Of Mice & (Wo)Men: When's the last time you saw an 5'4" 130 pound fat woman?
I'm always amused when a rodent study that seemingly counters the calorie-based theories on obesity comes down the pike. In predictable fashion, someone in the LC webosphere will pick up on it and use it as an example to counter calorie-based theories on weight/obesity. A recent example of this is brought to us by low carbers' favorite comedian edutainer, Tom Naughton: Fat Mice & The Laws of Thermodynamics that referenced the following study: Mild calorie Restriction Induces Fat Accumulation in Female c57BL/6J Mice.
Now Tom starts out misrepresenting things by picturing a fat mouse, likely an ob/ob. This study actually involved females of the strain pictured below:
Kind of a cute little critter, no? The study was also conducted in the context of calorie restriction and its demonstrated increase in longevity of mice. They are not a mutant strain genetically predisposed to obesity.
These mice can live almost 3 years and average about half that. So the two experiments were conducted during normal growth (4 weeks for 8 week old mice in one study, 3 weeks for 10 week old mice in the other). The mice were not made obese then put on a calorie restricted diet. Both groups of mice grew slightly or not at all during the studies. So this study was NOT looking at weight loss in the obese, it was looking at the effect of restricting calories in a normal mouse and testing the response. Now reproductively these mice were adults, but these mice continue to grow throughout their lives. So this might be somewhat akin to putting normal weight young children on calorie restricted diets and seeing what happens. The results may well hold a clue to those impoverished cultures with high rates of true undernutrition in childhood leading paradoxically to obesity in adulthood, but that's not what CDS sufferers see.
Now, before I continue on to discuss this study and its implications, I simply can't help but point out that the last link in the previous paragraph is to a study entitled The High-Fat Diet–Fed Mouse. In this study they fed this very same strain of mouse the usual (11%) fat chow and a high (58%) fat diet. The regular diet was quite high carb (63%) while the high fat diet was fairly low carb (~25%). The results: "Body weight was higher in mice fed the high-fat diet already after the first week, due to higher dietary intake in combination with lower metabolic efficiency." Why did these mice ACTUALLY *get fat*? They ate more! Someone ought to write a book on this stuff. 
(I guess Marta forgot to turn up their thermostats and get those futile cycles spinnin, but I digress ...) Something else happened to the fattening mice, they became hyperglycemic, hyperinsulinemic, and had impaired glucose tolerance. This sounds to me like mice overeating on a high fat diet getting obese and diabetic while those eating low fat/high carb diets maintain proper energy balance for normal growth and metabolic regulation to me. Oh wait ... that can't be right! Yeah, I forgot ... this is a mouse study and therefore has no relevance to humans after all. Phew! Explained that one away nicely. Nothing to see here folks, let's move on ...
Sorry, but before we do, let's summarize: This mouse grows relatively insignificantly in mass over the span of 3-4 weeks when fed a low fat - high carb diet in either ad libitum or calorie restricted fashion. With CR, the metabolism slows so that these mice divert more intake towards fat stores than lean mass. The very same strain of mouse fed a relatively low carb high fat diet gets fatter and heavier because the mice eat more.
OK ... So back to the original study, thermodynamics, etc. All of the mice were acclimated to eating ad libitum (AL) throughout their lives up to the start of the study. There were two study "legs":
I: 8 week old mice divided into 2 groups AL v. CR for four weeks. Lean and fat mass were assessed.
II: 10 week old mice divided into 2 groups AL v. CR for three weeks. Total fat mass, distribution between various fat depots, resting energy and total energy expenditures (REE,TEE) were measured.
In Study I, both groups increased body weight slightly and similarly. But the AL added more lean mass while the CR added more fat mass. The result reporting as percents is a bit misleading IMO. Note that we're talking mice that weighed around 20g. After 4 weeks the CR mice had 3.37 ± 0.23 g fat mass vs. 2.00 ± 0.09 g. So while the CR group added 68% more fat mass, we're talking 1.37 g of a 20 g mouse - e.g. a redistribution of <7% bodyweight in a period. I also note the variability for the CR mice is quite a bit higher than that for the AL mice indicating that some of the CR mice faired differently than others.
OK, so the CR mice got fatt-I-er, but not "fatter", hence the title of this blog post. The CR mice accumulated more fat tissue compared to the AL mice, and added less lean mass, but, they didn't gain more weight. In other words, they did not become obese. This is important because if we're talking "Why We Get Fat" and saying that it's all about dysregulated fat that accumulates lipid, this study simply does not support such a thesis.
For the overweight ladies in the audience (since this study was in females) who became so in adulthood, think now about how you got fat for a moment. Did you start out a 130 lb woman (or whatever "normal" is for your height/build) with 20-25% body fat and start noticing that despite weighing 130 lb week in and week out for a period of years you started turning to goo and found yourself with 50% body fat? Of course not. When we get fatter, we see the weight on the scale increase week in and week out as we become, say, a 180 lb woman. Does that mean each of us gained 50 lbs of fat? Of course not. I discussed this HERE.
Back to the study, in Part II, they measured energy expenditure and lo and behold TFLOT holds up pretty well. In this part of the study, both groups of mice were relatively weight stable for three weeks. The 5% CR corresponded to a 5% reduction in TEE and both groups were thus in energy balance. The resting energy expenditure (REE) dropped 20% (from 6.09 to 4.83 kcal/day, a difference of 1.26 kcal/day) while total energy expenditure dropped 5% (from 8.38 to 7.97 kcal/day, a difference of 0.41 kcal/day). For the AL mice REE/TEE was ~73% while it was only ~61% of the CR group. Doing the math, the other energy expenditures in the CR group must have gone up even though it wasn't noticeable with the locomotive activity or BAT (brown adipose tissue) thermogenesis (although they didn't measure body temp, rather UCP activity so it is possible that there was temperature compensation not related to BAT). Seems the mice were conserving energy by lowering the "idle" on the engine, all the while expending a bit more on something - could that be the mouse equivalent of fidgeting or other nervous behavior resulting from sensing minor starvation? Who knows. But, the mice that accumulated the most fat also expended a greater proportion of their intake on something other than basal metabolism.
So, where does this leave us in the end? Well, we do know that a certain level of body fat does seem to improve survival rates for disease and injury (sorry no handy reference at the moment). Perhaps CR, by causing the mice to be more efficient at storing energy and putting a bit less into bone/muscle/organ growth end up with bodies that require fewer calories to maintain later in life and allow for sufficient reserves to get through harder times. Makes sense to me. I'm being repetitive, but it is important to note: they did NOT become obese or even fat. The mouse's organs and systems were not strained by managing a significantly heavier body. Even on a small mouse, about one and a third gram is just not a lot of fat spread around several depots - that's like 1/4th of one teaspoon of butter.
OK, so how does this translate to humans, weight gain and weight loss? Well, firstly, when we get fat we GAIN weight. We don't just start redistributing lean and fat mass. And what of losing weight. Isn't that 5% change in TEE in response to a 5% CR proof that the body is adaptable so, that whole 100 cal/day = 10 lbs in a year is totally wrong? Well, for this we could go on and on with the rodent studies, OR, we could acknowledge that we have a crap load of data for what happens to actual humans who are already over-fat and look at that to see if there's really much to be learned here. From the discussion in this very paper we have the following:
A growing body of literature has demonstrated that moderate or severe CR (30–60%) leads to significant changes in body composition including reduced body fat mass and/or lean mass, with or without weight loss (4–6,22,23). For example, 25% CR in humans resulted in a clear decline of body fat mass and fat-free mass after 6 months (5). In 6-month-old mice, 55% CR resulted in a 71% reduction in total fat mass after 6 months (22).
Let us also keep in mind the metabolic rates vs. body masses for various mammals as well. The energy expenditure:body weight ratio is substantially higher for mice than humans. See, for example, the graphic below:
Considering that body temp maintenance is a major component of REE, the mice seem to have a disproportionately large ability to conserve energy as compared to, for example, us humans, because it's a bigger "cost" per unit mass for them.
Here is just one study that quantified both REE and TDEE for actual free-living humans (as luck would have it obese women), that I've blogged on previously. The study looked at LC vs. LF diets and EX (3X 45 min moderate cardio) vs. NX (no exercise) by comparing 4 groups of dieters. The changes in body composition, REE and even TEF did not differ between the two diet groups. For both diets, REE was reduced by ~130 cal/day. This is GOING to happen folks! IF you are losing weight without changing activity, you are in caloric deficit from eating less. Even TEF wasn't different - I've long suspected that this is because the Atwater factors represent metabolizable energy that seems to have been partially if not fully adjusted for the "cost" of extracting the energy.
What influenced body composition most? The much maligned slogging cardio. Yeah, 3X 45 minutes of 15 minute sessions on one of three cardio machines. From the discussion:
More important than total weight losses [of which LC were slightly more than LF], however, are the relative changes in FFM and FM. Exercise training was a major determinant of the changes in body composition, with FM comprising 89.4% of the weight loss in the Ex group, compared with only 71.3% in the Nx group.
So much for exercise being useless for fat loss, but I digress ... In any case, the exercisers had their intake matched to approximate the caloric cost of the exercise itself so that the "calculated" caloric deficit would be the same for both groups: e.g. they got to eat a bit more. But let's look at TDEE:
Directly due to Exercise: EX: +0.07 ± 1.23 NX: -1.46 ± 1.04 MJ/d
Not attributable to Exercise: EX: +0.75 ± 1.06 NX: -0.61 ± 1.03 MJ/d
As I've stated before, I'm not sure these are additive, but +0.82 MJ vs -2.07 MJ between the two. This is a swing of almost 3 MJ or ~ 700 calories!! The result is that the exercisers lost 2.7 kg more on average (that's almost 6 pounds) of FAT. And why? Because they actually increased TDEE from baseline rather than reducing it. And not just from the exercise, but because NEAT (non-exercise activity thermogenesis) increased. So much for the theory that exercisers just lounge around on couches more the rest of the day to compensate. But again, I digress ...
If there is a real lesson to be learned here folks, it is that we should strive for our children to eat a diet that allows them to grow normally and remain lean eating ad libitum, because once we get fat, it's a minefield out there what to do about it. And if we find ourselves as overweight adults, there's no easy fix. We gain and lose both lean and fat mass and we have limited control over it. When we lose weight, TDEE goes down in part because REE decreases (and stays there for the most part) but NEAT goes down too. Exercising can help counter this.
Eat Less, Move More ... Move More you can eat a little more.
Comments
Quote "That second part of that sentence ["ingest fewer calories than calories expended in a day"] is, of course, correct."
He also doesn't seem to deny that weight loss or gain is strictly related to eating/moving patterns:
Quote: "Yup … if you get fat, by gosh, it means you’re either eating more or moving less."
His point is how little relevance a certain physical law has in obesity research and weight/fat regulation. I don't think that he would argue that any of the actual study outcomes (changes of fat, weight, REE, TEE, NEAT in the mice) have necessarily the same or even similar implications in humans. But that wasn't his point to begin with.
Quote: "Yup … if you get fat, by gosh, it means you’re either eating more or moving less."
Umm... that would be Fat Head mocking Jillian Michaels because lord knows she didn't get the midriff in an ad that occasionally graces his blog of late because she knows a thing or two about weight loss. Guess it makes these two big men feel a bit more impo'tant putting her down rather than putting forth some sort of consistent theory. She must have hurt his feelings or something: http://www.youtube.com/watch?v=5LNH0RPXI0M
Naughton like his teacher can't spin his way t a consistent explanation because TFLOT and the carb/insulin magical fattening macro/hormone theories don't mix.
To your last sentence: Actually I would say, TFLOT and carb/insulin magical fattening theory are two non-related "issues" - while the former is always right but meaningless, the latter can or cannot be right but certainly without being magical - but we've been over this ;).
On a related note, I've staid shy of 1800 cals a day since october, eating primarly protein and carbohydrate (berries, fruit, lean cuts of meat and a whole lot of wholegrain bread and oats, vegetables and lowfat cheese). I'm currently down 37 lbs.
Prof. Lampert calls it "important but dull". http://secondlaw.oxy.edu/. Replace meaningless with "dull" then ;)
The question in my mind is can(autonomous)NEAT be increased in people with a low propensity for it.
@Christian: TFLOT doesn't need to indicate direction of causality, but it explains perfectly well why surpluses leads to gains and deficits to losses. Ultimately you put too much or not enough food in your body to meet needs, signalling telling you to do so is part of what makes us living beings, but it never goes in reverse. Or are you aware of some humans for whom urine, CO2 and feces are pumped backwards through through their bodies and a steak with a side of spinach, roasted potatoes and a glass of wine and some oxygen comes out of their mouths?
Reverse means cause and effect are switched, not time going backwards. I gave an example before, not sure if you read that:
"Say two identical twins eat two different, yet isocaloric meals both worth, say, 300 kcal. Lets assume over a 3 hour period the metabolic rate of those twins requires precisely 300 kcal. Twin 1 who eats a healthy diet partitions the energy perfectly, leaving the body with the same amount of fat and other energy stores at 3-hour baseline. The other twin however eats a bad diet: 50 kcal of his meal are partitioned into fat storage, the energy difference is replaced by, say, glycogen. So at 3-hour baseline, the second twin is both 50kcal “fatter” and slightly glycogen depleted. Somehow the body senses the glycogen depletion and is signalling slight hunger. Twin number 2 eats an apple worth 50kcal. And boom - thats why we get fat ;)."
Yeah the metabolic pathsways and numbers are invented - i honestly don't care ;). The thing is in this situation - without violating energy balance - the second twin overate because he was getting fatter, not the other way around. You could also say shitty energy partitioning or wrong settling point because of shitty diet. It is perfectly possible for "overeating" to be an effect rather than a cause. At least physics doesn't forbid that.
There's no evidence of any kind that a "bad diet" would lead to more calories partitioned as fat storage. No proof of any kind that certain foods are more conductive to fait gain, not even marshmallows, as long as the caloric intake itself is not conductive to fat gain. And no proof of any kind that certain foods, not even top sirloin and spinach, are less conductive to fat gain, as long as the caloric intake is conductive to fat gain instead.
So there's no evidence that regardless of calorie intake certain foods are more likely to be stored. But even if they were, fat storage per se is meaningless because it is ungoing process. The only thing that matters is fat balance at the end of the day (or the week) meaning fat stored vs. fat mobilized and the only thing that controls this process is your caloric intake vs. your caloric expenditure.
I don't think we can do much about the fidget stuff, but we can do other little things. Y'know initially I did it consciously. Now it's like auto pilot for me.
http://www.ajcn.org/content/83/6/1442.full
protein is the only variable.
Isocaloric diets that are inadequate in proteins are worse for weight loss. Isocaloric diets that are adequate in proteins are not worse for fat loss than diets that are higher in proteins and the ratio of fat to carbohydrates is irrelevant as long as the diet is isocaloric.
@Christian: Please think about the evolutionary consequences of what you (and Taubes) propose. Isn't the whole point of fat cells to store energy in times of plenty so we can survive through times of scarcity? But according to you, when a hunter gatherer killed a large fat animal and had plenty of fat and calories for dinner, their body would not store any of those excess calories, because the meal was zero carb. When the hunter gatherer didn't manage to hunt anything and had to survive eating roots and vegetables and fruits, who are fibrous and poor sources of calories, their fat cells would not release any energy. It was like having a bank account that doesn't let you put money into it when you have plenty and doesn't let you withdraw money when you need it. Does that make sense to you? Do you honestly believe that was what happened? Please tell me how humankind manage to survive to this day.
I also take one day a week where I eat 300-400 grams of carbohydrate, to increase leptin. Wholegrain bread with honey. Delicious :)
It sounds easy, but it's literally taken me years to really get the groove going (six years ago I weighed 330 lbs, today I weigh just above 200). What got me fat was never carbs in the first place. It was the overconsumption of calories, in the form of burgers, pizza, chips, cookies, chocolate and stuff like that. I don't eat any of that stuff any more (just the occasional slice of pizza and the occasional burger). I made a concious effort to change my diet for good, and it's finally sticking.
A few years ago I gave lowcarb a try for quite a while. It worked, but not any better than having my carbs like I do now, and having to avoid carbs all the time turned into a huge mental chore. In short, I figured it wasn't all it was cracked up to be. Reading the science about how carbs work (I think I've read every post on this blog), makes me realize I was right to bring carbs back into my diet.
"There's no evidence of any kind that a "bad diet" would lead to more calories partitioned as fat storage."
Well, if that really is so then case closed. But again - physics can't tell, only "evidence".
And btw if you ever read a book about nutrition for weight lifters (e.g. by Lyle McDonald) you would know that this is precisely what these people are mostly occupied with: energy partitioning aka when can I eat how much of what that it goes to my muscles and not to my hips.
And a last point: Yes, if you adjust for caloric intake this discussion about macronutrients might all have little relevance. But if you don't and just eat till full, wait till hungry again and repeat - then this might become relevant.
Do I make sense to anyone?
As for Lyle's books, keep in mind that the methods you're thinking of when referring to him are the cyclic diets that are meant to let you lose weight while sparing muscle (or UD2, which is total glycogen depletion followed by a massive carbup). For muscle gain, Lyle has specifically said that the best course of action is to cycle between a modest calorie excess for a period of time, and then diet off the fat that accompanies muscle gain. Remember, Lyle is concentrating on the guys that have very little bodyfat. For those people, losing bodyfat without losing muscle is a big struggle. For the rest of us, these things are overkill.
Whatever you eat, the body will handle. What it won't do is flush out food undigested, which is the only way calories from food would be made unavailable to the body.
Yes but that's because they are on hypercaloric eating and when you are eating 2000 calories more to gain weight you need to make sure the excess is not used as energy to store but as energy to build muscles. And most weight lifters screw it up anyway because they eat more energ than their body needs to build muscles since muscle growth is limited by protein synthesis and they become fat anyway, although it's concealed by bigger muscles.
There may be clues in this study that explain obesity in adults in impoverished cultures. Topic for another post.
Excellent comment! I don't think anyone questions that our bodies have compensatory mechanisms, but there's no evidence for carbs causing our bodies to starve our lean tissue in favor of accumulating fat. This study might seem to imply this, but it seems that restriction during growth does cause an animal to put a bit less into growing bigger and a bit more into reserves. The generation that grew up during WWII with rations, etc., is filled with examples of stunted growth.
The LC community, unfortunately, seems to ridicule those who are successful with the conventional approach. LOTS of them out there. Why is this? Because you don't fit the rebel mode and the theories. They are not content to promote low carbing as another, healthy, possible solution to the problem. Most people cannot live on consistently <20g carb/day and what do you tell the rest? What do you tell those who do not lose on low carb diets? These people get accused of not really doing low carb the right way, and now they're being told that they may be so carb sensitive they can't tolerate leafy greens.
Dr. Dansinger reported in an interview with Jimmy that about 1/3rd of The Biggest Loser contestants keep all the weight off, another 1/3 gain back about half, and the rest gain it all back. In the overall scheme of things, that's a pretty good track record.
Hmm, if you think so. But as far as I can tell Tom mentions neither carbs nor insulin in his post and it was actually not about strengthening Taubes insulin theory. It was about the simple fact, that if (<- you notice the big "if" there, right?) is true, it would not violate any laws of physics. A subtle point, that makes all the difference but is somehow difficult to propagate to people who are constantly mixing "the insulin fattening theory" and "the implications of physics for weight regulation". Tom's post was about the latter.
He got roped in by the title of the article and the %'s of change in body composition and ran with it. He talked of "fat mice" - they weren't fat - and calorie restriction making you fatter. Mocking Jillian is his way of saying ELMM doesn't work and "here's proof" because CR made these mice "fat". But he neglected to put it in proper context.
I asked him some questions on his blog, but again, he's a-scareded of being "stalked" so he opted to delete the comments.
Indeed, just as I think GT et al are mistaken in holding to a narrow view of cho/insulin, I think FLOT shouters are equally myopic in ignoring the interplay of insulin/leptin on hypothalamic appetite stimulation as it relates to ad libitum diets. A calorie sure is a calorie, no doubt about it, but "stop shoveling food into your fat face" has not been very effective advice, and it seems to be almost absurd advice when treating 5-6 year olds who become obese even when they have the same access to food and the same physical routines as their lean siblings. I find Lustig's take on insulin/leptin interplay in obese children fascinating (http://www.nature.com/nrendo/journal/v2/n8/full/ncpendmet0220.html).
@CarbSane- do you (or anyone you know) by any chance have access to two of the other studies referenced in the Manninen letter? I would like to see M&M and detailed results of the insulin receptor-knockout mice and intensive insulin therapy weight gain in IDDM studies:
http://diabetes.diabetesjournals.org/content/42/12/1700
http://www.ncbi.nlm.nih.gov/pubmed/12110165?dopt=Abstract
The full text of your second link (the FIRKO mice study) is available for free. Click on the "Cell Press" button and then the PDF link to the right. You should be able to download it.
:)
according to James Krieger insulin doesn't stimulate appetite. What's your opinion on his claims?
The TRUTH is the caloric bank account model is wrong.
The TRUTH is that obesity is a hellishly complex , multifactorial disease of which calories are only ONE FACTOR AMONG DOZENS UPON DOZENS UPON DOZENS, and whose genetic component is the SAME AS HEIGHT.
Mice are used by Dr Friedman and others for good reason. Our reward pathways are VERY similar.
You caloric hypothesis people are so stubborn. I do not understand this.
Defenbding a failed theory is NOT what science ius about, nor will you ever come closer to the TRUTH about obesity which we all are trying to figure out.
Science does NOT understand the CHEMICAL BEHAVIOR of fat cell receptors currently.
Science does NOT know enough about obesity for such assuredness that you have. ( as well as the Internet gurus)
Actually it has been quite effective for those who heed it. When I was obese I ate a lot. I had convinced myself that it wasn't really that much, but it was. Why does the fact that people lose weight eating LC diets because they eat less need some contorted explanation. Sure genetics play a part. I had a friend with 3 boys - two looked like her (she was obese), one looked like the Dad (thin). The former were overweight, the latter rather scrawny, yet they ate the same diet. However they didn't eat the same amount, the fatter boys ate more. They were also cuddlers when "auntie" came over while the thin kid, even when playing video games, was fidgety. I know not how to treat such a situation, but putting them on a low carb "diet" is not likely to be all that much more effective than any other diet.
Sorry can't even find full text link for that first one, LMD found the second one.
Insulin therapy is not analogous to physiological endogenous insulin behavior. As noted in the comments elsewhere, there are different types with different half-lives that are longer than endogenous insulin. Knock-outs are useful to discern pathways, etc.
Postprandial insulin release does not cause hyperinsulinemia unless, I suppose, a person is eating starch and sugar every few hours around the clock. I suggest such a person has other problems besides insulin ;-)
Razwell, nobody here claims to have all the answers as to what causes obesity or how to reverse it in free-living humans. But we DO know HOW we get obese - a consistent positive caloric balance - and HOW, technically, to reverse it. If you lock an obese person up and give them limited access to food, and perhaps only the electricity they can generate on a stationary bike, they will lose weight (fat and lean).
The problem we have is that there's far more to obesity is that there are multiple causes that have nothing to do with energy balance or fat cell regulation and all that. These are the things that lead people to regain the weight. You need to read a bit over at my personal blog to get an idea of where I'm coming from with that. You see, I know I was never genetically programmed to be obese or even overweight, and that there is an epidemic of obesity really cannot be denied. To say that we are on average only like 7 pounds heavier masks the fact that the percent of the population that is 50 lbs overweight has grown considerably. We need to prevent this from happening which means find out what foods cause overeating (and I suggest tasty carb+fats and liquid calories) to begin with, not concocting theories to demonize a macronutrient that helps sustain the human population (eliminate most carbs and there's just not enough of what's left to sustain all of us) with many examples of doing so with impressively low obesity and disease rates and impressive longevity. Then we need to find ways to enable obese people to get into and sustain an energy deficit so as to normalize their weights. That last part is FAR easier said than done. And I might point out that low carb diets seem to have no better track record than any others.
> @kds: "stop shoveling food into your fat face"
> has not been very effective advice
Has anyone else ever put it that way on this blog, or was that a first?
The weight loss curve by Mark Sisson is awesome :)
Reverse means cause and effect are switched, not time going backwards. I gave an example before, not sure if you read that:
"Say two identical twins eat two different, yet isocaloric meals both worth, say, 300 kcal. Lets assume over a 3 hour period the metabolic rate of those twins requires precisely 300 kcal. Twin 1 who eats a healthy diet partitions the energy perfectly, leaving the body with the same amount of fat and other energy stores at 3-hour baseline. The other twin however eats a bad diet: 50 kcal of his meal are partitioned into fat storage, the energy difference is replaced by, say, glycogen. So at 3-hour baseline, the second twin is both 50kcal “fatter” and slightly glycogen depleted. Somehow the body senses the glycogen depletion and is signalling slight hunger. Twin number 2 eats an apple worth 50kcal. And boom - thats why we get fat ;)."
_______________
And at the end of the month you weigh the 2 and the 2nd twin has less fat mass. First law will tell you what to do: go back and find the input or output stream you missed. (you missed that he's a contestant on Biggest Loser & is exercising)
"Insulin makes you fat" will tell you nothing.
First law explains the situation and gives you avenues to troubleshoot. Insulin theory tells you next to nothing (besides being wrong).
I was referring to that statement from a public health/epidemiological perspective. No one disputes that consuming fewer calories than you expend will make you lose weight. This is a ridiculously simple fact, most fat people know this fact while simultaneously not wanting to be fat, and yet obesity/diabetes rates are absolutely absurd. CI/CO is the obvious how, but it says nothing about the why. 'Why' are some able to heed the advice and stop stuffing their faces? Why can some keep off the weight once they lose it yet others seem almost predestined to yo-yo or regain? Why is it near impossible to make some of the folks in this BBC documentary (http://www.youtube.com/watch?v=_6-A0iHSdcA) gain weight and hold on to it permanently even with thousands of calories/day worth of overfeeding?
Portion control, declining physical activity, increased palatability of food, failure of character/ willpower, too many carbs, too much fat, ad inf. are just not satisfying enough answers. I agree with Lustig in that biochemistry drives both metabolism and behavior- I'm just waiting for some well-done primary research that succinctly elucidates some meaningful mechanism(s).
face the facts. The claoric model FAILS. Maneul woould lose organ bone and muscle before losing a large amount of fat.
he would sadly pass away of malnutrition and starvation beofre he ver became leanbecause has has FAT CELL DISREGULATION.
You caloric people are stubborn
manuel
uribe ?
or
Sam Clemens?
Uribe ?
Where low carbers are concerned, too many are convinced that all they have to do is cut out the carbs for "effortless" weight loss and maintenance. There's those stories out there of folks who no longer have to watch what they eat and the sky is blue every day. But that is not reality for most. There's this new whiff that if LC only gets you so far, that's the best you can resign yourself that you can do and ever experiencing a hunger pang is akin to torture.
How can we "eat when hungry stop when full" if we never let ourselves experience hunger?
We Americans, especially it seems, have a very bad idea of how much we should be eating and actually are eating. I really think the Starbucks, energy drink, etc. fads are huge culprits in this. When I was a kid we didn't drink with dinner, although most of my friends usually had a glass of milk. I don't remember Mom having a drink in her hand 24/7. She had a cup or two of coffee in the morning, and maybe one in the afternoon. A normal cup, not the huge mugs I have >:) McD's is advertising a caramel mocha coffee thing these days. A medium is almost 300 calories. Just a coffee, with cream and regular sugar would be like half that. And there are people who have these things and chai and whatnot daily. This would have been unheard of in the 70's & 80's. I knew a few soda junkies but few drank regular soda or KoolAid all day long. We drink constantly, even "push" water. I question the wisdom of this, even with non-caloric beverages.
Where I keep getting tripped up over trying to pin the cause of the obesity epidemic on metabolic dysregulation is twofold:
1. Sugar, wheat, refined carbs, potatoes, all manner of junk food to pastries, etc. have all been around long before this epidemic. So have the percentage of those predisposed changed considerably? There is *some* evidence for this being multigenerational relating to fetal nutrition in the womb, birthweight, etc. something I plan to address in coming weeks. But I don't understand why we keep trying to construct elaborate theories when we KNOW folks are eating more. The "why" is not insulin per se from any evidence I've seen.
Sanjeev put it brilliantly: TFLOT gives us tools to troubleshoot the problem. LC gives us one tool to control intake.
See also Insulin Resistance: Solutions to problems.
When a system is not working, we systematically troubleshoot areas that could be culprits. Does TFLOT offer up all troubleshooting possibilities? No. But looking at TFLOT in that way I though was quite brilliant. Not every brilliant statement must be a ground shattering scientific masterpiece.
OK ... so now for the hand slap. You're comments are devolving into nasty little personal attacks here. Please let's stop that now. OK?
If people eat less on low carb and lose weight, why concoct some alternate explanation for the obvious? But when people don't and they start looking for obscure explanations before addressing the obvious, that leads to frustration and wasted money, time and effort. When I see someone like Jimmy (to whom I have commented several times on his menus blog) frustrated with his weight regain struggles and unable to see the forest for the trees (e.g. when he eats less he loses, when he eats more he does not or he gains) it genuinely saddens me. Folks can believe that or not, but it's the truth.
http://anthonycolpo.com/?p=1088
The Adventures of Chris “Razzi” Razwell
1) Calorie denial: I fully support you in so far that many, many people read Taubes first book and got away thinking they could eat all the palatable low/no-carb food in the world and still lose weight. I am convinced that Gary himself thought that at that time (although to a much lesser extend maybe) because of the whole GP-rate-limiting-conjecture. That is not true of course. As Lyle McDonald says you can get shredded on an all carb diet and you can get fat on a no-carb one.
2) Troubleshooting: I think "fiddling with metabolic regulation to our advantage" by means of directly addressing the metabolic pathways in our body that control fat metabolism and hunger signalling is one key player in preventing / curing obesity. The fact that it will - of course - impact a term in TFLOT is trivial.
I read Keith Frayn's Metabolic Regulation. I am not pretending that I understood much of it but the chapter "energy balance and bwr" just upsets me. This guy is literally trapped in his one-way interpretation of thermodynamics which is bizarre to me. I am not proposing that he should do a complete turn-over and suddenly propose that carbs->insulin->obesity or anything like that. But he says that "insulin and leptin are important signals involved in longer-term regulation [of fat depots]". At some other part he does the calculations that a teeny weeny caloric offset is sufficient to explain considerable weight gain or loss over prolonged periods of time. Yet - all he has to offer as a treatment is that we must eat less than we expend (a tautology), that this is difficult to do because we are fighting a massive regulatory system which his whole book is all about and that it is "dispiriting" that long term success with this treatment advice is ineffective at best.
3) That is the reason why I want to have a real explanation for "the obvious". If people lose weight on a low carb diet - it just has to be that they eat less than they expand. I want to know precisely "why". Is it because we ruled out a large proportion of palatable foodstuffs? Is it because they now eat protein and are just more satiated? Is it because we affected the metabolic regulation of the body to their advantage? Is it because of some other reason?
"The obvious" can be a sufficient explanation in some cases (maybe Jimmys case belongs to this category) but must not be one in others.
Re #2: You're actually hung up on the wrong thing regarding TFLOT and directionality. Taubes has utterly confused this situation by misrepresenting TFLOT. The correct energy balance equation for the process is: Ein = Eout + Estored (alternately Ein - Estored = Eout). This describes the process of energy use. Mathematically you can write Ein - Eout = Estored and then say the right drives the left for some convoluted chapter in a book, but the whole discussion is nonsense. Frayn's treatment is in no way misguided and Taubes' attempts to show it is driven by the right side of an incorrectly arranged equation is a distraction. Regulation is just that - insulin is a traffic cop in the regulation - but we can't make something out of nothing. Taubes proposed causality is that fat starts to accumulate and then you eat more. It's utter nonsense. He does not present any evidence for this and believes it's everybody else's job to prove it wrong. That's not how science works.
As to why most people eat less on low carb it IS the protein. Nitrogen balance is a critical thing that our bodies seek to maintain in the face of varying input. Taubes acts like nobody's been looking at this sort of thing. A quick Google scholar on keywords protein satiety demonstrates otherwise. I've posted a few here, see my protein label. There's also a lot of info out there implicating branch chain amino acids BCAA's, leucine in particular playing a key role.
I don't think there's any one single explanation for why we get fat. Taubes totally ignores any societal/psychological issues and yet I know that's how I ultimately got this way. My husband was a low birthweight premie, so one article I read says he was actually born "fatter" and more susceptible to IR and obesity. So when he got up to almost 300 lbs it would be easy to blame this, when it was because he was out of work,depressed over the death of a loved one, eating a boatload of food and drinking beer. Or maybe it's like so many men I know who can eat a ton and stay thin through their 30's and fail to adjust when their metabolisms start to mysteriously slow down when they reach a certain age. Same for women. Maybe it's because too many of us HAVE gone on a diet at some point and try to micromanage our intake rather than listening to our bodies. There's no single cause, no single macronutrient cause.
High-intensity exercise builds/retains lean mass and burns glucogen.
Low-intensity exercise doesn't build/retain lean mass and burns fat.
Therefore, do both e.g. HIIT, Tabata, Zumba!
My point still remains that Frayn's treatment options are highly misguided. Regulation (or better dysregulation) is "not just that", it could be a crucial key factor here.
Some people can do any manner of training and just never be able to add much if any muscular bulk. Me? I do. I suppose this is one of my saving graces and something low carb seems to encourage partitioning to lean tissue because most people who don't know me or my weight history peg me at ~150-60 lbs. A bit OT, but you know you've made it when young men (e.g. friends of my hubby) will comment on certain fat women in your presence. It bothered me that they did at first, and I mentioned it to my husband - something like "don't they realize they're insulting me?" - and he said something like "See? They see you as a thin person".
Obesity is treated by creating an energy deficit sustainable for a sufficient period of time to deplete energy stores.
OK ... now that's the clinical/technical truth. So how do we accomplish that in the real world? Hormonal "tweaks" will affect weight loss only if they alter some term in the TFLOT equation.
I think "craze" is quite the apt choice of word. I don't really know how many people made an honest go at a low-carb way of eating back then, but one thing I'm certain of is that "fat makes you fat" was still as much an overwhelming part of the zeitgeist then as it is now. At any rate, I agree that making permanent changes in one's lifestyle is what really matters. Indeed, what does the data say about compliance to a reduced calorie LC vs. reduced calorie LF diet?
--As an adult, I actually don't give a crap how I got obese. We all know for ourselves how that happened.--
As I've been saying, the 'how' (CI/CO) is fairly obvious and mostly irrelevant inasfar as treating the underlying 'why' in the general population. I feel like we're stuck at a root issue of causation,and I believe Taubes is only somewhat off the mark in his simplified analogy regarding fatness preceding overeating. Instead, I think the focus should be on a hypothalamic physiologic/behavioral setpoint. What are your thoughts on leptin/insulin signaling and how it relates to the derangement of this weight setpoint. Stephan's blog series on the topic comes to mind:
http://wholehealthsource.blogspot.com/2009/12/body-fat-setpoint.html
http://wholehealthsource.blogspot.com/2010/01/body-fat-setpoint-part-ii-mechanisms-of.html
http://wholehealthsource.blogspot.com/2010/01/body-fat-setpoint-part-iii-dietary.html
http://wholehealthsource.blogspot.com/2010/01/body-fat-setpoint-part-iv-changing.html
While, at an individual level, there are multiple causes for obesity, and while the technical explanation always concurs with TFLOT, I believe the best -catch-all' hypothesis on the 'WHY' question goes like this;
1) Most human beings are largely products of their environment...this is true of moral, aesthetic, and behavioural choices (including eating behaviours).
2) The environment in many developed and developing countries has become increasingly obesogenic (highly palatable foods that are calorie dense and cheap, sweetened and calorie-dense beverages, the rise of the 'food as entertainment' culture, the changing of aesthetic and social norms to accommodate the change of weight norms etc.).
3) Human beings have evolved to eat to excess in times of food abundance.
Add these three things together, and I think you get a simple picture of why things are going awry (hopefully the simplicity of the saint, and not the simplicity of the fool).
We haven't got more gluttonous than our forebears; we simply eat more because our environment cues us to do so (i.e. they would have done the same thing had they been transported forward in time; just as indigenous cultures alter eating behaviours when exposed to western 'abundance').
I'm not claiming it IS a myth, just that there may be much less to explain that most people assume.
Here are some of the massive, expensive public scare campaigns that stand out in my memory-
What happened to the "death of the age of antibiotics" and the "return to the bad old days of infectious deseases" I read about in the 80s?
What happened to the "explosive rise" in diabetes that would overwhelm and bankrupt the Canadian health care system by the late 90s?
And of course AIDS was going to kill all of us ... sparing only those who could capture a unicorn.
What happened to the something Taubes himself wrote about, the blood pressure and salt tsunami from the late 70s to the early 90s? Given his history, it surprises me he's never raised the possibility (that I've found) that the obesity epidemic might be a variation of that.
I've always said that if all the fast foods, restaurants, theaters, starbucks and so on started to serve only LC while keeping the prices low, we would have the same rate of obesity. The LC breakfast bowl at Hardees is aroud 1000 calories.
It's food abundance, availability and our drive to overeat when food is abundant that makes getting fatter so easy in the modern times. Food quality or food type has nothing to do with it.
It's going to get really tricky at some point figuring out how to cover "lifestyle diseases". Many of our states are looking to add sodas to the "sin tax" list ... where does that end? They claim its in a public health interest (like all the ciggy taxes), but it's to raise revenue plain and simple.
You've mentioned this a few times, and I just don't get it. How can drinking water, even lots of water cause obesity? If it's all about calories then water should make no difference at all since it has none. I've even heard arguments to the contrary: that drinking lots of water can help to curb appetite.
Drinking large amounts of water stretches the stomach. This means that the stomach secretes ghrelin sooner than it should, which stimulates appetite.
The nutritional control of ghrelin secretion in humans: the effects of enteral vs. parenteral nutrition.
http://www.ncbi.nlm.nih.gov/pubmed/17061019
It's not particularly new so maybe everyone has seen it. They tested the ghrelin response to various "foods" over the course of 3 hours. The only one that significantly reduced ghrelin was glucose. I found it surprising. Just sharing.
When I was a kid-teenager I was a tom boy-jock. And yet we would line up for a few sips out of a water fountain after lengthy recess/game/practice, etc. I was a babysitter and camp counselor and I do not recall worrying over the kids ever dehydrating. Now? We were descended upon at a hotel pool once by a kids group outing to said pool and after a half hour the coordinator whistles everyone out of the pool for a water break! A bit extreme, but ...
The first time I did the water thing was along with my first diet, because it helps you to feel full thus curb appetite. I think it also helps for the mindless boredom snacking to just have a non-caloric beverage instead. But it is well known that some of our hunger-signalling hormones are secreted simply in response to distension of the stomach. For a while you'll feel full drinking water, but in the long run your brain may begin to associate a level of fullness with a lack of nutrient availability prompting you to need to eat more so as to be even more full to sense satiety. This is just a theory of mine.
There's no evidence for any benefit to water drinking. I take a lesson from my cat. A year and a half ago both were a bit overweight and kitty #1 was looking sick, kitty #2 had stinky poop but was otherwise spritely and the vet was not concerned by anything at his last checkup. Switched them both from quality dry food to canned tuna (cat food version). They got leaner (not lean), one died (#2, age 10) and #1 is still kicking. I avoid gluten in his diet and his allergic skin condition is better (not cured by any stretch). When they ate dry food I had to change water almost daily in their bowl. Now? My kitty is almost never seen drinking water ... he seems to get what he needs from about 1.5 cans of wet food a day.
Bottom line: Why tell someone to drink when they're not thirsty - overriding natural impulse?
"I've always said that if all the fast foods, restaurants, theaters, starbucks and so on started to serve only LC while keeping the prices low, we would have the same rate of obesity. The LC breakfast bowl at Hardees is aroud 1000 calories."
Yeah, except most people who eat a 1000 calorie HP, HF, LC meal like that are satiated for much, much longer than they would be eating a bagel or a donut or a stack of pancakes. I would contend that there isn't a single person described by a metabolic syndrome picture who got that way de novo by eating strictly low carb. The one thing that these people have in common is that their high fat intake is coupled with a high refined carb intake. I think it's clear that many dieting fat people can stall or somewhat reverse their weight loss by consuming too many low carb calories, but I find it near impossible to imagine that someone (otherwise lacking a hypothalamic disorder) would be able to start out lean and later develop diabesity without significant consumption of grain-based desserts, pizza, pasta, french fries, cheeseburgers, and especially sodas and other liquid calories.
Probably not if eating *real* whole low carb foods. But the same could probably be said for a low fat diet devoid of Snackwells and other processed crap.
Just about everything you list carries a high dose of both fat and carbs. A metabolic assault on the body!
Only because right now pizza, french fried and cheeseburger are the cheap and abundant foods so if you're following a paleo, LC or something diet you're surrouded by forbidden temptation.
But if for any reason LC and paleo foods became the cheap and abundant food that you can buy at any corned of the street, in any fast food, theaters, playground... then it would be the norm for people to become fat eating nothing but LC and paleo foods. That's because way more important than caloric density or type of food is cultural food abudancy.
We're wired to overeat whenever we have a chance to increase our endogeous stores. This means that the lack of processed and caloric dense foods in nature has never been an obstacle to our overeating and fat-gaining needs. Only food availability is.
We've never been as obese as we're today because food has never been this cheap and available. Changing the type of food won't change anything, because the most important, and pretty recent, cause of obesity would still be there: extreme food availaibility and abundance.
CS- I agree that the same could possibly be said for the low-fat diet, but "diet" is really the key word since I'm specifically interested in ad lib over decades, aka the way people really eat. LF ways of eating always involve restriction of calories, so yeah, if we take 200 kids and start half on LC and half on CR/LF and follow them for 25 years we would probably see equal incidence of metabolic derangement. Now let's say we run the same experiment with ad lib LF. This is mere speculation based on anecdotal experience, but I suspect the LF group would be crushing the LC in incidence of metabolic syndrome.
Additionally, what foods are you referring to by whole LC? If in regard to non-whole you're talking about those maltitol-loaded frankendesserts, then I would hesitate to call them LC let alone whole. And what exactly constitutes "processed crap" on LF? Snackwells are low-fat, low-protein and contain about half sugar and half enriched wheat flour, so therefore we should shun them? Artisan ciabatta and a little strawberry jam probably has the exact same nutritional profile but is acceptable? Because it's not processed? Too confusing for me.
It's been done. It's called "the Kitavans". For months you couldn't swing a cat without hitting a Kitavan related blog post.
From the reports, they are NOT starving - they get as much food as they want and they seem healthier than the low carbers I've been exposed to. Myself included.
> list ... where does that end?
Riverdance
> @Harry & Leo: Abundance + Convenience + Palatability = Overeating sounds about right
IMHO this is missing key pieces
knowing when to stop (not necessarily consciously)
being able to stop once you know to stop
_____
Riverdance: no, it doesn't mean anything.
Leo, I still highly doubt this is the whole truth.
http://www.ncbi.nlm.nih.gov/pubmed/19209185
This is a very small cross over study with only nine participants and no control group. But in my book large results in small groups ought to ring a bell. Apart from improving any health parameter you can think of, leaving out 'neolithic' items led to spontaneous undereating. Even crazier: the ivestigators had to force feed the participants more than 300 extra kcal per day in order to keep them weight stable on the 'paleo diet'.
The same phenomenon has been observed and documented by Lindeberg and, for what it's worth, I know several confirming anecdotes myself. Something in our food besides energy content (partly) controls our intake and even body composition (I don't say weight, although the mentioned experiment suggests such blasphemia).
Leo, I still highly doubt this.
http://www.ncbi.nlm.nih.gov/pubmed/19209185
This is a very small cross over study with only nine participants and no control group, but in my book large results in small groups ought to ring a bell. Apart from improving any health parameter you can think of, leaving out 'neolithic' items led to spontaneous undereating. Even crazier: the ivestigators had to force feed the participants with more than 300 extra kcal per day in order to keep them weight stable on the 'paleo diet'.
The same phenomenon has been observed and documented by Lindeberg and, for what it's worth, I know several confirming anecdotes myself. Something in our food besides energy content (partly) controls our intake and even body composition (I don't say weight, although the mentioned experiment suggests such blasphemia).
Regardless, my experiment with 200 kids was conceived with modern Western culture in mind, i.e. ad lib LC vs LF for kids whose parents shop in supermarkets rather than spend 8 hrs a day gathering coconuts and tubers.
> experiment with 200 kids was conceived with
> modern Western culture
I didn't catch the emphasis, I should have from the context, thanks for clarifying.
> not to mention the Kitavans eat no refined
> grains and negligible sugar)
I came away with the impression of a huge amount of fruit, so I assume a decent amount of sugar.
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