiry in its infancy. Back in 2004 was the whole nutrition blogosphere discussing obesity arguing about ancient history if they weren't looking at leptin?

As to "we still have people quoting 50-100 year old research to support their arguments", well there are certainly some people doing that. I'm not one of them for the most part. Frankly, I'm not sure which nutrition bloggers out there you're referring to who are not reading the current literature.

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