Gary Debunks Taubes II ~ It's the Frucose Stupid, revisited

Gary Taubes had a problem on his hands for his "Alternate Hypothesis" on the cause of obesity. While Why We Get Fat was in the writing stage, a couple of NIH biophysicists remained pesky thorns in Gary's side having challenged him on a lynch-pin of TWICHOO (Taubes Wrong Insulin-Carbohydrate Hypothesis Of Obesity).   Not to mention an equally pesky then-anonymous bunny-eared blogger who posted some pretty damning stuff on the subject, especially when she looked at his seminal reference on the subject from GCBC.  Downplay as he might, try to move on and have everyone forget, as he eventually relented and did, Taubes' original WWGF remains enshrined in the first journalistic effort on the topic: Good Calories Bad Calories.

It wasn't all that long ago that people were shouted down in forums and comment sections of the low carb persuasion for daring to suggest that people could gain weight on low carb.  Remember the meme?  At least you won't gain weight being a fat glutton?  Can't gain weight so long as there's no carb around?  It was all there in black and white in GCBC-- you need glucose to make alpha glycerol phosphate (aka glycerol-3-phosphate) to store fat.  

Well ... he was forced to abandon that one and come up with some more imaginative ways carbs really make us fat after all for WWGF.  Since then his lecture schtick has also evolved to include a new mechanism for obesity -- one that the Japanese don't thwart so brazenly provided you buy that they eat virtually no sugar.  
TWICHOO 1.0:  carbohydrates → insulin spikes → hyperinsulinemia → glucose to fat & fatty acids trapped in adipocytes → fat accumulation/obesity    
... ancillary to this version was this notion that insulin spikes → insulin resistance in muscles first → more glucose to fat in adipocytes. 
TWICHOO X.0:  fructose → insulin resistance → hyperinsulinemia → fat trapped in cells → overeating and/or wasting of lean tissue → obesity      
... in this version, Taubes posits that the "metabolically healthy" can likely eat insulin-stimulating starches to no ill effect so long as they remain insulin sensitive (e.g. don't consume fructose).
There are problems with the evolution of TWICHOO.  A scientist -- as Gary likes to play in journalistic arenas -- is entitled to tweaking and altering their hypothesis in the face of new evidence. Actually, they are compelled to do so. And do so unambiguously they should. This is not what Taubes has done. He's simultaneously jumped on another bandwagon (fructose = bad, bad, evil, and more bad) while never clarifying the gaping holes in his first hypothesis. Version X.0 (the tweaks were subtle so we don't know what number we have finally arrived at, hence the X) has not been completely fleshed out and put forth to replace v. 1.0. Fructose has never really fit into the TWICHOO "it's all about insulin" hypothesis. I'll save the big problem with X.0 for another post -- that being the dietary factor most easily manipulated to produce insulin resistance is fat.  One cannot heed evidence implicating fructose and ignore more compelling evidence implicating fat in this regard. But that's for another day.

Now onto the title of this post.  Around a year ago, Gary Taubes began putting the written finishing touches on TWICHOO X.0 in the wake of making an utter ass hat of himself at AHS11.  Rather than discuss the points Stephan Guyenet made in his follow-up post countering the 1.0 version of his hypothesis, Gary offered up a five part "rebuttal" of food reward.  But he stepped in it in doing so.  In that blog post, he referenced some studies by PJ Havel's group:
The second and third papers, both published in October, were randomized controlled trials in humans — rather than primates or rodents — which is always a nice attraction in nutrition research since there’s no guarantee any animal model really reflects the physiological situation in, well, us.  The second paper reported that overweight and obese older adults (40 to 72 years-old) getting a quarter of their calories from fructose-sweetened beverages used less fat for fuel and actually expended less energy than did the same subjects when they were getting the equivalent calories from glucose drinks. So the calories were the same; the metabolic effects were different. For the fructose, the effects were what we’d expect (okay, what I’d expect) if the fructose beverages were causing or exacerbating insulin resistance, an observation that Havel et al had published earlier. The more insulin resistant these people became, the less fat they used for fuel—hence, we can assume, the more fat they stored—and the lower their basal metabolic rate. 
NEITHER of the papers (I bolded his links and directed the first to the free full text) make Taubes' original case about carbs and insulin.  They just don't.  If it's carbs spiking insulin that leads to fat trapping (that we still hear about 90 some percent of the time, often from people citing Taubes), how do a pair of studies demonstrating that fructose -- a non-insulin spiking carb -- elicits metabolic mahem whilst glucose does not, work in your favor?  By changing your hypothesis and hoping nobody notices I suppose...

Considered together with a third study Taubes wrote:
What can we take away from these studies? Well, these three papers certainly support the contention that the sugars consumed in western diets have very specific deleterious metabolic effects, and that maybe these sugars are the, or at least proximate cause of insulin resistance and metabolic syndrome, and so, we can assume, obesity and type 2 diabetes and perhaps all the other chronic diseases that associate with these two conditions (cancer anyone?). 
OK ... let's back up the bus here ;-)  I already weighed in on this smoke-and-mirrors game back then with: Gary Debunks Taubes ~ It's the Fructose Stupid!  Of the three, the study entitled "Consuming fructose-sweetened, not glucose sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans" is the most troublesome for TWICHOO.  

Go back to GCBC, in it he wrote:
"Over the years, prominent diabetologists and endocrinologists -- from Yalow and Berson in the 1960's through Dennis McGarry in the 1990's -- have speculated on this train of causation from hyperinsulinemia to Type 2 diabetes and obesity.  Anything that increases insulin, induces insulin resistance, and induces the pancreas to compensate by secreting still more insulin, will also lead to an excess accumulation of body fat. 
What? Yet another "oh nevermind??"  He's taken back the G3P stuff, but never the carbs cause IR stuff that permeates LC theology to this day!  How to reconcile how fructose, that does not directly increase insulin, causes IR.  How Gary?  

There are still far too many who have been misled by Taubes-inspired mouthpieces, if not Taubes himself, that carbs cause insulin resistance.  Many of these same people believe they've pooped out their pancreata by consuming too many carbs in their misguided yoots.  Neither is true for the vast majority if not essentially all people.  The evidence on that is pretty clear folks.  You can fashion more elaborate scenarios about how carbs cause you to overeat and all of that, but the evidence remains.

... Can we get to the present Ev?  OK!!

So just before Thanksgiving, Gary Taubes treated us to a rare blog appearance.  What would happen if…? Thoughts (and thought experiments) on the calorie issue.   I'm beginning to wonder if NuSI is planning on funding actual experiments after all, or if we'll just get more of these "thought experiments" from the likes of Gary Taubes.  

Gary posits we perform an experiment on the holodeck metabolic ward of the Starship TWICH-UCAN.    We find two healthy young male twins in prime energy balance at 3000 cal/day and confine them to the ward for 20 years.   The experiment he proposes is so minor as to be silly.  The twins, I'll call them F&G instead of A&B are manipulated differently in all of 5% of their caloric intake.  Gary wants to feed F&G exactly as before, but with one difference.  Twin F gets 10% or 300 cals as sugar, thus 5% or 150 cal or 37.5g as fructose, while Twin G gets the 10% as glucose, thus 5% or 150 cal or 37.5g glucose.  Yes folks, he's really *thinking* on this one!  Or as he would say in his wannabe-physicist days, he's been all nachdenken über over it.  He specified the scenario, not I.  To demostrate the reason Taubes gedankenexperiment is such a dud, we have to put the rest of the 3000 calories in context.  Let's do a reasonable SAD macro of 50/35/15 for C/F/P to begin with, and let's assume we take the 10% "control" out of the carbs, leaving the rest alone.  So F&P are each consuming 375g carb/day to begin with, of whatever composition, and Gary proposes in tiefe gedanken that we fix the composition of 300g of that at whatever their current carb intake is, leave fat and protein alone, dictate 37.5g glucose to each, and either an additional 37.5g glucose for G or 37.5g fructose for F.  

Come back in 20 years and what do you expect to find?  I'm going to go out on a limb here and say, NO DIFFERENCE DUE TO DIET.  There might be something that goes on in F vs. G, but is there a person reading this who believes that altering the carb composition of 5% of one's diet in energy balance is going to set metabolic mahem in motion??   The ever dogmatic Taubes, perhaps.  The result of his gedankenloseexperiment is as follows:

What happens? Care to guess?  Will A and B still be identical after 20 years of A eating 300 calories of sugar every day that B does not eat?
We know sugar is metabolized differently from the glucose in starch because of the fructose component. Glucose is metabolized by cells throughout the body; fructose is metabolized primarily in the liver. We know the liver will turn some of this fructose into fat and if the fructose is delivered quickly enough (say in liquid form as sugar water), it  likely to cause insulin resistance in the liver, which in turn might cause systemic insulin resistance.  The extra 150 calories of glucose in B’s diet will stimulate more insulin secretion, although for B this will come in the absence of any fructose-induced effects in the liver. One way or the other, A and B will experience different metabolic and hormonal effects, despite eating precisely the same amount of calories in diets that are otherwise 90 percent identical. Their fat cells, for instance, will be on the receiving end of different hormonal and metabolic signals. As Claude Bernard would say, the fat cells would be living in a different  milieu intérieur and this will effect how they change over time.
Cut the french crap Gary.  Do you really believe this will change much?  It might change things ever so slightly.  No where near enough to make a difference, even over 20 years I'd wager.  Perhaps if all of Frick's carbs were designated to come from sugar, and all of Guac's from starch, or at least 90% or so, then we might see a difference.  And before going on, let's address this strawman, shall we?   I don't know how many times it bears repeating, and Lyle McDonald's Energy Balance Equation treatise still remains one of the best on this, nobody claims all calories are identical.  But on balance, unless you are at the uber extremes of macro composition, it all seems to marvelously balance out in the end.  Carbs are about 4 cal/g, as are proteins, and fats around 9 cal/g.  These are and have always been approximations.  If people ate the same exact thing day in and day out and then varied one component, they'd probably react.  If their homeostatic machinery is intact, their metabolisms and such should react to such a change.  After all, isn't that what Taubes and company have been telling us?  That calorie restriction is useless because we'll just turn down the thermostat and burn fewer calories?  Nobody denies adaptive measures.  

The question with this experiment is whether we believe such would be even perceptible switching out 150 cal glucose for fructose.  Gary is so into his new evil sugar manufactured schtick these days, however, that he apparently does.  After going on a bit more on the what if's, Gary proposes his scenario of what he proposes happens:  (I've replaced A with F, B with G, we'll call our twins Frick and Guac)
...  let’s assume two things for the sake of argument. First, the sugar in Frick’s diet causes Frick to become insulin resistant. And second, insulin works to put fat in fat tissue. There’s some evidence for our first assumption and the second assumption is in the textbooks; there’s a lot of evidence for that.
Now as Frick becomes insulin resistant, his pancreas has to secrete more insulin than G’s to handle the equivalent carbohydrate load. So Frick now might have higher circulating levels of insulin than Guac. If he does, this means more calories might be fixed in Frick’s fat tissue than in Guac’s.  Put simply, Frick might now be getting fatter than Guac. And as Frick gets fatter, his body has to compensate for the calories that are being locked away in the fat tissue and for the greater metabolic demands of a heavier body. What does Frick do?
Before we answer that riddle, answer me this.  Whatever happened to the fact that Guac is spiking his insulin more with each meal as a result of consuming glucose?  Back to the holodeck... 
What Frick can’t do is eat more, because we’ve fixed his caloric consumption at 3000 calories per day. One option is he could cannibalize his lean mass to feed his growing fat tissue. This can certainly be done without violating any thermodynamic laws. Now Frick gets fatter while simultaneously losing muscle mass and his weight remains more or less the same. A second option is that Frick’s body merely expends less energy to make up for the calories being locked away in fat tissue and the greater caloric requirement that comes from being heavier.
Again, why isn't Guac's fat being locked away from the insulin his extra glucose is spiking?  Here we have the same old rehashed and unsubstantiated pile of goo theory of obesity which is rather nonsensical. 
Now Frick gets fatter while his energy expenditure goes down. While Guac remains in energy balance throughout the experiment — eating 3000 calories a day to match the 3000 calories he expends — Frick moves into positive energy balance. He’s still consuming 3000 calories every day, but he’s expending less. And the reason he’s in positive energy balance is because he’s amassing fat in his fat tissue and getting heavier (Although a naive observer, wedded to the energy balance, might decide that Frick has become a couch potato and that’s why he’s getting fatter. In this case, the direct effect of the sugar is to make Frick expend less energy and this in turn causes the energy imbalance that makes Frick fat. The causality is reversed.)
Yeah, Gary, this is the funniest one of all, because we all know that the way to turn an active kidlet into a couch potato is to feed him some sugar ... right?  Eh ... when has observation ever swayed Gary's hypothesizing, right?   Now I'm convinced he had one of the Havel studies in his mind when writing this.  Those studies were actually one clinical protocol with two different write-ups.  The overweight subjects ate a regular diet for 2 weeks to establish a baseline weight-maintaining caloric intake.  They were then instructed to consume 25% of this baseline caloric intake as either fructose-only or glucose-only sweetened beverages. But ... and this is a biggie ... the remainder of their intake was not restricted.  Both groups consumed more non-sugary beverage calories, equally and gained weight.   Now the second paper, makes two points:  1.  resting metabolic rate was lower in the fructose consuming group (-.09 from 1.19 = -7.6%) and fat oxidation rates were lower.  Ding ding ding!!!  The first paper outlines all the very bad insulin resistance related stuff not covered in the second.  Slam dunk! 

Not so fast.  It's buried a bit in the initial paper, and all the talk of fat oxidation and metabolic rates is distracting.  For sure if your metabolism is slower you should gain more weight -- the glucose group ate 8.4% more while the fructose group only 7.4% more, a statistically insignificant amount that wouldn't have countered the REE changes anyway.  So what went on here?  Did the fructose drinkers gain more weight?  Surprisingly NO.  Again, the difference is not significant, but glucosers gained 1.8%  body weight vs. 1.4%  for fructose group.  They also gained more body fat, 3.2% vs. 2.8%.    However what fat was gained, was disproportionately put on the middle by the fructose consumers.  

Changes in Total Body Weight                                                              Abdominal Fat Changes
Now, this looks super crappy for the fructose folks, so yeah, don't go out and exchange 1/4 of your dietary intake for fructose-only sweetened beverages.  And if for some reason you're hell-bent on consuming 1/4 of your daily caloric intake as SSB's, be careful to scale back your other calories so you're not overeating and gaining weight!!  It's not good for your general risk profile or metabolic health.  

That said ... these folks were Frick and Guac from our experiment to a degree.  They consumed other carbs along side their prescribed sugary drinks.  Only Frick and Guak are envisioned to be calorie restricted.  So what do you think happens then?  I'm guessing nothing really.  At calorie balance, the fructose is likely just refilling glycogen.  No IR to speak of, but even with the IR in the Havel studies, this did NOT produce greater fat gain overall.  

So TWICHOO X.0 is out the window too.  Is NuSI planning to study this in the future?   Fund longer, better controlled (from an intake/compliance standpoint) studies, perhaps by Havel's relatively local group?  We'll see.  

There are more thoughtless experiments from Taubes post to tackle, and perhaps a few of the comments, both hilarious and saddening as this level of confusion only remains at this point because of the deliberate deception of a science writer who fancies himself a visionary.

Oh ... and to avoid abdominal obesity and it's concurrent metabolic woes, if you're going to overeat, perhaps choose an insulin-stimulating food.  
Now, assuming this did happen, or at least could happen, it would lead us to some other interesting observations as well. For instance, if A puts on this fat above the waist, it will increase his heart disease risk. The more fat he gains, the greater his risk of diabetes. In fact, depending on the size of the effect, he might become diabetic over the course of the study. His brother might not. A’s cancer risk goes up, as well, with his adiposity. So does his risk of getting Alzheimer’s. All without consuming a single calorie more than his twin brother did. In fact, if we run the experiment long enough, the brothers might die of different diseases and one might out live the other by a significant amount
No comment.


blogblog said…
I deliberately gained 10kg in 8 weeks on a VLC diet just by drinking a lot of cream.

Luckily I lost the weight just as quickly when I stopped the cream.
Chris said…
Superb. A tour de force. Thanks for your work on this Evelyn.
Unknown said…
The evidence on that is pretty clear folks. You can fashion more elaborate scenarios about how carbs cause you to overeat and all of that, but the evidence remains.
Unknown said…
What possessed you to deliberately do something so drastic?
Anonymous said…

I posted this previously (off-topic) but it seems pertinent to the 'what possessed you' type question.

'The first people to recognise and codify what was happening were a pair of Wired magazine journalists from the Bay Area in California, Gary Wolf and Kevin Kelly. They called it "self-tracking" and in 2007 founded a blog named the Quantified Self. They wanted to create an informal support group for people such as Clements (the "extreme experimenters") and for curious individuals interested in self-improvement (for example, a friend of theirs who was investigating the connection between caffeine and productivity).'
I think Beeminder is kind of cool!

I've been supplementing with vitamin D and fish oil. Recently, I received a solicitation from a hospital research group to take part in a study, in which I would take - you guessed it - vitamin D and fish oil. If I actually travel in to visit the hospital (within driving distance), they will pay me - something like $400. The study will take something like 5 years (don't have the letter in front of me); I decided against it because not only will I be submitting information about my food intake (that's OK) but I WON'T be able to take some other supplements (not OK).

The advantage, besides the money? They would give me the supplements, which are almost exactly the dosage I'm taking now!
Puddleg said…
As a longtime fan of the unstoppable Taubes I was disappointed by this gendanken-thingy. It seems so half-hearted. If you want to test whether a calorie really is any kind of a calorie, why not switch all the carb calories in the first twin's diet for alcohol calories?
blogblog said…
"What possessed you to deliberately do something so drastic?'

It's a basic scientific process called self-experimentation.
Mr. Wrong said…
I do this experiment on myself every weekend. the alcohol calories seem to improve mood quite a bit but has severe side effects the next morning...
Jane said…
Yes Taubes sounds half-hearted to me too. Maybe he's realised something doesn't add up here. Lustig tells him how fructose causes everything under the sun but neglects to mention that high fructose feeding in lab animals gives them copper deficiency. Does Lustig know this? I can't imagine he doesn't. But he probably doesn't read what the copper people say and realise most Americans have marginal copper deficiency and would be very sensitive to fructose because of it. So he and Taubes are groping around in the dark together.
Unknown said…
Wow. Really? Amazing.

I guess tomorrow I'll go and try out some poison ivy, you know, for SCIENCE, especially since I've shown resistance to it during childhood.

Actually, scratch the above and let me rephrase my question. . .

What motivated such a self-experiment? Did you actually feel that you needed to give a fair trial to some of the claimed merits of a high-cream VLC diet? If so, was there a time when you subscribed to a strict low carb diet?
Galina L. said…
It is the first time I returned from visiting my mom and my country with 5 extra pounds. I mostly blame it on being much more relaxed with the consumption of alcohol socially than before. Partially I have LCarbing to blame, because before I avoided all drinking since the age 35 because it used to make my asthma and eczema noticeably worse. Now I can drink and visit my friends who have cats. For the sake of the clarity of experimentation, I must add that it is possible I was reacting on gluten with higher readiness for allergies.
Galina L. said…
I think GT was half-hearted when he released WWGF.
Galina L. said…
We all experiment with our diets. Some even experiment with substances. When I first heard about Atkins diet after moving to Canada from Russia, I thought it was plane insane and didn't make sense. Approximately in 10 years I got it a try because I was truly desperate. It worked. It also allowed me to eat less without being hungry.
I don't think any longer that calories don't matter, so the over-drinking of cream is not what I plan for experimenting.
CarbSane said…
He had to be. He's got to know somewhere deep down that his hypotheses don't hold water. The anti-sugar frenzy is greater these days than the anti-fat, so it's the obvious bandwagon to jump on.
CarbSane said…
I think what Kade is getting at is that experimentation is one thing, but why would one engage in one that they know will have detrimental effects? I'm willing to try most things, but I would at least be hoping for something positive to come about, and I would abandon it if not.

Speaking of deliberate weight gaining (presuming one doesn't need to legitimately do so) -- anyone know the status of that trainer fit to fat to fit or whatever? He deliberately gained like 50 lbs and was trying to get it off last I checked in. Too lazy to look for a link right now.
Galina L. said…
The comparison of cream with poison ivy set me off a little bit. I remember the story about the brave trainer, no link is needed. I would never try to deliberately gain so much weight. At my age even 5 extra lb I brought from Russia could take a while to loose in a dark time of the year. At least it will keep me less carefree during Christmas season. I am getting deeper in the pre-menopause, and it means things can get more complicated metabolically.
One of my lady-friends started HRT and wears a progesterone patch. I think it should be counterproductive (like making one more grumpy,hungry and bloated), and I am not prepared to experiment with hormones yet.
Unknown said…
Did anyone have the misfortune of hearing Robb Wolf's latest podcast with Kiefer ("Carb-Backloading")? Really a dire interview, mounds of pseudoscience with anything legit having been taken right from Lyle MacDonald. As soon as someone says, "and then my research led me to the work of Gary Taubes" you know you're in for a treat... I couldn't listen to the whole thing. (Sorry if this is a repost Evelyn, I posted before from an old version of IE at work and despite saying "posted" it didn't show up.)
Unknown said…
Heh. Evelyn's got the right idea.

And the comparison was very much tongue in cheek and not so much between cream and poison ivy as it was between two people doing self-experimentation without any clarification or details as to why they're doing these experiments that come at a certain price without anything obvious in return. I can only guess that Blogblog's scientific quest with the intentional 10kg weight gain via VLC-cream edition was to either disprove that on VLC excess fat calories don't count, or to disprove that calories count at all on VLC, even from dense sources of fat such as cream.

Unknown said…
Jane, I have read your comments on various blogs with regards to copper and iron and the relationship they share.

My question to you: What kind of copper to iron ratio (in milligrams) would you consider realistic and healthful?
Lerner said…
That trainer was given minor coverage in followup news a few months ago. He did get back to how he started, of course; but that did not make a big splash. The masses want to hear "it's not your fault" and "exercise is counterproductive" and "here is a gimmick you can use", not "you can do it with lots of effort".
nthmost said…
Kiefer doesn't read anything Lyle has written, but Lyle loves to go looking for Kiefer's articles and dispute everything he says. So you can forget about the "Kiefer's just stealing Lyle's stuff" argument.

Kiefer also doesn't think Gary Taubes has everything right, particularly when it comes to the role of carbs vis-a-vis exercise and long-term success on low-carb.

I haven't listened to the interview yet. I just know this stuff because I was Kiefer's business partner until earlier this year.
nthmost said…
Taubes sounds half-hearted because that's his voice. If you've ever heard him talk, even when it's a topic he knows well and is passionate about, he still sounds half-hearted.

Check him out on the Dr Oz show:

This video is also worth watching just for horror-tainment. The number of nutritional fallacies Dr Oz is ready to go on record spouting is unbelievable. I mean, I knew he was bad, but WOW.
nthmost said…
Entertain an alternate hypothesis, if you will.

He was "half-hearted" when he released WWGF because it involved no new research or novel writing, being basically a more layman-friend version of GC,BC, and Taubes (as a scientist) wasn't intellectually stimulated in producing it.
Galina L. said…
"It is not your fault" message still warms my heart,to tell you the truth. I remember how justified I felt(and still do) when I found out that indeed it was not my fault that I had to be streaker in my diet than my husband,that I was hungry all the time not because I was a gluttonous freak, but because my body reacted wrongly on carbs, and no amount of exercise will let me eat plates of pasta like he did. Now my husband is the one who is freaking out when there is now food in a usual meal time (when we are not at home, of course) .
garymar said…
Naomi reads Evelyn! Small world! I just clicked and found out that you do a lot more blogging than Postpartum Punk.
Jane said…
Hi Kade, this is an interesting question. How much copper does your brain need? It's really important because copper regulates iron and iron overload is implicated in Alzheimer's. Klevay has a paper entitled 'Alzheimer's disease as copper deficiency'.

The water has been seriously muddied here by a paper published in 2006 apparently showing that copper is bad for the brain. Its title is 'Dietary copper and high saturated and trans fat intakes associated with cognitive decline'. From that title, you'd conclude a high copper intake means poor cognition, wouldn't you? Well their Table 1 shows the exact opposite. Cognitive score INCREASED with increasing copper intake, and almost unbelievably, the highest quintile had a cognitive score six times higher than the lowest. Now the highest quintile had a copper intake of up to 8mg/day, which is very high indeed, but obviously not too high. An iron intake of 8mg/day is plenty, which means, in answer to your question, that a 1:1 ratio of iron to copper is almost certainly better than the recommended ~10:1 ratio.

BTW, I emailed the lead author of this abominable paper, and she confirmed the data in Table I are correct.
CarbSane said…
Wonder if that's the reason my FIL's wife wanted him to replace all the copper pipes in his home with PVC!
Jane said…
I'm sitting here feeling very puzzled. I just watched that video. I don't know anything about this Dr Oz but I did not hear him spouting any fallacies. Did I misunderstand your comment? Did you mean Taubes was spouting fallacies?
CarbSane said…
Oops, I get it now! That'll teach me for reading in the feed reader.

Welcome nthmost! I was not familiar with your work and have bookmarked it to check it out when my semester winds down.
Unknown said…

Thank you for the response.

Now here's the real question: how does one cap their iron intake and up their copper intake on say, a kind of high-grain vegetarian diet that you recommend? Seems awfully hard, even when using a McDougall starch oriented approach. Typically, by just 1400 calories, one is already looking at 14mg of iron with just 2.2 mg of copper and 5.9 mg of manganese (Can be achieved with a combination of millet, brown rice and lentils with only a small side of vegetables). Are we supposed to compensate for this through supplementation? Perhaps there's also some consideration to be made for heme iron versus non-heme iron.

Jane said…
Hi Kade
Yes you're right, a 1:1 ratio is not achievable in practice. This is difficult, because the copper content of food has fallen alarmingly in recent years - here in the UK, copper in veggies has fallen since 1940 by 75%!

The iron:copper ratio in my diet is probably around 5 or 6. But then my food is full of phytic acid which inhibits absorption of iron, and according to Klevay, promotes absorption of copper.

I eat a lot of dairy products, which is a bit dodgy because they are so low in copper that milk has been used in the lab to make animals copper-deficient. I thought, 30 years ago, well if the Hunza do it, I can do it, and it seems to be OK. Perhaps as long as you eat the dairy together with grains, their copper and phytic acid take care of things.

There's something else potentially bad about dairy products. Saturated fat has been found to inhibit absorption of copper and manganese (in rats) and promote absorption of iron. I suspect all the controversy about whether saturated fat causes heart disease boils down to this. But I also suspect that so long as you don't live on meat and saturated fat (are you listening Taubes) it's OK.
Unknown said…
Hi Jane,

Interesting points. I have heard the noise that's been raised with regards to the drop in copper content in our vegetables.

Also, saturated fat does raise LDL count. Now I remember getting into an unwarranted confrontation with someone over the same topic a while back where he argued that while it isn't the ONLY risk factor, there is no harm in working towards keeping LDL cholesterol on the lower side. I am going to have to agree with that guy. Shouldn't be an issue if it is only a small fraction of the diet.

I would still like to know your thoughts on the iron content of plant foods. Should we not be as alarmed with the numbers if it is plant iron?
Jane said…
Kade, the thing about meat iron is that meat is very low in manganese. Plants are much higher: wheat for instance has an iron-manganese ratio of 1, and in beef muscle, it's around 100. Yes, 100. Manganese protects mitochondria and much else from iron-induced damage. There is a favourite paper of mine showing that iron-induced parkinsonism in rats can be completely prevented by manganese. I sent this paper to a friend who works on Alzheimer's and he couldn't believe it. It means, copper deficiency + manganese deficiency = Alzheimer's/Parkinson's. The drug giants have recently given up the search for an Alzheimer drug. They've wasted billions.

'Manganese: a transition metal protects nigrostriatal neurons from oxidative stress in the iron-induced animal model of parkinsonism'
Unknown said…
I hear you, Jane. I've always wanted to look further into the topic of iron overload, even in those who are not genetically predisposed to haemochromatosis since a lot of food products on the market come 'iron fortified'.

Good call on the manganese ratio. Well, again, this seems to be a bit low on the grain-diet that I outlined above. On a similar add up of millet with brown rice, lentils, vegetables and tubers, I am looking at almost 1600 calories and a rather large 24.4 mg of iron with 7.5 mg of manganese. Certainly a better ratio than beef, but not 1 to 1. Again though, this is non-heme iron, along with phytic acid and reasonable amounts of manganese.

I just had a look at 50 grams of beef liver, which while low in manganese, provides a much higher amount of copper to iron.
Sanjeev said…
manganese in humans:

a massive, important distinction according to mouse/rat models and micro-mechanistic molecular pathway studies ...

but if your criteria include high quality evidence, a distinction that makes ZERO difference in real humans, measuring real outcomes, in controlled trials. Hundred year old observational studies are not high quality evidence. Rat and mouse studies are not high quality evidence.
Sanjeev said…
phhhhttt... not to say the studies debunk its importance. If there have been studies, the proponents are not producing them to prove their points.

The studies that are presented remind me of the beta carotene studies ... and when beta carotene was given (for example, to smokers) lung cancer rates went up.

The have been a couple of other cases that escape me at the moment "rat models prove this" or "people with blood levels of xxx are healthier"

and when the real studies were done the people whose levels were brought up experienced WORSE overall outcomes.

mass quantities of low quality evidence do NOT aggregate into high quality evidence.
Sanjeev said…
> Lustig tells him how fructose causes everything under the sun but neglects to mention that high fructose feeding in lab animals gives them copper deficiency
"Lustig and Taubes focus on their own micro-mechanistic, too-tightly-focused views using observational studies, micro-mechanistic molecular pathway models ... they should focus on my (90 year old) observational studies, micro-mechanistic molecular pathway models and mouse/rat studies instead"

... irony much, Jane?
Jane said…
Hi Sanjeev
I think I detect biochemistry phobia. As I'm sure you know by now, I have spent 30 years studying the biomedical literature. It took me 20 years to get to grips with metabolic pathways and their ramifications. If what I say sounds wrong to you it's because you can't see the connections I can see. If you think I should be communicating with other scientists instead of commenting on blogs, you have a point. But actually I do both. I need to know what ordinary people think, and what information is available to them. You have been quite helpful.
Unknown said…
Furthermore, putting the above exchange aside. I did willingly approach you for the information and discussion, Jane. It's not like I've professed outright allegiance to the ideas based upon a few back and forth comments.

Jane, thanks again for sharing your thoughts and being a good sport.
Sanjeev said…
If I criticize Paul Jaminet's stance on wheat germ agglutinin as an adjuvant as being largely untested, if I criticize Lustig's "sugar high" as being thoroughly debunked by controlled studies that measured actual behaviour in children given blinded sugar or artificial sweeteners, if I criticize Taubes' ideas as the "fallacy of composition" how can i NOT crriticize your untested or unproven ideas? they're all ideas. They all demand proof. And if this involves health claims and recommendatins they require far more proof.

If you want a more detailed response I'll provide it.

"connections" are NOT exempt; Get over it.

"connections that you cannot see" is a red flag that raises suspicion.

Accusations of phobia and blindness are NOT proof. These only serve to increase suspicion.
Sanjeev said…
> WGA is an immunologic adjuvant as being largely untested

as far as health outcomes in real people
Jane said…
Which of my 'ideas' is unproven or untested? It's true I'm suggesting the prevention by manganese of iron-induced parkinsonism in rats has relevance to human Parkinson's. Are you saying I shouldn't suggest that until the experiment has been done in humans? Injecting iron into their brains? We already know Parkinson patients have iron overload.

Do I want a more detailed response? Yes, I do. I write short comments because I don't want to bore people or confuse them. There is a limit to how much evidence I can give, obviously. That doesn't mean it doesn't exist.

If I say 'it's been a pleasure' Sanjeev will wet himself laughing. But it has.
Jane said…

'If you want a more detailed response I'll provide it.' Yes, I do want it. Either you are putting in a lot of time and effort building a case against me, or you have realised there is no case. I shall check this space tomorrow and not again.
Alex said…
I guess you never read GCBC where he goes on endlessly about HFCS, but yeah let's pretend Taubes just discovered that fructose is evil.
CarbSane said…
Please, let's dispense with the nonsense "you haven't read GCBC" crap, can we? I've read it. Yes he goes on and on about sugar, nobody's "pretending" otherwise. But he does not implicate fructose in insulin resistance. That's his new schtick. Here's the old one:

consumption, or due to the consumption of refined and easily digestible carbohydrates, might have a similar effect. One question that will be addressed in the coming chapters is why medical investigators and public-health authorities, like Landsberg, will accept the effects of insulin on chronic diseases as real and potentially of great significance, and yet inevitably interpret their evidence in ways that say nothing about the unique ability of refined and easily digestible carbohydrates to chronically elevate insulin levels. This is the dilemma that haunts the past fifty years of nutrition research, and it is
critical to the evolution of the science of metabolic syndrome. As we will discuss, the observation of diseases of civilization was hardly the only evidence implicating sugar and refined carbohydrates in these diseases. The laboratory research inevitably did, too. Yet the straightforward interpretation of the evidence—from carbohydrates to the chronic elevation of insulin to disease—was consistently downplayed or ignored in light of the overwhelming belief that Keys’s dietary-fat
hypothesis had been proved correct, which was not the case.

Regarding the potential dangers of sugar in the diet, it is important to keep in mind that fructose is converted more efficiently into glycerol phosphate than is glucose. This is another reason why fructose stimulates the liver so readily to convert it to triglycerides, and why fructose is considered the most lipogenic carbohydrate. Fructose, however, does not stimulate the pancreas to secrete insulin, so glucose is still needed for that purpose. This suggests that the combination of glucose and fructose—either the 50–50 mixture of table sugar (sucrose) or the 55–45 mixture of high-fructose corn syrup —stimulates fat synthesis and fixes fat in the fat tissue more than does glucose alone, which comes from the digestion of bread and starches.

Old Taubes: Fructose stimulates DNL, and makes the most G3P, glucose stimulates insulin. Refined carbs cause chronically elevated insulin.
New Taubes: Fructose causes IR causing hyperinsulinemia.
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