tag:blogger.com,1999:blog-36840063.post8230086759897088358..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: A glimmer of lightPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger61125tag:blogger.com,1999:blog-36840063.post-31876238348845554312012-06-17T18:37:12.912+00:002012-06-17T18:37:12.912+00:00My biggest problem with SG is not the FR hypothesi...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.Margaretrchttps://www.blogger.com/profile/17160051189722454020noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-80846187475926093172012-06-13T05:05:35.366+00:002012-06-13T05:05:35.366+00:00@engineering: "calorie balance" is gibb...@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.<br /><br />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.js290https://www.blogger.com/profile/08157385596237909630noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-79458340855083241592012-06-13T04:52:20.026+00:002012-06-13T04:52:20.026+00:00Falling from a window causes broken bones. <---...Falling from a window causes broken bones. <--- true usually.<br /><br />Broken bones, therefore, are always caused by falling from windows. <--- false. <br /><br /><br />Hypothalamic / central brain defect leads to thrifty metabolism and fat tissue growth. <--- true.<br /><br />WHenever you see a fat person, you know the problem is a brain disorder, and insulin always follows brain activity, right? <--- lol no.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-34020694214573355112012-06-13T04:48:38.594+00:002012-06-13T04:48:38.594+00:00@Engineering
It is illogical to state research in...@Engineering <br />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.<br />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.<br /><br />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.<br /><br />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.<br /><br />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.<br /><br />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. <br /><br />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.<br /><br />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.<br /><br />Who's laughing now?<br /><br />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? <br /><br />I am not leptin resistant. I respond to low dose leptin powerfully, and I have the published studies to prove it.<br /><br />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.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-52158230499689371022012-06-12T23:20:57.833+00:002012-06-12T23:20:57.833+00:00@FrankG:
I agree with John that set-points exist ...@FrankG:<br /><br />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.<br /><br />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. <br /><br />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.<br /><br />Overall we can't really talk about food reward unless we can first agree that:<br />1) The application of control theory to biology is useful and results in testable hypotheses.<br />2) A lipostasis system exists, which uses leptin as an adipose mass signal.<br />3) The hypothalmus regulates energy intake and expenditure to defend a range of leptin levels.<br /><br />If we can agree on these then we could talk about the possible specific mechanisms of leptin resistance. <br /><br />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.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-66661346266064601812012-06-12T22:17:21.472+00:002012-06-12T22:17:21.472+00:00@engineering wrote: "Set-point is a valid con...@engineering wrote: <i>"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."</i><br /><br />Was this meant as a rebuttal, or in agreement with John's <i>"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..."</i> ?<br /><br />Accepting the idea of set-point <i>-- implicit in the word "<a href="http://en.wikipedia.org/wiki/Homeostasis" rel="nofollow">Homeostasis</a>" word used to describe this feedback system --</i> does not require a leap (as performed by Stephan Guyenet) to that set-point being <i>brain-centered</i>. 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.<br /><br />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.<br /><br />Similarly look to the flocking behaviour of birds or schooling of fish: to a visiting alien a <a href="http://www.youtube.com/watch?v=iRNqhi2ka9k" rel="nofollow">murmuration</a> 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"FrankGhttps://www.blogger.com/profile/01980497914756341565noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-11993757719499656742012-06-12T19:52:40.458+00:002012-06-12T19:52:40.458+00:00The reason the "sloth/gluttony" or "...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. <br /><br />I don't think obesity research in general will make much progress until we start talking about feedback and closed loop control.<br /><br />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.<br /><br />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).Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-60463747908771966232012-06-12T19:31:51.117+00:002012-06-12T19:31:51.117+00:00Set-point is a valid concept that applies to almos...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.<br /><br />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."<br /><br />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.<br /><br />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.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-45131302356804844772012-06-12T04:26:49.300+00:002012-06-12T04:26:49.300+00:00engineering,
It is unfalsifiable and violates Occ...engineering,<br /><br />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. <br /><br />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.Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-57407286906211861702012-06-10T00:02:03.314+00:002012-06-10T00:02:03.314+00:00@engineering, "...food reward modulates the s...@engineering, "...food reward modulates the set point of leptin defended by the hypothalamus..."<br /><br />First, what does that mean exactly? What does "set point of leptin" mean? And how is it "defended by the hypothalamus?"<br /><br />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?"<br /><br />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?js290https://www.blogger.com/profile/08157385596237909630noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-82575998729056626172012-06-09T05:04:43.144+00:002012-06-09T05:04:43.144+00:00If low carb diets work by reducing food reward, wh...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? <br /><br />Why am I always better to eat peanuts and an atkins bar, than cold pasta with my nose held?<br /><br />The idea that low carb diets work via reduced reward simply does not apply to me.<br /><br />PS: "reward", pleasure/motivational attributes of food, cannot make your blood sugar and energy zig zag, but macro/micronutrients can do that.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48915593962588146202012-06-09T04:59:20.714+00:002012-06-09T04:59:20.714+00:00@engineering health No, I understand that "re...@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.<br /><br />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. <br /><br />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.<br /><br />Flaws this huge can only be explained by cognitive biases, an emotional drive to make what is not true, true. <br /><br /><br />Regarding your argument that insulin hypothesis proponents say we can cure obesity by avoiding some foods... yea, the fact <b>a few random nuts believe carbohydrate causes obesity is irrelevant</b>. <br /><br />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.<br /><br />People constantly confuse the most simplistic forms of CIH with the insulin hypothesis in general, these are not the same. <a href="http://itsthewooo.blogspot.com/2012/03/insulin-hypothesis-is-not-same-as-cih.html" rel="nofollow">Here's my rant on that</a>. <br /><br />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.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-74443950229547298512012-06-09T03:55:38.232+00:002012-06-09T03:55:38.232+00:00@Elliot:
Can you clarify the question? What princ...@Elliot:<br /><br />Can you clarify the question? What principle did I use for what exactly?<br /><br />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?Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-76937092642164118882012-06-09T02:57:11.932+00:002012-06-09T02:57:11.932+00:00@engineering
Setting aside the statements about s...@engineering<br /><br />Setting aside the statements about sugar diets for the moment, what I'm getting after here is this:<br /><br />How did you come up with diet soda? How did you rule out sugar water? What <i>principle</i> did you use?<br /><br />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?<br /><br />'[...] low food reward diets: low fat diets, most high in rice asian diets, "feeding tube" diets, and kitava-like starchy paleo diets.'<br /><br />Same questions as above.Elliothttps://www.blogger.com/profile/05609032995818591810noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-78865883153188842232012-06-09T00:59:53.732+00:002012-06-09T00:59:53.732+00:00@Gro-up,
All that crusade against packaged food is...@Gro-up,<br />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. <br /><br />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.<br />1weentrGalina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-58014059092491678032012-06-09T00:59:29.032+00:002012-06-09T00:59:29.032+00:00This comment has been removed by the author.Galina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48020961586773089772012-06-09T00:59:05.494+00:002012-06-09T00:59:05.494+00:00This comment has been removed by the author.Galina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48988913537350593902012-06-09T00:57:43.418+00:002012-06-09T00:57:43.418+00:00This comment has been removed by the author.Galina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-58811272179065208622012-06-09T00:56:42.909+00:002012-06-09T00:56:42.909+00:00This comment has been removed by the author.Galina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-38335993882061471932012-06-08T22:58:57.943+00:002012-06-08T22:58:57.943+00:00@Grow Up:
No, it does not- that's not the evi...@Grow Up:<br /><br />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. <br /><br />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.<br /><br />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.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-46747833924179806812012-06-08T22:32:58.963+00:002012-06-08T22:32:58.963+00:00Engineering-health: "virtually any modern pac...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.""<br /><br />THANK YOU!<br /><br />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. <br /><br />This reconciles "food reward" and "low-carb" perfectly!Archie Robertsonhttps://www.blogger.com/profile/03023132179697037438noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-19807947085672140662012-06-08T21:43:59.641+00:002012-06-08T21:43:59.641+00:00Of course, I don't advocate pure sugar water a...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.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-33303526378523698932012-06-08T21:20:00.202+00:002012-06-08T21:20:00.202+00:00@Elliot:
You're asking for specific examples ...@Elliot:<br /><br />You're asking for specific examples of high reward foods to replace with low reward foods?<br /><br />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."<br /><br />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.<br /><br />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.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-41887122570162084892012-06-08T20:58:04.593+00:002012-06-08T20:58:04.593+00:00@engineering
"[...] a disease that can be tr...@engineering<br /><br />"[...] a disease that can be treated by replacing specific foods with other foods *if* you know which foods to replace with which."<br /><br />And which specific foods are those, for Stephan's theory? More specifically than "the ones that are rewarding", I mean.Elliothttps://www.blogger.com/profile/05609032995818591810noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-37922400332331750602012-06-08T20:31:36.434+00:002012-06-08T20:31:36.434+00:00@js290:
Food reward does explain the calories out...@js290:<br /><br />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.<br /><br />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.<br /><br />@ItsTheWooo:<br /><br />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.<br /><br />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.<br /><br />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.<br /><br />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.<br /><br />@john:<br /><br />Can you please point me to some of the worthy criticisms of the food reward hypothesis?<br /><br />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).<br /><br />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.Anonymousnoreply@blogger.com