Wednesday, June 06, 2012

A glimmer of light

For those who do not have the supplies of anti emetic necessary to read main stream nutrition opinion it's worth noting that not all obesity researchers are idiots. I rather like this article. Woo might too, after her last foray on the WHS for the Noddy guide to obesity.

Peter

61 comments:

LeonRover said...

Nice (enough)new conjecture.

Better than "Whale tagging dog".

js290 said...

The conservation of energy, as with every other Laws of Science, is a necessary effects, not the causes. People still confused about this have a fundamental misunderstanding of science.

Sidereal said...

I admire you guys for being able to venture to WHS. I find my cortisol and hypertension issues much improved if I stay away from teh stoopid. ;)

tess said...

what she said.... if there's anything more annoying than reading "the new Stephan" it's reading his commenters.

ItsTheWooo said...

WANT FULL TXT.

MY OBESE GLUTTON NATURE DEMANDS IT.

ItsTheWooo said...

@Sidereal these days when a new WHS link pops up in google reader, I skip over like a child running past a haunted house. I still subscribe.

I could not resist the title this time: "Calories Still Matter". I was hoping he went entertainingly hysterical like carbsane (the title, almost INFLAMMATORY), but unfortunately he remains emotionally reserved quasi-lobotomized per usual.


@tess I can't help but notice he receives just as much hate as acclaim. Every other commenter is like "lol ur dumb".
Of course he remains in good standing with the paleo elite lunch table, presumably because he is a VIP who is also is quasi-paleo. It's sort of like how scientologists will defend tom cruise no matter HOW BATSHIT.

bopes said...

Full text available at link at bottom of page Peter linked to.

Nigel Kinbrum said...

The fact that Wells JC, and Siervo M. use the words "Gluttony" and "Sloth" makes them lose all credibility.

If they don't know the difference between doing things consciously and unconsciously, their opinion is invalid.

engineering-health.org said...

It's disappointing to see you guys dismissing Stephan's ideas at "crazy" and "stupid" without the well reasoned scientific rebuttal it deserves.

He is a rigorous scientist and critical thinker, and his views seem to me well supported by the data. I wonder if you guys are somehow misunderstanding his reasoning and arguments if you find them to easy to dismiss?

I find the biggest problem with his most of his arguments is that they're subtle and easy to mistake for something entirely different.

For example, in his debate with Taubes on food reward, it's clear to me that Taubes never understood the food reward theory and was instead attacking a straw man, probably unintentionally.

js290 said...

@engineering-health.org, in light of Peter's last two posts, I humbly present the question I posted on gnolls.org:

JS, does food reward adequately explain the calories out component? That is, if we accept that metabolism can be slowed by restricting energy input, then it stands to reason that metabolism can be increased by increasing energy input. In other words, energy input and output are coupled [in the mathematical sense]; they can’t be treated independently. So, if one is to argue that highly palatable foods cause excessive energy input, would they not also have to explain why those same palatable foods reduce energy output? Maybe I missed this part of the food reward theory?

J Stanton's response is directly below it.

Also, the data will always support the idea of "food reward" because the idea of food reward as it relates to obesity, specifically, appears to be a specious re-explanation of the Conservation of Energy.

ItsTheWooo said...

@engineering-health SEW TIRED of the accusation that we don't "understand" FR if we disagree.

I understand it very well, and I disagree entirely, for very good reasons.

IMO people who support FR hypothesis fall into one of two camps. They are either grossly ignorant of the totality of evidence (e.g. being unaware it is false to conceptualize dopamine as an "addiction" marker rather than an arbiter of the energy conservation response) ...or alternatively they are moral / religious / irrational zealots who DESPERATELY want to believe it's CICO and gluttony and sloth and ELMM (...usually for reasons which usually have nothing to do with petty obesity.)

@Nigel your interpretation of FR is MEANINGLESS. You just don't seem to understand this. It's MEANINGLESS. No one cares what you personally think. Sorry, harsh truth, but your subjective interpretation is just that: your subjective interpretation.

Even if we are assuming you are being truthful (I doubt you are, I am pretty sure you absolutely think obesity is caused by gluttony/sloth... on my blog a few days ago you described your behavior as "a pig laying in filth". If that isn't a moralistic statement describing sloth and gluttony I don't know what is)... the fact remains the vast majority of people including researchers think obesity is a choice, a person chooses to put this in their mouth and to not exercise. Cold hard truthiness.

AGain, if you really are being truthful, why would you describe your own inactivity as akin to a pig laying in filth? This is not a descriptor that suggests moral/emotional neutrality.

Nigel Kinbrum said...

Woo, no one (of any importance) cares what you personally think, either. I blog and leave comments on other people's blogs for shits & giggles. What's your excuse?

Provide a link to the comment I wrote. I don't recall writing any such thing about my behaviour being like "a pig laying in filth".

People read what I write, pass it through some weird "cognitive bias" filter in their brain and translate it into something completely different, which they then argue against. The cognitive bias is strong in you, Woo!

Makro said...

@Woo Just to stir things a bit - let´s formulate "alternative FR hypothesis":

"obesity is a choice, a person chooses to put this in their mouth and to not exercise. Cold hard truthiness."

FR 2.0: Tasty but nutritionally terrible (I.e. it is the opposite of what Dr. Terry Wahls of TED fame has self-experimented with) food is consumed by people because it is "rewarding" (potato chips, Ben n' Jerry´s, Big Gulps).

Because hunger / calorie management still works properly, total calories consumed stay pretty normal, and excess leads to compensatory activity, yadda yadda.

However, over time, this deficient (but tasty) diet leads to mitochondrial deterioration, chronic insulin management issues, etc. (perhaps boosted by other modern hazards like stress and insufficient sleep, etc.) Metabolic syndrome sets in, lethargy and gluttony manifest themselves.

Metabolic havoc ensues.

I.e. FR->Poor nutrition (nota bene, not "overeating")->MetSyn -> Gluttony and Sloth.

Nigel Kinbrum said...

Woo, see Simile.

If I wrote "I'm as happy as a pig in shit", it means "my happiness can be equated to that of a pig in shit" and NOT "my lifestyle can be equated to that of a pig in shit".

If you seriously think that I mean the latter, you are either as thick as two short planks or my guess-> as mad as a March hare <-my guess.

If I had written "I'm as happy as a sand-boy", I expect that you would have accused me of having an obsession with Silicon Dioxide!

LeonRover said...
This comment has been removed by the author.
LeonRover said...

Well, Nige,

I believe you have just been the object of an "ad porcum" argument.

"In silico, veritas", information on the interwebz.

Slainte

PS "Simile and the world similes with you." See song by Verita Lynn

ItsTheWooo said...

@Nigel
My opinion is indeed worthless, however I do not conflate my opinion with popular scientific hypothesis, as you do pretty much constantly. If I offer my opinon, it's my loudmouth ass opinion. On the other hand, you will barge in center stage and speak for Stephen Guyenet and make up random qualifiers and caveats and argue people from the perspective of a hypothesis you did not invent.

This could all be avoided entirely if you just said "In my opinion, I think..." before you described your ideas. Instead you insist on saying "FOOD REWARD is..."


Re: the comment...Sorry, not convinced.
You are basically refusing to admit your choice of words implied moral judgement. The phrase "happier than a pig in shit" is always applied to examples of people being content in immorality/bad behavior particularly gluttony and sloth... unless it is used ironically. Only an autistic or a non-english speaker would believe this crap.

gallier2 said...

@Makro

However, over time, this deficient (but tasty) diet leads to mitochondrial deterioration, chronic insulin management issues, etc. (perhaps boosted by other modern hazards like stress and insufficient sleep, etc.) Metabolic syndrome sets in, lethargy and gluttony manifest themselves.

Yes, but that is exactly what SG and his ilks deny.

bopes said...

Food Reward spelled backwards is Doof Drawer.

That's a fact.

Sidereal said...

@Makro
Totally reasonable hypothesis, entirely consistent with the CIH and exactly contrary to what Guyenet argues. His central claim is that tasty food leads to overconsumption and brain damage which CAUSE obesity. (I think, but since I'm too dumb to understand the writings of that subtle and nuanced thinker, I'm open to correction.) On the other hand, you're saying that the core issue is actually mitochondrial damage from nutritionally defunct CIAB like refined carbs bathed in transfats and PUFA which causes overconsumption and sedentary behaviour. This is exactly the opposite of what Guyenet argues. He explicitly rejects the idea that gluttony and sloth are the consequence of the metabolic syndrome / mitochondrial crapout. From his latest post:

I know someone out there is thinking about the "alternative hypothesis" that we're eating more because our fat mass is expanding. Anyone can come up with a hypothesis, but not all hypotheses are supported by evidence from the scientific literature. There is a mountain of evidence demonstrating that experimentally increasing calorie intake increases fat mass, regardless of whether the calories are coming from carbohydrate or fat, and regardless of changes in circulating insulin (5, 6, 7, 8). When someone publishes evidence that the reverse occurs-- that fat mass expansion causes increased food intake in humans, and that this is not only biologically possible but actually occurs in common obesity-- I'll begin taking the idea seriously. Until that time, it will remain unfounded speculation that is unnecessary due to the existence of explanations that are more parsimonious and better supported.

Makro said...

@Sidereal

As for insulin, etc. being irrelevant to weight gain, I would be curious to hear him discuss why (for instance):

- "Acute post-challenge hyperinsulinemia predicts weight gain: a prospective study." (The title says it all) Doesn´t this make the whole "fat causes insulin resistance / hypersecretion" far less plausible? (If stuff like the preceding Hyperlipid post wasn´t enough, that is...)

(Sigal et al. Diabetes 46:1024, 1997)

- Why insulin-suppressing (low-carb) diets comparatively (with somewhat less insulin-suppressing low-calorie / low fat diets) work (much) better amongst people who have insulin regulation problems.

(See, for example, "Effects of a Low–Glycemic Load vs Low-Fat Diet in Obese Young Adults, A Randomized Trial", Ebbeling et al, JAMA (2007).

- Why insulin suppressing drugs lead to weight loss in obese people. With the degree of response to the drug correlating strongly with the degree of weight loss, nota bene.

(See, for example, Velasquez-Mieyer et al "Suppression of insulin secretion is associated with weight loss and altered macronutrient intake and preference in a subset of obese adults", International Journal of Obesity (2003) )

- Why blood sugar suppressants (I.e. metformin) lead to weight loss in obese people.

(See, for example:

Freemark and Bursey (2001)
Kay and Alemzadeh (2002)
Srinivasan et al (2006)
Burgert et al (2008)
Klein et al (2006)
Love-Osborne et al (2008)
Atabek et al (2008)
Clarson et al (2009)
Wilson et al (2009)
Yanovski et al (2011)

- Finally, because Dr. G has (ab)used them so much, let´s just note our favorite family of knockout mice:

(LIRKO)
(NIRKO)
(MIRKO)
(FIRKO)
(BATIRKO)
(VSMCIRKO)
(PODIRKO)

How come knocking out insulin receptors have such striking effects in causing or preventing obesity if insulin has no causative role in... obesity?

Feel free to add to the "mountain of evidence" above.

Ed said...

Huh, it sure seems to me that the food reward hypothesis is supported by a much tinier minority than those who think carbs cause obesity, and even tinier than those who think gluttony & sloth cause obesity (as evidenced by your link). I'd hardly call Guyenet's position "main stream." I mean, I've actually met, in real life, spontaneously, a number of people over the past few years, who are "cutting carbs to lose weight." I sure as hell have never met someone who "was eating less rewarding foot to lose weight." As far as "common knowledge" goes, I'd call food reward an important alternative hypothesis, it just happens to be supported by a number of, you know, researchers. Oh well. Sometimes the enemy of my enemy is my friend. And sometimes everyone's just stupider than me, I am the way and the light :-) (Wait, Peter, I thought you said "no gurus"??)

In any case, the linked paper seems to go after fructose, not potatoes. I thought this crowd was anti-carb. Why do you "rather like" an approach that is not anti-carb? (Sorry, maybe it's explained in the full text, which I admit I haven't read.) Shrug. It's like the hostility towards Guyenet, maybe, comes from 2 places: 1) the apostate ("I used to trust him! Now he's turned on me!") or 2) The theory he supports explains the success of the low-carb approach via a different mechanism, and oh crap, he might be right!

This is meant in the spirit of friendly but pointed discussion, perhaps impossible with Woo but maybe with others. Ok, pile on me!

Ed said...

@Sidereal:

"He explicitly rejects the idea that gluttony and sloth are the consequence of the metabolic syndrome / mitochondrial crapout."

The casual (or hostile) reader might read your comment to believe that he espouses the notion that gluttony and sloth are caused by "nothing" -- eg they're character defects (my cursory read of Woo suggests that that's her perspective of Guyenet.)

My read, however, is that he believes gluttony and sloth are instead consequences of Snickers bars, Doritos, and blooming onions. My guess is metabolic syndrome is a parallel consequence of those foods, and is inter-twined with obesity and other subsequent problems.

In any case, Guyenet has explicitly stated that he does not believe the food reward hypothesis explains all obesity. That many commenters characterize the hypothesis as meant to exclude all other hypothesis strikes me as an exaggeration arising from petulance. Shrug. It's all very complicated.

Elliot said...

@Ed

"In any case, Guyenet has explicitly stated that he does not believe the food reward hypothesis explains all obesity. That many commenters characterize the hypothesis as meant to exclude all other hypothesis strikes me as an exaggeration arising from petulance. Shrug. It's all very complicated."

I'm pretty sure we all agree that there are multiple causal factors in obesity. Guyenet does agree with this but essentially rules out metabolic causes out of hand. Once you've ruled out metabolic causes, what's left? Some very specific diseases and then mental factors like gluttony/sloth/"addiction"/food reward.

john said...

engineering-health,

I think it's that you read this post without first the existing arguments on this and other blogs. Many have provided worthy criticisms. js290 brings up an obvious flaw.

It reminds me of that one guy cwaind or whatever who went crazy on Peter's light and humorous post on fruits and vegetables, though your comment is much more reasonable.

It seems to me that Stephan carefully avoids speaking in terms of concrete physiology because doing so would invalidate a hypothesis that is based soley on "calories in," disregarding hormonal/etc influence on calorie destination. He beats around the bush regarding logical criticisms and focuses on strawmen-type arguments like "Calories still matter." Also, he'll nitpick prominent low carbers and generalize to, "See, the insulin hypothesis is incorrect" (CarbSane seems to be a big fan of that tactic).

Using a totally abstract concept like "set-point" to *explain* weight changes and measuring food reward only in post hoc fashion are *not* the actions of a critical thinker or rigorous scientist. The implication is nothing more than fat people need to eat less of the foods they eat the most.

Ed,

I'm not as critical as Woo in that I don't think Stephan is disguising "character defects" of gluttony and sloth as FR, but the bit about FR not explaining all obesity is probably just a side effect of having a non-aggressive, cautious personality. He has stated that he thinks the hormonal disruption/inflammation/etc associated with a obesity is a result of that obesity. What else is left?

Galina L. said...

Mine main problem with FR theory is that not only different foods are rewarding to different degrees for different people (it was endlessly discussed before, and I am not going there), but also a food reward quality of foods for individuals often depends on the individual's metabolic state and is a function of such state, not over-wise, so it could be changed. After couple of years spent on a LC diet, maybe earlier, all groups of foods became less desirable for me. Nuts are still problematic, but to smaller degree as well,and it is minor. Some garbage like Oreo cookies and Dr. Pepper is an exception, I couldn't consume it even before when a cardboard looked promising (with a right souse, of course). What changed in my physiology? I have no numbers to point to besides my weight (merely 30+ lb lighter).
I could speculate using Macro's comment, that since there is a question

"(Sigal et al. Diabetes 46:1024, 1997)

- Why insulin-suppressing (low-carb) diets comparatively (with somewhat less insulin-suppressing low-calorie / low fat diets) work (much) better amongst people who have insulin regulation problems."

pointing toward certain metabolic state, in my case the insulin-regulation problems got resolved. FR didn't cause anything and didn't resolve anything while being a part of a picture.

There is nothing wrong with discussing rewarding qualities of food, I am sure there is plenty of research that could be done about the subject, but I would hate it to be labeled with the "main cause of obesity" tag. For me addressing food flavors as the mass obesity problem cause is the same as healing diabetes with taking care of peripheral neuropathy and dialysis.

I am just another non-important commenter, of course, but I can testify about changes in my body.

Nigel Kinbrum said...

ItsTheWooo said...
@Nigel
My opinion is indeed worthless, blah blah blah...
This could all be avoided entirely if you just said "In my opinion, I think..." before you described your ideas..."
Everything that I write is my opinions/beliefs/thoughts. It's therefore completely redundant to preface everything that I write with IMO or IMHO. IMHO, of course!

"Re: the comment...Sorry, not convinced. You are basically refusing to admit your choice of words implied moral judgement. The phrase "happier than a pig in shit" is always applied to examples of people being content in immorality/bad behavior particularly gluttony and sloth... unless it is used ironically. Only an autistic or a non-english speaker would believe this crap."
Only a nut-case could come to the above conclusion. I often use that simile because, to we Brits, shit (and farting) is funny.

LeonRover said...
"Well, Nige,
I believe you have just been the object of an "ad porcum" argument."
Woo's argument is not strictly Kosher.

Sam Knox said...

"Doof Drawer"

That cracked me up.

ItsTheWooo said...

@Makro as gallier2 & sidereal said, the idea that reward/palatability of food increases vulnerability to metabolic disease is staunchly denied by Guyenet. If FR operated within the realm of reality like this, I wouldn't have rejected it entirely.

I too came to this thought (that perhaps novel engineered foods lead people to overconsume a diet that can destroy metabolic health/lead to hyperinsulinemia...sounsd reasonable and I do sort of believe this is part of hte obesity epidemic). However, Guyenet has told us in no uncertain terms this is not the case...:

-The obese are NOT hungry, suffering instead from a compulsive eating/craving problem...
-The obese do NOT have unstable blood sugar, sugar/fatty acids never decrease from insulin so as to provoke hunger...
-Insulin simply does NOT lead to obesity, high blood insulin is always a reaction to growing fatter.
-Insulin is always appropriately matched to food intake, and high insulin in obesity is a reflection of insulin resistance which was caused by growing fatter, which was caused by calories, which was caused by rewarding food.

etc etc etc.

Basically he is so full of crap it makes me want to puke, as everything he is telling his audience is counter/opposed to real human obesity and how it manifests. They just eat it up because they lack the experience or personal insight to see it. Seeing as Guyenet has not much studied human obesity, it is understandable how he can make these errors. All he knows are strains of rats and misrepresented studies.

Makro, your examples are all good, but they are like drops of rain in a thunderstorm. The evidence for insulin driving fat storage is OVE-R-WHELM-ING. Only a moron or a person who wants to believe can deny that. It's madness that people without a primary insanity can sit there and say things like "Insulin does not cause fat gain". Brainwashing is strong?

Oh, the popular retort to the efficacy of LC diets: they reduce reward more than low fat/low cal diets.

The retort to the octreotide / metformin studies: leads to weight loss via other mechanisms; insulin reduction is incidental (I KNOW, OMG :x !!)

ItsTheWooo said...

Dear Mr Ed:

Why so ready to characterize me as a baddie? I do like discussion if you want to :D

I do not believe Guyenet will admit gluttony/sloth causes obesity, any more than mel gibson will spontaneously admit he hates jews. He has a reputation to protect and that is not becoming of an obesity researcher.

The FR hypothesis, however, is still the same old gluttony/sloth thing make no mistake! It makes the assumption that we can stop all of this if we avoid the "bad" foods, as if choosing to eat like an unsupervised 5 year old is the reason we have these disorders. Even in the best light, it is hard to ignore the obvious judgement inherent. "Just stop buying snickers bars fatass. If you can't control yourself stop the junkfood11!!!"
When you see a 400 pound lady in the store, YOU KNOW its because of the snickers bars. That simple, thanks FR!

What about fat/diabetic people who never ate soda and chips and candy? Guyenets response to this question: Lalala I cant hear you.

What about people who are IR but slim, or people who are diabetic and slim? Where does FR fit?

No, Ed, the reason we reject the FR hypothesis is precisely because Guyenet made it abundantly clear the insulin hypothesis is FALSE, and FR is TRUE. If we have to sacrifice a lamb here it ain't gonna be the insulin hypothesis which is clearly overwhelmingly true. Again, he has made it ABUNDANTLY CLEAR that he believes FR explains the majority of obesity, and insulin hypothesis explains 0 percent of obesity. Guyenet has not allowed for any possibility that these are both true.

As an obese person my entire life history is easily explained by Taubes and Atkins' and others work ... to hand wave dismiss what I live through, to tell me all along it was just a food adidction and my OBVIOUS GLUCOSE DISORDER isn't real, is infuriating and offensive.

It is all the moreso infuriating / offensive that I know it is hurting thousands of people who can benefit greatly by controlling the insulin response to food choice // maximizing glucose tolerance with supplements and so on... but they are misguided into believing there is no such thing as hypoglycemia and hyperinsulinemia after meals does not lead to hunger/ fat gain and other such bullshit.

Makro said...

@Woo "Makro, your examples are all good, but they are like drops of rain in a thunderstorm."

Oh, I know, but one has to start somewhere.

"The evidence for insulin driving fat storage is OVE-R-WHELM-ING."

Yep, but I think a straight-up, easily accessible compendium of all lines of evidence (with extensive references) pointing in that direction (and discussion of contrary evidence as well, of course), is what is most sorely needed in this debate.

"Only a moron or a person who wants to believe can deny that."

Well, or an obesity researcher.

"It's madness that people without a primary insanity can sit there and say things like "Insulin does not cause fat gain". Brainwashing is strong?"

Well, it´t not that absurd, given that that´s what you would expect for dietarily induced insulin release in healthy people under most circumstances.

Well, also, I guess you could spray insulin up someone´s nose and note that it causes satiety. (Let´s not dwell too long on what happens if you should happen to make brain insulin receptors resistant to insulin(1)...)

(1)http://www.sciencemag.org/content/289/5487/2122.abstract

Makro said...

"Why so ready to characterize me as a baddie?"

Cuz lots of people use politeness as a discussion filter. You are many things, and abrasive is one of 'em. ;)

Nigel Kinbrum said...

Funny how insulin drives muscle mass storage in bodybuilders who do lean bulking.

I used that particular post from Martin Berkhan deliberately.

Insulin only causes fat mass gain in people who eat way too much and move way too little.

*Sits back and awaits the usual rant from cognitively-biased individuals about how I am "obviously" implying gluttony and sloth. Oy!*

LeonRover said...

"So oft in theologic wars,
The disputants, I ween,
Rail on in utter ignorance
Of what each other mean,
And prate about an Elephant
Not one of them has seen."

"A plague on both your houses."
Mercutio to Romeo.

The modern Verona of "Diet & Exercise" contains many more than a couple a' houses.

Slainte

Galina L. said...

Usual rants against gluttony could sound pretty annoying . Here is the typical example from some comments on the link from the Diet Doctor blog

"All these obese people must be prety dumb as well.

Want to lose weight? Eat less, excercise more. It really is that simple. "

Ya , I sure know how simple it is ...

IcedCoffee said...

@Nigel,
I don't think anyone contests that insulin does beneficial things as well. We need insulin to survive, and insulin can certainly be used to promote muscle growth. But we aren't talking about normal postprandial insulin elevation, we're talking about chronic elevated insulin. Bodybuilders tend to have remarkably normal fasting insulin. Not to mention that bodybuilding requires extremely strict caloric monitoring, otherwise that awesome insulin will still lead to fat gain. (<--- Personal experience)

Furthermore, whats your point? All obese people should just become bodybuilders? Problem solved!

As a side note, Martin's "leangains" protocol involves carbohydrate restriction on rest days. Thoughts why?

engineering-health.org said...

@js290:

Food reward does explain the calories out component- food reward modulates the set point of leptin defended by the hypothalamus, which controls hunger, metabolism, and desire to exercise.

It's not simply causing people to eat more food- it seems to cause the hypothalamus to use all of the "tools" available to it to increase adipose mass.

@ItsTheWooo:

You say that you're understanding the food reward hypothesis, but your rebuttals of it suggest that you're confusing it with the "sloth/gluttony" idea, which is the same mistake I was making as well until very recently. In fact it's radically opposed to that idea: it suggests that high calorie intake isn't the product of a conscious choice, but a disease that can be treated by replacing specific foods with other foods *if* you know which foods to replace with which.

I'd like to point out that low carb/inulin explanation makes the exact same assumption that we can stop obesity by avoiding specific "bad" foods. The insulin hypothesis of obesity suggests that obesity can be treated by avoiding "high carb" foods. The food reward hypothesis suggests that obesity can be treated by eating lower reward foods, which includes (but isn't limited to) lower carb foods. For many people, low carb is likely the best way to actually lower food reward.

I am not interested in defending certain hypotheses, I'm interested in understanding the truth and I suspect the truth is far more complex than either theory. The thing is existing data from many experiments (and lean populations with high carb diets) contradicts the insulin hypothesis, and supports the food reward hypothesis.

Your getting angry and insulting people who disagree with you isn't helping things any, I have no vendetta against people subscribing to the insulin hypothesis… I subscribed to it myself until I recently decided that the food reward hypothesis both explains the evidence that seems to support the insulin hypothesis, and other evidence which the insulin hypothesis fails to explain.

@john:

Can you please point me to some of the worthy criticisms of the food reward hypothesis?

Also, "set-point" isn't a totally abstract concept, it's a specific feedback system that's been heavily studied. Nearly every biological system operates with feedback and set-points, some seem not to, but they're a rare exception (if they don't in fact actually have feedback we haven't identified yet).

Insulin itself is of course a hormone primarily for maintaining glucostasis. I suspect that insulin resistance has evolved primarily as a load balancing mechanism to equalize glucose uptake between cells, and when the lipostasis system fails it suddenly experiences the burden of trying to control glucose uptake in an environment far outside the range over which it evolved to operate. This behavior makes the glucostasis system look and act as if it's intended to serve as a lipostasis system, yet it lacks the capacity to do so under many real world conditions.

Elliot said...

@engineering

"[...] a disease that can be treated by replacing specific foods with other foods *if* you know which foods to replace with which."

And which specific foods are those, for Stephan's theory? More specifically than "the ones that are rewarding", I mean.

engineering-health.org said...

@Elliot:

You're asking for specific examples of high reward foods to replace with low reward foods?

It seems weird to point out specific examples when virtually any modern packaged food with a brand name is likely to be a "high reward" food, and most anything that is a simply cooked plant or animal product is likely "low reward."

The most striking example to me is this one: replacing zero calorie diet soda (high reward value/zero calories or carbs) with pure sugar water (high in carbs and calories, essentially the basis of Seth Roberts Shangri-La diet) should reduce hunger and calorie intake.

This is a testable prediction made by the food reward hypothesis, which is *the exact opposite* of the prediction made by the sloth/gluttony hypothesis it's often confused with.

engineering-health.org said...

Of course, I don't advocate pure sugar water as a healthy food, it's just a striking and counter-intuitive example of the effect of food reward.

Grow Up said...

Engineering-health: "virtually any modern packaged food with a brand name is likely to be a "high reward" food, and most anything that is a simply cooked plant or animal product is likely "low reward.""

THANK YOU!

Considering that "modern packaged foods with brand names" invariably contain high quantities of sugars and/or wheat, you have just defined hidden high-carb products.

This reconciles "food reward" and "low-carb" perfectly!

engineering-health.org said...

@Grow Up:

No, it does not- that's not the evidence the theory is based on, but one way to apply it to lose weight in practice. To distinguish two hypotheses, you need to look at experiments under which those two hypotheses make different predictions.

Replacing packaged foods with a low carb diet of natural foods has identical predictions under both hypotheses. It's one piece of information that utterly fails to distinguish the two hypotheses, and therefore is simply irrelevant in this discussion.

One thing that does distinguish the two hypotheses is that people also lose weight on very high-carb low food reward diets: low fat diets, most high in rice asian diets, "feeding tube" diets, and kitava-like starchy paleo diets.

Galina L. said...
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Galina L. said...
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Galina L. said...
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Galina L. said...
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Galina L. said...

@Gro-up,
All that crusade against packaged food is a fight against very local phenomenon(on the World scale), very recent in a historic perspective. Of course super-availability of food helps population to grow bigger, but for somebody like me and many others who came to live in the USA from a different food environment, it doesn't look like the core case of the obesity. We saw people dealing with weight issues in our native countries(on a smaller scale),and such maladies as diabetes, cancer, stroke, high blood pressure are all common in places where people rely on self-cooked meals, but consume too much carbs. They may look thinner than an American crowd, but the difference is mostly in a scale. Also, for most people who have been eating so called "real food" all their lives, boxed and cafeteria food just doesn't taste good, especially on a long run, after a novelty wears off.

I can assure you, replacing self-made low-fat, full of fruits, vegetables and whole grains food with a low-carb fare, even the one containing questionable mayo, causes a very positive change in a weight, health and the normalization of appetite and energy level for many people.
1weentr

Elliot said...

@engineering

Setting aside the statements about sugar diets for the moment, what I'm getting after here is this:

How did you come up with diet soda? How did you rule out sugar water? What principle did you use?

For example: what's the difference? Is it the bubbles? Is it the caffeine? Is it the calories? Is it that diet soda comes in a package with a brand on it?

'[...] low food reward diets: low fat diets, most high in rice asian diets, "feeding tube" diets, and kitava-like starchy paleo diets.'

Same questions as above.

engineering-health.org said...

@Elliot:

Can you clarify the question? What principle did I use for what exactly?

Are you asking how one tells if a food is "high reward" or "low reward" independently of it's effect on weight gain or are you asking something else?

ItsTheWooo said...

@engineering health No, I understand that "reward" defines the reinforcing nature of a behavior/substance, which is considered a dopamine mediated phenomenon. I understand this, but I think it is all a psuedoscience justification for good ol' "GLUTTONY & SLOTH". It's sort of how in the south circa 50s you had white racists saying we should keep blacks and whites "separate but equal". People are very clever at dreaming up confabulations to disguise or justify irrational bias.

For example, Guyenet is TOTALLY UNINTERESTED in the huuuuuuge body of evidence suggesting dopamine primarily mediates energy conservation states (and only incidentally is implicated in compulsive / rewarding behavior, which is a sub-function of dopamine's larger role as a seasonal indicator promoting motivation and energy wastefulness and opportunism). To conceptualize dopamine as an "addiction chemical" is myopic, perhaps willfully so. Dopamine signalling in animals will control the pre-hibernation response which exhibits a striking resemblance to human obesity and metabolic syndrome.

Given what science understands about dopamine in relation to metabolic thriftiness, saying obese people are addicts based on the finding of a low dopaminergic tone, is like saying a 1980's hemophiliac must be an IV drug user when it turns out he is positive for HIV. The most likely cause of HIV in a hemophiliac is exposure to contaminated blood via transfusions. To state a hemophiliac having +HIV is evidence of IV drug use is MIND NUMBING stupid. It is similarly irrational to use a low dopaminergic tone to evidence addiction in obesity, given the larger understanding of dopamine as pertaining to glucose tolerance/insulinemia/weight gain/movement and activity.

Flaws this huge can only be explained by cognitive biases, an emotional drive to make what is not true, true.


Regarding your argument that insulin hypothesis proponents say we can cure obesity by avoiding some foods... yea, the fact a few random nuts believe carbohydrate causes obesity is irrelevant.

The insulin hypothesis makes no argument that avoiding carbs prevents or cures obesity, it only argues all obesity is mediated by excessive fat tissue insulin signalling with facilitative calories (enhanced appetite from lower sugar/ffa) allowing for continued fat tissue growth. Most people who believe in the insulin hypothesis view diet as a method of therapy, not a cure, and carbs do not cause the problem, merely aggravate it like an allergy.

People constantly confuse the most simplistic forms of CIH with the insulin hypothesis in general, these are not the same. Here's my rant on that.

You may think FR supports the insulin hypothesis...I would say you must not understand the FR hypothesis as guyenet will inform you, that in no uncertain terms insulin NEVER causes obesity and merely is reactive to obesity/excessive eating.

ItsTheWooo said...

If low carb diets work by reducing food reward, why can I eat intensely flavorful low carb junky food and have no hypoglycemia/superior appetite control, but a big plate of bland starch will always result in hypoglycemia and hunger?

Why am I always better to eat peanuts and an atkins bar, than cold pasta with my nose held?

The idea that low carb diets work via reduced reward simply does not apply to me.

PS: "reward", pleasure/motivational attributes of food, cannot make your blood sugar and energy zig zag, but macro/micronutrients can do that.

js290 said...

@engineering, "...food reward modulates the set point of leptin defended by the hypothalamus..."

First, what does that mean exactly? What does "set point of leptin" mean? And how is it "defended by the hypothalamus?"

Second, would a more simple statement still describe the energy output component without losing clarity? That is, how is the above statement better than something like "leptin resistance leads to less energy expenditure and more energy storage?"

If a more simple and more generalized description works, how does the concept of "food reward" and "set points" improve our understanding of nature? That is to ask, how is science advanced with the concepts of "food reward" and "set points" when the concept of hormonal signaling can explain the observed phenomenon unaided?

john said...

engineering,

It is unfalsifiable and violates Occam's razor. That's what makes it an unscientific idea, but sycophants and suckers fall for it for some reason.

There exists a "set-point," or "settling point," of fat mass, bone mass, heart mass, etc. Even the pond down the street has a water set-point. Of course nobody says osteoporosis is caused by the brain lowering the bone set-point, because direct concrete explanations for bone loss/growth [and water gain/evaporation, etc] exist, just like fat mass. Guyenet clouds and "dematerializes" physiology in the same way with food reward by measuring only post-hoc, so that his ideas are more flexible and resistant to criticism.

engineering-health.org said...

Set-point is a valid concept that applies to almost every biological system- nearly every biological process is controlled by feedback to keep it's output within a range compatible with life.

The mathematics and methods for understanding this behavior were first formalized by Norbert Wiener in his book "Cybernetics: or the Control and Communication in the Animal and the Machine."

Of course, it's not adequate to simply state that something has a "set point" and leave it at that, you need to try and understand specifics of each molecular step in the system to understand how it behaves, so that you can understand exactly what is going wrong when it fails to operate correctly. Modern molecular biology tools are only now giving us the raw data necessary to build mathematical and computational models which accurately represent the behavior of such systems. Such models are falsifiable hypotheses- if accurate they will predict the systems behavior under new conditions which have never been observed.

Talking about biological mechanisms without evoking control theory opens the possibility of getting lost in specific interactions within a small subset of the system, while missing the dynamic behavior of the whole system. The dynamic behavior of the whole system, and the conditions under which it fails to maintain homeostasis compatible with health is generally what you're concerned about when treating disease.

engineering-health.org said...

The reason the "sloth/gluttony" or "calorie balance" hypothesis is complete gibberish, is because it's the result of applying "open loop" thinking to understand a "closed loop" control system.

I don't think obesity research in general will make much progress until we start talking about feedback and closed loop control.

Trying to treat obesity by ignoring this behavior is like trying to cool down a house with central heat/AC by opening the windows, or slow down a car with cruise control by applying the parking brake.

It's critical to realize that the "sloth/gluttony" hypothesis makes *different* predictions under the same conditions as the food reward hypothesis. They cannot possibly be the same idea, when they predict vastly different results from the same experiments (such as the diet soda vs sugar water scenario I mentioned above).

FrankG said...

@engineering wrote: "Set-point is a valid concept that applies to almost every biological system- nearly every biological process is controlled by feedback to keep it's output within a range compatible with life."

Was this meant as a rebuttal, or in agreement with John's "There exists a "set-point," or "settling point," of fat mass, bone mass, heart mass, etc. Even the pond down the street has a water set-point. Of course nobody says osteoporosis is caused by the brain lowering the bone set-point..." ?

Accepting the idea of set-point -- implicit in the word "Homeostasis" word used to describe this feedback system -- does not require a leap (as performed by Stephan Guyenet) to that set-point being brain-centered. I see no need for the brain to be controlling how much fat I need to store, when relatively simple, local processes can accomplish the same thing.

As John mentions: a pond or other body of water can maintain a relatively stable "shore-line" despite multiple and variable inputs and outputs, all without a central controller turning on or off taps and drains.

Similarly look to the flocking behaviour of birds or schooling of fish: to a visiting alien a murmuration of Starlings might be mistaken for a single large entity moving and whirling about the sky, controlled and directed by a central brain... where in reality it is a vast collection of relatively simple individuals, each with a small set of basic instructions such as "fly as close as you can to the bird(s) around you without colliding"

engineering-health.org said...

@FrankG:

I agree with John that set-points exist for almost everything, but there are different mechanisms for defending those set-points. Bone mass and heart mass are mostly controlled directly by local feedback mechanisms, whereas lakes (without manmade dams) use no feedback at all and are an example of "open loop" control. Osmotic diuresis is an example of biological open loop control.

The primary reason to think a "lipostasis system" with the hypothalamus as a closed loop controller actually exists is the research done on leptin in mice and rats which I won't attempt to summarize in a single blog comment.

It may be possible to have a lipostasis system which doesn't directly use the hypothalamus as controller but I've seen no evidence that such a system exists, and the role of the hypothalamus in lipostasis has been well studied. Such a system wouldn't fit any of the published literature on leptin that I've seen.

Overall we can't really talk about food reward unless we can first agree that:
1) The application of control theory to biology is useful and results in testable hypotheses.
2) A lipostasis system exists, which uses leptin as an adipose mass signal.
3) The hypothalmus regulates energy intake and expenditure to defend a range of leptin levels.

If we can agree on these then we could talk about the possible specific mechanisms of leptin resistance.

Now, the system does seem far more complicated than this, and has many more inputs than just leptin. Woo's example above is a good one, reactive hypoglycemia is one scenario where hunger gets cranked up all the way regardless of leptin levels. However, clearly there's plenty of obese people not suffering merely from chronic reactive hypoglycemia.

ItsTheWooo said...

@Engineering
It is illogical to state research into leptin proves that leptin is the ONLY influencing factor/controller of the fat mass settling point. If a lack of leptin centrally leads to severe obesity and non-termianting metabolic thriftiness (indeed it does!) ... this does not mean that ONLY LEPTIN controls the settling point. For example, one may have ample leptin, but be afflicted with a metabolic disorder which leads to gross hyperinsulinemia/inhibited/deficient fat oxidation when presented with a high glucose diet. An example of this: taking a dopaminergic blocking medication. WHen someone takes a dopamine receptor blocking med, the body will simply NOT oxidize glucose normally any longer, and hyperinsulinemia ensues shortly. The lack of normal dopamine will reduce motivation and motor activity at the same time, which only worsens the hyperinsulinemia.
Weight will be gained as a directly result of this lack of dopamine activity in the body and the brain. Glucose tolerance becomes non-existent, and you stop wanting / being able to move easily.

However, centrally, the leptin receptors are still working just as they always were... what happened was a DIRECT deficiency of dopamine, leading to energy conservation as if preparing for fall/winter, or if actively starving.

FYI, much of the way leptin modulates body weight is by affecting dopamine levels. A good chunk of the glucose intolerance/inactivity/fatigue/low motivation/passive personality associated with congenital or aquired leptin deficiency is secondary to the fact adequate leptin is required to make the dopmine system in your brain work properly. Dopamine synthesis drops to nothingness without leptin.

If you leave leptin signalling grossly in tact but cut the heart out of dopamine with a chunk of antipsychotic meds, you can produce some of the symptoms of leptin deficiency.

The point I am making here. It is false to assume body fat is controlled by one mechanism, it is false to assume settling point only has one effector, it is FALSE to state ONLY the brain affects fat mass growth. The brain is very important, but this is only because the brain is very influential in determining glucose sensitivity and insulin dynamics in the fat tissue.

If there exists a cell level mitochondrial defect in energy use, or a local abnormality in fat tissue, it is hypothetically possible to grow body fat abnormally even if central process are on deck.... or, the central abnormalities are merely reactive to the fat tissue abnormalities.

I am a real world fat ass. Let me tell you, sir, when I went on a ketogenic diet, it was like I was a naturally thin person. I weighed 280 pounds. TWO HUNDRED EIGHTY pounds of fatass. Within 48 hrs of ketosis I waddled into my family room and announced to my family I would be thin, because I cured my obesity, because I discovered the cause of it. They all laughed at me.

Who's laughing now?

If my brain was broken, I sincerely doubt a ketogenic diet would have cured me... but absolutely a ketogenic diet would cure a local abnormality in glucose oxidation, don't you think?

I am not leptin resistant. I respond to low dose leptin powerfully, and I have the published studies to prove it.

The FIRKO mouse is all the evidence we need that, ultimately, local action at the site of fat tissue via insulin 100% controls body fatness. The brain, hypothalamus, only controls how the fat tissue behaves. This does not logically mean or translate into all abnormal fat tissue behavior being a brain problem. Error, massive one.

ItsTheWooo said...

Falling from a window causes broken bones. <--- true usually.

Broken bones, therefore, are always caused by falling from windows. <--- false.


Hypothalamic / central brain defect leads to thrifty metabolism and fat tissue growth. <--- true.

WHenever you see a fat person, you know the problem is a brain disorder, and insulin always follows brain activity, right? <--- lol no.

js290 said...

@engineering: "calorie balance" is gibberish only because the religious calorie counters misunderstand what the Conservation of Energy is telling us. Conservation of Energy is a boundary condition in the control system you're interested in, in fact it's a boundary condition in ALL systems in this physical universe. Hence, it's a necessary effect. Religious calorie counters incorrectly attribute it as a cause. Similarly, are these homeostasis set points causes or effects? My guess is the latter.

In the control system that is human metabolism, does the concept of "food reward" improve the model that would describe the system? Or, would it simply be part of the overall reward feedback system? My guess is it's closer to what J Stanton writes about that we have a centralized reward system that drives all of our behaviors not just one specific to food preferences.

Margaretrc said...

My biggest problem with SG is not the FR hypothesis, but the complete dismissal of the validity of the CIH "no scientist takes the CIH seriously" or something to that effect, attempting (?) to make those of us who see the basic logic of the CIH as stupid, dumb, not scientists, etc. Sorry. I like biochemistry, too(even have a degree in it), and while I'm not willing to completely dismiss the idea that some foods (sugar?) have an effect on the brain's reward center, likewise I can in no way dismiss or buy his dismissal of the fact (yes fact) that insulin does regulate fat storage and that, while a diet high in carbs won't necessarily lead to obesity, obesity without the presence of carbs is simply not going to happen. Show me the fat person who got that way eating nothing but highly rewarding fat and protein and very few carbs.