Not only did the VLC diet lead to a higher total energy expenditure than the LF and LGI diets, the most remarkable finding is that it led to a higher resting energy expenditure. Basically, people on the VLC diet woke up in the morning burning more energy than people on the LGI diet, and people on the LGI diet woke up burning more than people on the LF diet. The VLC dieters burned 326 more calories than the LF dieters, and 200 more than the LGI dieters.
It's always tempting to view each new study in isolation, without considering the numerous studies that came before it, but in this case it's essential to see this study through a skeptical lens that places it into the proper scientific context. Previous studies have suggested that:
- The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are not trying to lose weight (2, 3).
- The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are being experimentally overfed, and if anything carbohydrate increases energy expenditure more than fat (4, 5).
- The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure during weight loss (6, 7, 8), and does not influence the rate of fat loss when calories are precisely controlled.
With that, let's see what could have accounted for the differences observed in Dr. Ludwig's study.
Was it Insulin?
I know it will be tempting to some people to attribute these results to changes in circulating insulin*. The hypothesis here is that lowering insulin increases energy expenditure. Let's see how plausible that is.
The first thing to point out is that the paper didn't actually report levels of fasting or meal-stimulated insulin, so we have no idea whether they differed, or if so, by how much. Most studies have shown that fasting insulin tends to be lower on diets that are very low in carbohydrate, but again this was not reported in the current study so all we can do is speculate. One would expect that the higher carbohydrate content of the low-fat diet in particular would lead to higher insulin after meals. However, the VLC diet was the highest in protein (30% vs. 20%), which also stimulates insulin release to a surprisingly large degree-- often more than an equivalent serving of carbohydrate (9). The point here is that we simply don't know how much insulin differed between the three groups.
The second, more important point is that lowering insulin levels does not appear to increase energy expenditure. The drug diazoxide, in addition to its effects in the brain and elsewhere, reduces both fasting and post-meal insulin secretion substantially (35-50%). In some but not all studies, diazoxide accelerates fat loss, and this may be related to its effects in a part of the brain called the hypothalamus
(10, 11, 12). When you give obese people diazoxide in conjunction with a low-calorie diet, it has no impact on energy expenditure, regardless of whether you look at the studies where it accelerated fat loss, or the ones where it didn't (13, 14). This suggests that when it works, it's because it reduces food intake.
Just to add more support to this idea, in free-living people, elevated insulin is associated with higher, not lower resting energy expenditure (15, 16). Insulin actually increases energy expenditure following a meal, at least in part via the brain, and so it is said to contribute to "diet-induced thermogenesis" (17). This is part of the reason why carbohydrate consumption is often associated with a higher post-meal energy expenditure than fat consumption (with protein being the highest, 18). It's worth noting that the difference in diet-induced thermogenesis between carbohydrate and fat is quite small.
Furthermore, it has been shown multiple times that on average, people with higher fasting insulin levels, and more insulin resistance, gain less fat over time than people with normal insulin levels (19). A recent study suggested that when you control for baseline fat mass however, this relationship disappears-- in other words, circulating insulin is not related to future fat gain (20). This is reminiscent of what we see in animal models, where a) increasing circulating insulin by making the liver insulin resistant does not cause fat gain (21), and b) preventing the increase in circulating insulin that normally occurs when they're given a fattening diet has no impact on the rate of fat gain (22). This shows that elevated circulating insulin is neither necessary nor sufficient to cause fat gain in animals, and suggests that the same is probably true in humans.
The overall point here is that insulin is not a compelling explanation for the effect they observed in this paper-- we need to look elsewhere.
Diet-induced Thermogenesis due to Increased Protein Intake
As mentioned above, protein increases energy expenditure following a meal (called 'diet-induced thermogenesis'), and differences in protein content between diets can result in differences in energy expenditure of up to 100 calories over the course of a day (23). The VLC diet was 30 percent protein, vs. 20 percent for the LGI and LF diets. This could account for a portion of the difference in total energy expenditure, although it can't account for the difference in resting energy expenditure because that's measured prior to eating.
Metabolic Inefficiency
The body contains and uses large quantities of protein, fat and carbohydrate. At macronutrient extremes, the body has to synthesize the missing macronutrient, and this is an energetically costly process. In the case of the VLC diet, participants' bodies would have had to make carbohydrate from amino acids and glycerol-- a process called gluconeogenesis. This uses energy, possibly accounting for a portion of the increased energy expenditure in that arm.
It would have been interesting to see a very low fat (10% or less) diet as a comparison group. It's possible that energy expenditure would have increased as participants approached the other end of macronutrient extremes.
How About Leptin and Insulin in the Brain?
One of the things I'd really like people to take away from my writing and talks is that where energy intake, energy expenditure, and body fatness are concerned, the brain is key. A particularly important system for fat mass regulation is the negative feedback loop between fat tissue and the brain that is completed by the hormone leptin. Leptin is by far the most important hormone for the regulation of body fatness in mammals. There are many things that influence food intake and energy expenditure, and some of these don't have a lot to do with leptin or physiology in general-- e.g. aunt Sally baked you a pie, or you're having drinks with friends, or you buy a dog and have to walk it twice a day. But leptin is the key hormone a circuit that does its best to regulate the balance between energy in, and energy out, and so it's always important to consider in cases like this.
As far as I know, the brain is the only organ that's capable of regulating energy expenditure, and it does so by controlling thyroid signaling, the HPA axis, the sympathetic/parasympathetic nervous systems, and physical movement. It has already been demonstrated that the metabolic response to fat loss in humans-- including the characteristic decline in energy expenditure per unit lean mass-- depends on the reduction in leptin that accompanies fat loss (24). The citation I just made was also in Dr. Ludwig's discussion section, and this is no coincidence! Although any explanation for Dr. Ludwig's finding is speculative at this point (duly acknowledged in the paper), leptin is a compelling possibility.
Leptin declined the most on the VLC diet, followed b the LGI diet, followed by LF. This doesn't tell us much about what's happening in the brain however, because we don't know how each diet affected leptin sensitivity. If changes in leptin signaling can account for the findings, then we would have to speculate that leptin sensitivity was increased in the VLC and LGI diets relative to the LF diet.
How the diets could have led to different leptin sensitivity in the brain is unknown. One intriguing possibility is that the decline in triglycerides improved leptin sensitivity. Dr. Bill Banks's research suggests that high circulating triglycerides impair leptin sensitivity in rodents (25). Dr. Banks is now at the University of Washington and I've had the pleasure of interacting with him a few times about this.
Another possibility is that the VLC diet led to improved insulin sensitivity in the brain. Insulin acts in the brain in a manner similar to leptin-- it suppresses food intake and increases energy expenditure, opposing fat gain (although to a much lesser degree than leptin, and the effect has historically been fickle). The VLC diet did appear to improve insulin sensitivity in the liver more than the other diets, so it's possible that it had such an effect in the brain as well.
Conclusion
It's always tempting to put the cart before the horse, and come to conclusions before we really know what's going on, but in this case all we can do is speculate. In my opinion, protein-induced thermogenesis, metabolic inefficiency, and alterations in the brain are the most likely explanations for the findings in this study, but we'll have to wait for future studies to see if this is true, and if so, why.
* Such as Gary Taubes's op-ed article in the NYT today. It proclaimed triumphantly that "a new study suggests that carbs, not calories, lead to weight gain". Back in reality-land, the study had nothing to do with what causes weight gain-- it was about fat loss maintenance in people who are already overweight (which are not metabolically analogous to pre-obese people as Taubes claims). There are numerous studies that compare the ability of fat and carbohydrate to actually cause fat gain, but these are inconvenient because they invariably show that 1) calorie intake is the dominant factor, and 2) fat is equally or more fattening than carbohydrate at a given calorie intake-- for example the study that concluded: "Excess dietary fat leads to greater fat accumulation than does excess dietary carbohydrate..." (26). In Dr. Ludwig's paper and the accompanying editorial in JAMA, they made no claims about carbohydrate being more fattening than fat, and they didn't even broach the topic, because Dr. Ludwig's study is not relevant to the question. I would love to see Dr. Ludwig set the record straight on this, but unfortunately most researchers don't fight back when their results are abused in the popular media.
174 comments:
Nice post stephan.
Can you speculate further about how leptin may have an effect upon resting metabolic rate via modulation of these systems you mentioned (i.e. sympathetic nervous system, HPA axis)?
Are we talking about increasing energy expenditure by increasing heart rate? or something more subtle such as increasing biochemical reactions that "burn energy"?
Stephan,
A few things struck me when I read the full text.
1. 1/3 of the study group dropped out, leaving only 21 people. When you look at the actual individual results for each person on the various diets, which are graphed, you see that some of these people did worse on the VLC diet than the other diets. You also see a very wide range in energy expenditures from person to person, which because this group is so small made me think that the average is not all that reproducible in a large group made up of different individuals. This is too small a sample from which to draw conclusions for the general population.
2. No one has remarked on the composition of the study group, which was 81% non-European whites. This is important, because we know that people of non-white ethnic heritages have different defective genes associated with abnormal blood sugars and obesity.
In addition, there were significantly more males than females in this study and their average age was quite young (30)
The very small size of the sample, and the skewing within the sample towards young black and hispanic males makes me think that it would be very foolish to extrapolate the results of this study to people of Western European extraction, females, and middle-aged people.
3. I wondered whether the order in which people did the 3 different diets might have had some effect on the outcome, too. The third month of maintenance might be harder than the first no matter what diet was done, which could also skew the results.
For now I'd put this into the "interesting but needs much more confirmation before it's taken as proof of anything" category.
Also, it's worth pointing out that while on average (but not in all cases) people burned more energy on the VLC diet they experienced a decrease in energy burning. And these people were still considerably overweight. People who lose weight on diets need to understand that whatever diet they do they have to eat a lot less than they did before starting their diet to maintain their new weight.
I appreciate Jenny's comment, which helped me save the time it would have taken to get squinty-eyed about some of the same factors. Thanks, Jenny! :-)
My money is on leptin/insulin resistance in POMC neurons, which have been found by Stephan's group to be damaged in obesity. They produce high levels of reactive oxygen species.
'.. the fact that satiety is associated with the highest level of ROS production in the hypothalamus – specifically, in the POMC neurons – indicates that POMC cells are more exposed to ROS-induced damage than NPY/AgRP neurons, which do not produce elevated ROS levels even if highly active. Thus, it is not unreasonable to anticipate that over time, POMC neurons might become impaired, a process that is in line with the declining ability of animals and humans to lose weight as they become older [132]. It is also projected that the more POMC neurons that are engaged in elevated firing (positive energy balance), the earlier the POMC system becomes impaired. Thus, the impairment of these neurons by elevated ROS could explain their resistance to signals in response to high-fat diet consumption. By contrast, NPY/AgRP neurons are inherently able to buffer ROS, so their increased activity during negative energy balance is not associated with ROS-induced degeneration.'
http://www.sciencedirect.com/science/article/pii/S1043276008001665
If we want to fit this in with Ludwig's findings, we have to say that the LF diet did not protect against oxidative damage as well as the VLC diet. If it contained a lot of refined carbs, this is to be expected.
Stephan is right. The brain plays the key role.This is verifiable by watching the lectures of top scientists who research obesity.
This is why real scientists such as himself, as well as Dr. Jeffrey Friedman and his colleagues, are conducting extremely important research on neural circuitry.We need to know MUCH more.
We even need to learn more about feeding behavior itself. Numerous things are involved in the initiation to eat ( some under control ,some not) but no one specific thing will guarantee you will eat.
Stick to good , quality, reputable , valid information from sources such as this blog, as well as Dr. Friedman, Dr. Leibel and Dr. Rosenbaum's lectures. All these people represent REAL science. Doing THIS will educate the public better.
At least 10 % of morbid obesity can be explained by a SINGLE gene defect. Dr. Friedman believes there is reason to suspect that number is siginificantly greater.
Leave the shyster fat loss blogs to the uneducated and gullible morons who read them and worship their said guru, as he /she lines their pockets.These "gurus" do not know what they do not know. The blind leading he blind.
Stephan, I'm very interested in knowing more about the brain's role in body fat regulation.
I don't believe they teach this in any sort of detail in med school but I really want to learn more as this is obviously extremely important.
In physiology they've briefly mentioned the role of the hypothalamus in hunger and satiety and the nuclei involved, but that's about it.
Is there a book that you can recommend that covers all of this, including leptin, insulin, the various other hormones, nuclei and brain pathways and the relevance of all this to human health?
i have to admit I find this site kind of confusing. I've been eating in a way based on Mark Sisson and Kurt Harris's sites (which you link to) and have been very happy with it. I read this site too, partly to make sure I'm not in an echo chamber because I don't like to get religious about things like this.
The confusing part is this site seems to basically rebut everything that the sites it links to say. This seems to basically come back around to weight watchers style calories counting yet I've never known that to work for anyone. In my own experience people eat primal/paleo do well while still eating a lot while low fat dieters struggle and fail. The exception being people who do high carb diets as part of lots of long distance cardio (bikers and runners).
I guess my questions comes down to "if the paleo crowd is wrong, why link to them?" and "what's your actual recommendation and how does it differ from weight watchers calorie counting?"
Hi Stephen,
I have a graduate background in Psychology/Neuroscience so maybe I'm biased towards your more academic approach, but I just wanted to say that your posts are a breath of fresh air in a sea of cherry-picking nutrition blogs. I also really respect your attempt to keep your scientific process public. Thank you, and keep up the good work.
Pictures speak a thousand words:
http://www.youtube.com/watch?v=2zVxA6yipv4
not to be overly pedantic, but I read taubes's editorial piece and couldn't find where he claimed "a new study suggests that carbs, not calories, lead to weight gain".
gunther, that's a joke right? ever seen dean ornish? how about mark sisson?
John Nicholas: low-carb and paleo diets are very effective, there are plenty of controlled trials to prove that.
I think the argument is rather about "why" they are effective than "if" they work.
It is also a fact that low-carb and paleo diets are more likely to improve other biomarkers of health (blood sugar, triglycerides, HDL, etc.) than just body fat.
I'm pretty sure Stephan agrees with this, but the mechanism behind "why" people gain weight on a certain diet and lose weight on others is a matter of debate.
Paul, ever seen Jimmy Moore?
Are you going to try to convince me all that increased energy expenditure of low carb is working for him?
gunther, i never made a claim that all low-carbers are thin (in fact, since most that try it do so because they're fat to start with). but your link to that video seems to imply the inverse; that all low-carbers are fat. this, of course, is patently ridiculous. and perhaps increased energy expenditure is working for jimmy; what did he look like before he started?
Jimmy lost a lot of weight on low carb, was still overweight the whole time, and then gained back some 170lbs of his weight loss in a few months. How can a guy like that prescribe dieting tips to people, or huck low carb bars, books and powders for bucks?
That is the very point of the clip. Not that all low carbers are fat. But that many of its main spokespersons making tons of money off this fad are fat. Atkins himself was 258 lbs and had congestive heart failure and high blood pressure.
Whether you like the clip or not, why would you take diet advice from these people?
i would take advice from those people because they've gone through the struggles that people who have been lean their whole lives can't seem to conceptualize (ppl who say things like "the move more, eat less").
also, you're playing a little loose with the facts on atkins. i'm surprised you didn't say he died of a heart attack. http://lowcarbdiets.about.com/od/atkinsdiet/a/dratkinsdeath.htm
Paul, here's a shot of Jimmy now, after years on low carb:
http://ancestralizeme.files.wordpress.com/2012/03/img_6822.jpg
You would take advice from people who obviously failed on the very diet they are prescribing (and making fortunes from promoting)?
Not very clever IMO, but well the world needs organ donors too.
i don't know if jimmy looks bad. what did he look like before?
and when I say "I", I'm not referring to me personally, but using it generically to represent someone who needs help with their weight/health. I don't seek/take advice much anymore, since I'm perfectly capable of reading, interpreting, and experimenting for myself. but whether you want to admit it or not, jimmy moore and all those fat low-carbers are pretty knowledgeable in regards to diet and health. so if someone needs help, they'd probably do much better to listen to jimmy than you're average mainstream nutritional "expert".
btw, didn't see any pics of mike eades, jay wortman, jeff volek, eric westman, gary taubes, or richard feinman in that video. is being lean really the best indicator of knowledge/expertise? i suppose we should all be begging steven tyler for his health tips, eh?
An article I recently found:
http://www.drmcdougall.com/misc/2012nl/jun/paleo2.htm
UCP increase, which happens with carbohydrate restriction, is a possible contributing factor. Protein is probably the macro with best association [negative] with body fat however.
The statement that carbohydrate is less fattening than fat in overfeeding isn't necessarily true; there are studies supporting both sides.
Carbohydrate restriction seems to increase leptin and insulin signaling in the brain; Lucas Tafur has written about it.
Blocking insulin does decrease fat storage. Diazoxide works sometimes, but that and TNF knockouts, which maintain adipocyte insulin signaling, are less convincing than direct & exclusive inhibition of insulin secretion by oxidized lipid consumption.
Hi, gunther
Jimmy's experience is not at all uncommon to people who suffer from significant to severe obesity. Real science would have predicted he would regain a lot of the weight. People like this are not that same as the average guy. The playing field is not at all level.
Dr. Michael Rosenbaum is extremely knowledge and qualified to give out obnesity advice. He is not lean himself. A person's own build has nothing at all to dio with what they know about morbid obesity.
You should never take someone's advice just because thet are very lean themselves.No person who understand science will ever do that.
Everybody on the Internet is trying to make money, gunther. There are PLENTY of lean naturally ectomorphic Internt shysters selling fat loss books etc- capitalizing on their physique.
It's the "cool thing" now to bash low carb diets.What is really disingenuous is that I can name you SEVERAL Internet shysters who were adamantly pushing low carb back in 2006 and before. It is not like they were always claimign low carb was a fad. These shady individuals were PART of the "fad'.
Back then it was "cool thing" to rail on high carb low fat. I have always been center of the road- leaning a bit more lower carb etc.
if this were the case my natural bodybuildign brother ( who has a physique FAR better than ANY Internet guru I have ever seen) should make hundred of thousands.
The truth is my brother's advice advice would not help Jimmy. Jimmy has a genuine medical condition- the phenomenon of obesity . GENES and a bit of work are why my brother is this way. He does not understand obesity at all.
Stick to the scientists, not people with lean builds etc. I am 6' 2" 160. That is very lean. I was the same way back in 1998. But this doe snot mean I can give anti- obesity advice to Jimmy. I simply am this way. The body is in control of weight far more than we are.
Remember, science can NEVER prove anything.NOTHING in science is ABSOLUTELY certain- NOTHING.
Einstein's General Relativity ( on eof the very TIGHTEST theories in all of sciecne history - and has been repeatedly tested and held ) is not "correct", it is ONLY the currently the best GUESS how Nature works at large scales. It is not absolutely " proven"
All we can be is less wrong. Newton was "less wrong" than the Ancient Greeks, Einstein was "less wrong" than Newton and inthe future the new theory will be "less wrong" than Einstein.
I see MANY Internet gurus who misuse and abuse science and have no clue hwo it actually works.
Hopefully this will help the public understand how science works.
I think it odd that we've long battled about low carb vs. low fat, etc., but have not brought into the discussion a thorough treatment of the effects of microbiota on weight loss. Consider, for example, FIAF and other hormones regulating fat loss but that are influenced (if not altogether controlled) by intestinal bugs.
To me, it is along these lines: people who are overweight or who have a history of obesity ALREADY have unhealthy (or un-diverse, or whatever) intestinal microbiota. In these people, whatever the genetics, low carbs helps because most bugs eat starch rather well (and then pump out toxins/hormones that control our metabolism). Low carbs, as long as they still provide enough glucose for a healthy immune system (which, in turn can modulate our intestinal microbota), reduces substrate for the intestinal bacteria, thereby limiting their potentially damaging effects. Intermittent Fasting also helps because it limits bacterial feeding frequency, in addition to up regulating nutrient absorption by us (because we've gone for a while without nutrients), thereby limiting bacterial feeding in sum. Hence why some people lose 10 pounds of fat out of the gate with digestive enzymes (less undigested food slipping down the bowls to the bugs).
Now in people who have never been fat and who have never had to worry much about what they eat, their intestines are probably housing a healthy array of diverse bacteria, and hence don’t suffer these effects. But our newest generations of antibiotics-treated, C-suction-begotten, formula-fed babies are absolutely screwed.
Further, few 12-week dietary trials will show these results very well.
@Razwell, do you have any links to good resources of information?
Hi, Dave :)
I use to have it organized but I will dig some up:
http://www.youtube.com/watch?v=NuWd1i6V87g&feature=related
http://www.youtube.com/watch?v=xcTNNThGsB8
http://www.youtube.com/watch?v=2i_cmltmQ6A
What I like about Dr. Jeffrey Friedman, Dr. Rudolph Leibel and Dr. Michael Rosenbaum is these guys are all super nuanced and go into great detail. They all collaborate and know each other. Leibel was on Friedman's team in 1994 for the leptin discovery. This research is their passion. And they are world class top researchers.
I hope you find this useful, Dave.
Take care,
Raz
Anyone who wants to understand the two diazoxide studies should read Hyperlipid Peter's analyses of them from some time back. (And if you do, you might see a familiar obesity researcher popping up in the comments with some interesting things to say...)
http://high-fat-nutrition.blogspot.com/2008/05/weight-loss-when-its-hard-2-diazoxide.html
http://high-fat-nutrition.blogspot.com/2008/05/weight-loss-when-its-hard-5-son-of.html
1. The 300 calorie per day "metabolic advantage" of a VLC diet has been previously described by Feinman and Fine (Metabolic Wyndrome and Related Disorders, Vol 1, #3, 2003)using the first and second laws of thermodynamics relative to gluconeogenesis.
2. while the authors expressed concern about a small difference in CRP (increased sligthly in the VLC group) they failed to discuss the counteracting reduction in PAI-1 in the VLC group, likely mediated by Leptin decrease (leptin upregulates PAI-1)
gunther gatherer, you might be interested to see this. It's a 2008 comment by low-carber ItsTheWooo on Hyperlipid (from Elliot's first link, thanks Elliot)
'.. LC/ high fat does help to keep me from feeling less hungry [I think she means more hungry], but it does not reverse the direct effect of low leptin I don't think. It's a type of hunger that has no relationship to meals, it's hard to explain... it's this constant desiring for food. And, you know how normal people get nauseated if they over eat? You kind of lose that too. It’s this hunger that is there all the time no matter how full or hungry you feel. It's a lot better now that I weigh more, but I am sure that if I was not psychologically trained to eat the way I eat, I would probably binge constantly, sadly enough. In rare moments when I let my mind relax, and I just eat, I eat an incredible amount. ..'
This, to my mind, is the problem with low carb: it does not get rid of hunger. The only thing that can do that is more leptin, as Wooo says, or less leptin resistance. If leptin resistance is due to oxidative stress in POMC neurons, low carb will only help to the extent that it eliminates refined carbs.
gunther gatherer, in your video you omitted the most prominent vegetarian of all time, the one that had the greatest impact on humanity: Adolph Hitler
Stephan, I have the exact same question for you as John Nicholas and I would be very curious to hear your thoughts on it. I too read Mark Sisson/Kurt Harris/Rob Wolf/Gary Taubes (especially Mark) and since I've been eating paleo I've been feeling much more energetic, I've lost some weight and I'm visibly gaining muscle mass at the same time, and I don't count calories at all nor do I get hungry. None of this was true while doing the conventional wisdom of low-fat, calorie-restricted eating, and the worst thing about it apart from seeing no difference was the constant hunger. I read your blog with interest because I'm concerned about getting all my information from one source, but you seem to be contradicting everything I'm experiencing as well as many people on the paleo. Can you elaborate on this?
Stalin, who said the video was mine? I do not have a vegan agenda, nor am I a vegan.
I was just directing you to the clip to show that any metabolic advantage of LC is obviously negated through some other pathway. We have lots of evidence of this by all the fat LC gurus out there.
Maybe researchers should stop trying to narrow everything down to macronutrients and actually think about what a lifestyle eating Real Food (with all of its necessary fiber and vitamins/minerals) will do.
This whole reductionist approach to diet, jumping on insulin, or leptin, or cortisol, or carbs, or fat, or whatever other thing they find next year, has been a mistake from the get-go. That is what I'm saying.
Gunter you are being intellectually dishonest by making noise about a few fat LC advocates. I have no dog in this race and I think both diets work if you stick to them, but it's also pretty clear that there are no other diets that have a success rate anywhere near that of low carb. (for whatever reason). Why not try to make your points instead of resorting to ad hominem attacks?
REE was measured by indirect calorimetry. Is it possible that different diets results in different discrepancies in indirect calorimetry measurements? Exactly what are we measuring?
Have you seen Peter Attia´s post on this study? The best and most rigorous interpretation I have seen so far:
http://eatingacademy.com/
Alex, the old "ad hominem" retort to distract people from pointing out the glaringly obvious. LC actually needs more of these "attacks" so people see what's under the hood.
If you have no stake in the game, why do you care? Is it fair for these people to make money hawking BS to people in need, BS which could actually get them killed?
Come on man, stop being a petunia. These people are not above being called out, and no one is going to die if they get named for what they are. It's not like they're hiding it themselves even, that is if they could hide it...
"Insulin acts in the brain in a manner similar to leptin-- it suppresses food intake and increases energy expenditure, opposing fat gain (although to a MUCH LESSER degree than leptin, and the effect has historically been fickle)."
REALLY?! On what basis do you make this claim? How could this even be measured or quantified, much less subjected to test? It's pretty much non-sensical, in addition to the obvious, well-demonstrated direct regulatory role of insulin in adipose tissue regulation and the apparent lack of even an indirect role for leptin (downstream signaling effects not included).
Hypotheses can only be disproven by arduous experiment, but they are trivial to espouse. What Taubes has chronicled has already apparently passed the test over centuries -- the standard contemporary dogma has been disproven over and over again. See GCBC section on S. Ranson for brain-related research. See GCBC citation of Woods and Porte from U. of Washington (sound familiar?) as well. Ah, but that's the hypothalamus which only controls homeostasis but can't be related to conscious control of eating behavior. Oh well!
Thanks for the link to Taubes' article. I enjoy his material -- he writes carefully, precisely, and elegantly. Nothing short of a superstar.
@Jane,
"This, to my mind, is the problem with low carb: it does not get rid of hunger."
In order to prove your point, you quoted what Wooo said about her experience with leptine injections. I just want to voice my opinion, that at the time she described in her comment her leptine could be too low after a massive weight loss when even LCarbing kept her too interested in food. I didn't loose too much weight (30+lb), and I didn't have too much to loose. I guess my leptive level didn't need to be corrected as much as hers. I had being straggling with an abnormal appetite and of being hungry to intolerable degree till I started a LC diet almost 5 years ago. It got better immediately, but it took time and the adaptation to IF before my ability to feel hunger hit so low that I started to guess how normal it is now. My always straggling with hunger mother got immediate relieve after her first LC breakfast. From reading other people comments, I can see that some continue being hungry even on LC, but I represent another group of individuals for whom LCarbing created unbelievable miracles.
@Ganter, I have being eating home-cooked well-balanced food with ample fiber content all my life and exercising. I can write a book about healthy eating, preparing sourdough breads, fermented veggies and organ meats. Probably it kept me from being really obese and my family members at optimal weight, but it was not enough to keep me metabolically healthy. I pat my back for being creating enough in applying a LC diet and be able to reach my goals, because, as you know, just carbs limitation will not get most people far enough.
@Paul: Oh lordie, which "before" are you talking? 1999 where he probably weighed less than his "goal" of 230 lbs following a successful stint of low FAT weight loss? Jan 1 2004 when he weighed 410 lbs? Jan 1 2005 when he weighted 230 lbs and where most of his "after" shots come from to this day? Jan 1 2010 at around 280, Jan 1 2011 at around 290, Jan 1 2012 at around 300? Or what of the lost years in between where his weight fluctuated wildly despite enthusiastically diligent LC adherence?
Nobody in their right mind would walk off the street, see a real picture of Jimmy Moore (not the years old avatar) and take diet advice from him. And in his case all that matters is his weight and health because he has NO other creds to discuss this than losing 180 lbs on Atkins in 2004.
Gunther's video is instructive though not definitive. Some of us may be "damaged" in that years of yo-yoing, dieting and whatnot have depressed our metabolisms, but LC is not a cure for that.
> REALLY?! On what basis do you make this claim?
Stephan's blog posts over the last 2 years cover much of the territory,
for other stuff here's a random scattering
of other sources
example: a big review article
http://rstb.royalsocietypublishing.org/content/361/1471/1219.full
Insulin acts directly at the liver to suppress the synthesis and secretion of glucose, and some plasma insulin is transported into the brain and especially the mediobasal hypothalamus where it elicits a net catabolic response, particularly reduced food intake and loss of body weight
> addition to the obvious, well-demonstrated direct regulatory role of insulin
If you don't keep up with science, science leaves you behind
Taubes has not even caught up to what was the state of the art on insulin and diabetics 5 years ago (it ain't mostly about storage), and until a year ago (maybe still) I had never read the words "doubly labeled water" in any of his corpus, so anything he writes on health, for self protection I must automatically disbelieve
Google James Krieger and insulin for a more balanced treatment of insulin.
Maybe get Todd Becker and Kurt Harris to outline the evolution of their views in the last 4 years.
Gunther, I'm surprised the light pressure from the flash didn't knock some of those vegetarians over.
gunter please provide any sort of justification for the statement that a low carb diet might get someone killed? I think you need to provide proof for that sort of statement.
And I care about this because I want to know the truth. I will call out low carb advocates who say stupid shit as well (and there are many).
same source as above (proceedings of a Royal Society meeting)
> The signal to reduce meal size
> generated by glucagon reaches the
> brain via sensory axons of the vagus
> nerve since total subdiaphragmatic
> vagotomy, selective hepatic vagotomy,
> or lesion of the vagal afferent
> terminal fields within the NTS all
> prevent glucagon's feeding-inhibitory
> effect (Geary & Smith 1983; MacIsaac &
> Geary 1985; Weatherford & Ritter 1986,
> 1988; Geary et al. 1993).
but the brain ain't got nuffin to do with huner and obesity; it's all about that evil insulin and "dysregulation [0] of [1] adipose [0] tissue[2]"
No one's claiming the brain's the ONLY thing, and "brain" does not necessarily mean "conscious"
[0] LOL, chortle, ROFL
[1] smirk
[2] guffaw
@Sanjeev --not to disturb you in the middle of your chortling, smirking and guffawing about your up to the second science knowledge-- but here's a puzzler for you.
Which has a greater effect on hunger: hypoglycemia or the famous satiety effects of insulin?
Loaded question, how many "hungry" people are in fact hypoglycemic?
"Nobody in their right mind would walk off the street, see a real picture of Jimmy Moore (not the years old avatar) and take diet advice from him."
LOL, same goes for you.
If oxidative stress in the POMC neurons results in leptin resistance, then the most likely scenario is that the pharmacological effect of ketone bodies is sufficient to reverse this on VLC.
That ketone bodies are able to restore the sensitivity of nerves that have been subject to metabolic stress is surely the least controversial aspect of VLC.
If these include nerves that regulate appetite and resting energy expenditure, Bob's your uncle.
In interpreting Ludwig's results, we should consider that low-GI is probably about the norm; VLC increases metabolic rate, and low-fat decreases it.
It seems quite clear to me that a relatively low carbohydrate diet, on the order of 20% of calories, is far less atherogenic than a conventional diet with 50% or more calories as carbs, and that 15% of calories as protein in more than adequate which leaves 65% of calories as fat.
A high ratio of TG/HDL indicates an atherogenic lipid profile and increased risk for coronary heart disease. In the examples study discussed by Stephen, The TG/HDL ratio of those with the low fat diet and 60% carbs was 2.67, the low glycemic diet with 40% carbs was 1.93, and those on the low carb diet, 10% carbs was 1.37. My own TG/HDL ratio after a decade on a high fat diet is 0.65 (58/90)
A recent study found that two primary factors that contribute to oxidation of LDL are smoking and high triglycerides. (21624357). Carbohydrates are inflammatory and increase triglycerides thereby increasing CHD risk.
The question of energy expenditure seems minor compared to the question of atherogenicity.
@Jenny, yes there were only 21 people, but it was a three-way crossover. So in a way it’s kind of like 63 people. And the order of the maintenance diets was varied, so some people did low fat first while others did low carb first, etc.
@Elliot, great links, especially the comments. A young Dr. Guyenet sure had a different take on insulin back in ’08.
@Galina, yes I know you have experienced miracles on LC. I have experienced miracles on high carb-high fat, which Wooo thinks is impossible. I know my miracles are long-lasting, 30 years and counting: are you sure yours will be?
I know you take supplements, which means you do not really trust your diet. I have never taken supplements, because I do trust my diet. I trust it because it is known to have produced excellent health in the past. Do you know that about yours?
Alex, I did paleo for 2 years and then VLC for 4 years. I developed dangerously high trigs and had several kidney stones before I stopped. The last stone was 5mm. This means I was pissing my bones down the toilet. The doctor did a CT scan and said I had fatty streaks on my liver. All that, and I was still always 20lbs overweight.
If you still want to debate whether dietary cholesterol is a causative factor in atherosclerosis, and whether high protein diets cause kidney problems, all that information has been in the literature for decades now.
Don't you think if there was a diet that caused you to shrink to your desired weight and make you as healthy as possible, we would all know about it by now? Taubes would like it to be LC, but this is consistently proven not to be the case.
@George
Good point. Ketones might well explain it. But only if the low fat diet did not contain white flour. White flour has had most of its manganese removed and replaced with iron. Ketones appear to work by reducing oxidative stress in mitochondria, which is what manganese does.
Don Matesz suggests the low-fat diet did contain refined carbs, because of its low fibre content.
'..[The low-fat diet] supplies only 30 g of fiber... they could have included at least 1500 kcal worth of low-fat whole plant foods, and if they did, they would have had a diet supplying more than 50 grams of fiber, yet still very low in fat. Instead they chose to include low-fiber high-glycemic load foods, most likely refined carbohydrates. ..'
http://donmatesz.blogspot.co.uk/
Gunter your n=1 experience doesn't invalidate or prove anything.
In fact, on this very blog Stephen showed very well that your idea is probably incorrect.
http://wholehealthsource.blogspot.ca/2011/01/does-dietary-saturated-fat-increase.html
LOL Alex, I'm not trying to prove anything. I really don't care what you do. You've obviously got a pro-LC bias, but I urge you to look this stuff up in the literature (and I mean studies that REFUTE your theory also) if you really do care about this topic, like you say.
I told you my story so you have a chance to avoid my experiences and do your own research before you listen to people who haven't even seen success themseves, yet claim to be experts.
Don't play games with your body based on theories espoused by internet gurus, is all I'm saying.
@alex-
"We describe a 16-year-old girl who had sudden onset of cardiorespiratory arrest while at school. She had recently attempted weight loss using a low-carbohydrate/high-protein, calorie-restricted dietary regimen that she had initiated on her own"
http://www.ncbi.nlm.nih.gov/pubmed/12356106
@Bill, 21 people doing 3 diets is still 21 people with those 21 people's individual characteristics and specific genetic makeups, not 63. And the order in which they did the diets might have an impact on the results.
The reaction to this study, and so many others, shows the extent to which people turn diets into religions and respond to them with a partisanship that precludes rational thought.
I have eaten a carb restricted diet since 1998, so it's not like I'm an anti-, but I've also seen how tough it is for most people to stick to the diet and believe that the fanaticism simply shuts off conversation and covers the quiet exodus of the multitude for whom the diet does not live up to the hype of its well-paid prophets.
@Jane,
I take nothing in order to correct a possible deficiency of my diet. There are other reasons for me using supplements. I take only magnesium as a daily supplement according to the advice of my neurologist in Russia who tested me in order to find the root cause of my migraines. The main health problems I have - allergies, migraines and an unfortunate desire of my body to be more chubby than I want it to be, are corrected to a different degree with my LC diet. I also take Taurine and sometimes glutamate during 3 - 4 days after the end of a menstrual period at the time when migraines are more possible. My only daily medicine is a desiccated Armour thyroid because my thyroid is partially destroyed due to a Hashimodo condition. I have been thinking about adding copper to what I take due to your convincing arguments about copper deficiency but have not done it yet. I sort-of unsure about changing something in my regiment. Sometimes a desire to improve what is working already just mess-up everything. I remember too well how my health hit a rock-bottom after I followed for one year an anty-inflammatory diet recommended by Dr. Andrew Weill. (In order to follow the diet I increased the amount of whole grains, limited red meat and saturated fat, I already ate plenty of veggies and fruits). Since then I am basically scared of eating more that a very limited amount of grains very sparingly. I don't trust the whole grain advise any longer. Why I should have doubts about my diet? Sure, 5 years is less than 30, but since my health issues are addressed, I have no reasons to worry so far. You warned in your comments about a danger of iron over-load for people who don't limit their red meat consumption and get their copper from a beef liver, like me. My guess it could be more so for post-menopause females, and I am not there yet.
Galina, the allergies, migraines and tendency towards chubbiness all sound like they are hormone related. Have you heard of the Estrogen Dominance theory?
It states that when estrogen outbalances progesterone in the body, you get a number of health issues including thyroid problems, fatigue, memory problems, and other symptoms which are quite like menopause.
http://en.wikipedia.org/wiki/Estrogen_dominance
Anyway, funny enough, it is dietary fiber that takes excess estrogen out of the body. If it is not absorbed in your dietary fiber (if you don't get enough fiber), the estrogen goes back into circulation and your levels grow, causing a lot of the hormonal problems we see both in women AND men (who have much less estrogen but still can have too much, think of that stubborn roll of fat around your stomach, guys).
Anyway it seems fiber can help rid the body of that hormonal excess and maybe help level you out. Neal Barnard talks about this a lot (I know he's a vegan, but just ignore that part if it's not your thing). There are a number of his lectures on youtube that talk about how to lower unnaturally high estrogen levels.
Gunter your experience is just as likely to be due to a hundred other things in your life. How about you read Stephen's article and get back to me.
I'm not advocating a low carb diet for anything other than weight loss, and I also recommend low calorie diets for weight loss if you can do it. So I don't think I'm biased because I disagree with your ridiculous assertion that low carb diets are life-threatening.
"I'm not advocating a low carb diet for anything other than weight loss"
That's great Alex, except it doesn't even work for that in long-term studies. So why do it if it has the potential to hurt you? Did you not read the link Cliff posted, or is any proof at all just n=1 to you?
I read Stephan's article. Did you read this one I posted above? It offers, yes, a different interpretation. Why not look at both instead of just those that support what you like to believe?
http://donmatesz.blogspot.fr/2012/06/low-fat-diet-suppresses-metabolism.html
Gee guys & gals,
It is so jolly amusing to see these targetted intellectual debates or mayhap it's more more like Poker.
You raise me WHS?
Well, Primal Don scuppers you!
So there.
Slainte
@Ganther,
When I added more fiber eating more while grains to already ample veggies consumption following Dr. A.Weill's diet, it didn't cause a positive change in my health issues, quite the opposite happened.
I don't have a favorable opinion of Dr. Neil Bernard who is first of all the founding president of the Physicians Committee for Responsible Medicine (PCRM), then everything else. When a psychiatrist out of blue became the specialist in the reversing of diabetes and in the menstrual disorders influenced by a diet while promoting his vegan agenda, I don't care what he has to say about anything. Dr. Weill also belongs to the PCRM, probably it influenced his anty-red-meat viwes as well.
@Alex,
I would recommend to try LC diets to people with high blood pressure, allergies, PMS, migraines, pre-menopause symptoms, mood disorders, frequent infections. My mom has a normal BP now, I have not getting any single flue or urinary tract infection during last 5 years (since I changed my diet), no hot flashes or killer moods for me now. I also off asthma medication, my list of cured conditions is abnormally long. I am not sure it would be so for everybody else, but it is definitely worth trying. A weight loss is just a pleasant side-effect compare to other massive positive changes in my health.
@ Cliff, Gunther:
I read the pubmed article about the girl who died of hypokalemia. None of the causes of hypokalemia (severe potassium deficiency)have anything at all to do with either low carbohydrate intake or high protein intake. In fact, proteins such as meat, milk, cheese and fish are very high in potassium. So the fact that the girl had undertaken "on her own" a low-carbohydrate high protein diet had absolutely nothing to do with her death.
On further investigation I learned that my earlier statement that a low fat high carbohydrate diet always results in an atherogenic lipid profile is not always true. According to a Berkley study (PMID 11160558), more than 70% of individuals experience an improved lipid profile on a high fat diet, but those with a genetically influenced atherogenic lipoprotein profile, a reduced fat intake (less than 25%)reduces numbers of small dense particles thereby reducing atherogenicity.
For the majority who experienced an improved lipid profile on a diet high in fats and low in carbohydrates it is nice to learn that such a diet increases energy expenditure and allows you therefore to get more nutrients without gaining weight.
Another advantage of a high fat diet is a great increase in intake of fat soluble vitamins such as vitamin K2 (menaquinone).
It is impossible to get adequate dietary vitamin K2 on a low fat diet a difficult on a paleo diet because it is hard to come by organ meats such as brains and kidneys that contain adequate vitamin K2. I therefor eat a lot of fermented cheese to get enough K2.
@Galina
It's difficult, isn't it. I expect your neurologist thought magnesium was better than a drug, and no-one would argue with that.
All I can say is that I think it's important for people to do their own experiments. Nobody is going to be healthy on a diet they have been forced to eat, whatever that diet is.
Galina, I've just re-read my comment and realised it might sound as if I'm telling you to do experiments. What I meant was, you ARE doing experiments, which is just what I think you should be doing.
Galina, correction again. I've just read the paper Cliff linked about the girl who died on a low carb diet. It's VERY scary. I think gunther gatherer is right.
@Jane,
Actually, the neurologist gave me also some actual prescriptions - anty-seizure medication because my migraines looked like an epilepsy on electroencephalogram and a Caventon (medication against spasms in blood vessels because other tests indicated I needed it). She mentioned ketogenic diet and advised a magnesium supplement. The anty-eppileptic medication worked great for a while, then the effect started to wear out and I began to feel sluggish, I tried a ketogenic diet instead, it worked as well as medication without wearing out and sluggishness. As a person who can have allergic reactions easily, I often have a problem with medications because it causes a flare in previously dormant asthma or eczema, especially if a medication taken long-term. In such situation a diet and a magnesium supplement which are also beneficial for allergies look like much better options.
I read the link provided by Ganther and didn't find much similarities with mine situation ."She had recently attempted weight loss using a low-carbohydrate/high-protein, calorie-restricted dietary regimen"(a teenager doing crash high protein diet). What caused the potassium to fell so low? No one knows what exactly she was doing to herself. Indeed people could be a danger to themselves. For example Ganther also gave links to videos with horribly looking vegans. A lot of people mistake extreme thinness for a marker of health.
Gunther,
Everything you guys have posted has been n=1 stuff.
- One teenager who died while doing both a low carb and a low calorie diet. So basically rabbit starvation or something.
- One blogger who's still fat..
- One philosophy major who seems to think that 30g of fiber costs 300 calories to digest or something? I didn't bother reading it all, frankly.
"I didn't bother to read it all, frankly"
You've illustrated the problem with the LC movement.
Funny how being a philosophy major is suddenly a disqualifier to you. Gary Taubes was a physics major and is neither a scientist nor a doctor. And Jimmy Moore??? LOL.
Hate to come in so late to this, but after reviewing the study I have some serious questions.
1) On the "Study outcomes" slide footnotes b and c seem to negate the conclusions of the study. None of the energy balance numbers were statically significant between diets.
2) Double labeled water has not been fully validated for use in obese subjects. The reason is that they seem to sequester the isotopes creating a bias in the results. I could totally see diet playing a role in the level of sequestering.
3) If the REE was so different for the LVC group why wasn't the findings corroborated by a change in weight over the 4 week period?
Where did I post anything about Taubes or Moore? I don't even know who Moore is except for you talking about him being fat.
I read enough from that link to know that Don doesn't even seem to understand basic statistics, or maybe he didn't read the study carefully.
from the study:
Compared with the pre–weight-loss baseline, [...] The decrease in TEE showed a similar pattern (mean [95% CI], −423 [–606 to –239] kcal/d; −297 [–479 to –115] kcal/d; and −97 [–281 to 86]
This is where the ~300 calorie number comes from. Don makes a big deal about it being 246 but he is comparing the actual expenditures rather than the difference from baseline which is the salient point.
BTW, I would trust a physics major over a philosophy major every day of the week.
We know you didn't read the post Alex, because if you had you'd know the TEE was not Don's main criticism with the study interpretation. It is the bizarre claim that low fat diet caused an unhealthy lipid pattern and insulin resistance. The researchers claimed to have based the LF diet on "fruits and vegetables", but on closer inspection the amount of fiber was pathetic. This means subjects didn't actually eat fruits and vegetables, the researchers just gave them refined low fat foods with high glycemic index. THIS is what Don is saying is disingenuous about the results.
If the researchers had let subjects actually eat real foods they would have received a lot more fiber, which in turn lowers overall glycemic index, lowers lipid values, lowers insulin resistance, causes more satiety (bc food volume is much higher) and hence causes subjects to eat much less.
The "LF diet" was a laboratory diet that bears no relationship to a whole foods diet naturally low in fat. Its comparison to other diets is flawed from the beginning.
This is where actually reading other opinions would do LCers some good.
The study wasn't about how much people ate, it was about their expenditure... his whole point is sort of irrelevant to the study.
You could always have more fiber so it's just him applying a no true scotsman fallacy. The 30g daily of fiber in the study is well within most recommendations of between 25g-35g. It was also about the same amount as the LGI diet AND, it was 20g a day MORE than the low carb diet. So I think it's absolutely ridiculous to criticize them for not loading up the low fat diet with fiber.
I stand by my decision not to bother with anything more than a skim.
What can I say? You obviously don't think fiber is important. Not surprising from a LC standpoint.
Here's what Boyd Eaton says about the diet evolved on by our primate ancestors:
"Simple carbohydrate intake would have been strikingly below that now common, and, somewhat counterintuitively, such diets would have provided only moderate levels of starch and other complex carbohydrates so that the total carbohydrate contribution to dietary energy would have been less, not more, than is typical in contemporary affluent nations. Dietary fiber would have exceeded current levels by an order of magnitude: 200 grams vs. 20 grams a day (Milton, 1993): for some ancestral hominoids, colonic fiber fermentation may have provided over 50% of total dietary energy. (Popovich, 1997)"
You can find the whole text here:
http://www.cast.uark.edu/local/icaes/conferences/wburg/posters/sboydeaton/eaton.htm
So you see, the 30g/day recommended daily intake now is woefully inadequate in comparison to what we're used to eating historically.
So the 20g "more" fiber in the LF diet compared to the LC diet is still pathetic. BOTH DIETS had paltry levels of fiber. But the LF diet would have had considerably more if subjects had eaten whole foods instead of low-fat yogurt and chicken breast.
Fiber is necessary to rid the body of excess estrogens (which cause weight gain and metabolic syndrome). Not to mention all the vitamins and minerals that go with the fruits and vegetables. The LF subjects didn't get those either.
If you can really believe a LF diet based on refined, high glycemic index foods is the same as a whole foods diet naturally low in fat, then there's no point in arguing this any more. You'll have to stay in the Taubes and Moore camp and take your chances. Good luck!
So what? All 3 diets were deficient in fiber? Maybe, (you need more than some historic precedent to prove that), but I don't see how that invalidates anything anyway.
30g of fiber is far closer to what people typically eat on a low fat/low cal diet. They could have added hundreds more diets to the study if they wanted to, with different wrinkles such as fiber intake or protein composition, or fat source. But I don't think it's fair to criticize them for not including your personal favorite diet. They picked these 3 diets which represent 3 different paradigms common in the world and showed very clearly the difference between them.
Would a 60g fiber a day low fat diet beat a 60g fiber a day low carb diet when it didn't with 30g vs 10g? I'm VERY skeptical of that.
The point, as I said more than once now and as Don said, is that this LF diet was not the "fruits and vegetables" diet the researchers claimed it was.
Hence any conclusions drawn from it are useless.
And you don't need to tell us you'd be skeptical if a LF diet beat a LC diet. It's obvious where your biases are.
This is the problem with LC diet theory in general. Anything that doesn't agree, doesn't exist.
@Alex: Fiber, MUFA and protein can dramatically alter insulin sensitivity among other things. Why not just control for obvious confounders if you're specifically trying to draw inferences for one macro?
BTW, regarding Don's discussion of values, he used the TEE's calculated using the actual measured RQ instead of FQ. Difference from baseline vs. difference from each other plays no role. If you have baseline value of 10 and group values of 8,6 and 4, the greatest difference between groups = 8-4 = 4 is the same as the differential in the differences (8-10) - (4-10) = 4 :D
Difference was 246 for RQ calc, 325 for FQ. My problem with all of this is not presenting SD's and using uniform %CI (derived) and paying no attention to measurement error.
Where's the weight loss or gain?
Gunter,
The diet was claimed to "emphasize whole grain products, and include a variety of vegetables and fruits"
That's doesn't mean it was exclusively composed of such. I have to state again I don't have a problem with low cal diets and have used them successfully myself but really I don't see why you are so militant against low carb. When you try to paint me negatively as an extremist it reflects poorly on you since it's you who actually holds such a position.
If you want to keep twisting my words to an extreme position that I've clearly stated several times I don't hold, then please go away, I'm done talking with you.
@Evelyn You're right about the values. For a minute I had forgotten that all groups tried all diets in random order, I was thinking the baseline would be different for each diet.
As for your other point, If the low carb diet 'won out', and it was the lowest in fiber by far, I would think then equalizing the fiber content is unlikely to change the results except to make the margin greater. At least unless by 'equal' you mean Gunter's idea that one diet should have a 10x higher fiber content than the others.
Good discussion everyone. Sorry I don't have time to participate more.
I think several people brought up meaningful critiques of the study. I found Eric's comments particularly insightful.
I spoke to a statistician colleague about this study, and he had some pretty serious reservations. One of them Eric touched on, and that is that the pairwise comparisons between diets were presumably not significant since they weren't reported. Another issue (if I understood him correctly) is that they mathematically corrected for too many factors for a sample size that small.
There is a lot of skepticism in my field about this study. It's basically semi-contradictory to a lot of other data. I think in the end we'll just need to wait for independent confirmation from other research groups. I hope that the high impact of the finding will mean that other groups will try to replicate/expand it soon. I also hope they'll publish their negative results if they aren't able to replicate it, rather than just letting them languish in science limbo.
@Galina
'What caused the potassium to fall so low?' [in the girl who died on a low carb diet]
The paper says ketone excretion depletes minerals including magnesium and potassium. Magnesium regulates potassium, and loss of both could explain the cardiac arrest, it seems to me.
Here is a list of symptoms found in epilepsy patients starting a ketogenic diet. They include low magnesium (hypomagnesemia).
'RESULTS: The most common early-onset complication was dehydration, especially in patients who started the KD with initial fasting. Gastrointestinal (GI) disturbances, such as nausea/vomiting, diarrhea, and constipation, also were frequently noted, sometimes associated with gastritis and fat intolerance. Other early-onset complications, in order of frequency, were hypertriglyceridemia, transient hyperuricemia, hypercholesterolemia, various infectious diseases, symptomatic hypoglycemia, hypoproteinemia, hypomagnesemia, repetitive hyponatremia, low concentrations of high-density lipoprotein, lipoid pneumonia due to aspiration, hepatitis, acute pancreatitis, and persistent metabolic acidosis. ..'
http://www.ncbi.nlm.nih.gov/pubmed/15329077
Jane,
I don't have the full text but cardiac deaths are not uncommon with starvation diets. This is why anorexia is a really bad thing. The low carb part of this is probably a red herring given that the diet was also low calorie. People need to be careful when dieting!
@Jane,
A ketogenic diet is one of variation of normal human ways of eating. It cant't be potentially deadly.(I mean a normal way of eating, not some crazy variation) As I understand from the article, no one knows for sure what else that girl was doing(taking diuretics maybe)or how much she ate. The ketogenic diet fed to epileptic children in hospitals was notoriously crappy and hard to tolerate, children were also put through initial fast. I can't believe you may seriously think that her case should make me alarmed or it is reasonable for me to be scared by potential health problem people experienced during the initial period of the adapting to the artificial anty-epilepsy diet. I am at least 4 years behind the adaptation period, my diet doesn't cause starvation. Do you really expect anyone in my case to disregard the resolving of all mine health issues as a result of limiting carbs after reading about some isolated case with murky details and watching videos with vegetarian propaganda? Really, how do you expect me to react? To start eating whole grains again? Besides, the water-damping ability of LC diet was what I needed, as many people with insulin resistance. Several months before adapting the diet I was prescribed a diuretic because over-wise my legs were swollen most of the time. My doctor told me such condition was very typical for females after 45, sortb of part of getting older prosess, and the standard of care in such case was a "water pill". He didn't mentioned electrolytes replacement or any potential side effect from fluids dumping (doesn't mean much,probably). The symptom returns every time if I eat more than a very modest amount of grains or overdo other foods that contain more than appropriate amount of the wrong (in my case) mackronutrient. My husband is the "everything in moderation " guy, but watching my swollen legs after I eat some carbs for social reasons prevents him from bugging me about my diet, which is convenient. Unlike children, many not very young people benefit from fluid dumping, many take diuretics for bp control. My mom's blood pressure (75 yo)became normal next day after she started LC, and stays normal since then, her face used to look bloated before but not now.
ketogenic diets for epilepsy also included dehydration which can account for many of the negative side effects.
By included dehydration I meant that the patients were intentionally deprived of water as part of the treatment.
Wow! This was an amazing read. I felt like a ping pong ball bouncing between opinions. Guess none of you have this all figured out and still have your work cut out. Nothing like working on an experiment with about a thousand variables and trying to figure a predictable combination when you know it is really impossible...Just my opinion.
"The low carb part of this is probably a red herring given that the diet was also low calorie."
Come on Alex, how can you say you're not biased towards LC? All diets which cause weight loss do so because calorie intake goes down.
Knowing that, we can say low calorie is the real red herring because it's not a variable between successful diets, whether LF, LC or anything in between.
So gunter, everyone who doesn't believe your heart will stop with low carb is some sort of fanatic?
There are two things being conflated here, there is low calorie and there is LOW CALORIE, you know? If you're trying to lose weight there is a difference between being at a healthy -10% and unhealthy -60%. The difference is called anorexia and everything she suffered is a pretty common side effect of extreme starvation. Her problems were not due to a healthy low calorie diet, I suppose I should have said starvation diet instead. My bad, but that's also how it was described. Given her age and the sparse description of the diet I'm far more inclined to attribute it to starvation rather than missing a few carbs (or a few calories). Now, that being said, I wasn't able to read the full text, but when there is a huge amount of literature related to heart problems and anorexia I don't think it's a crazy assumption to make.
> don't have the full text but cardiac deaths are not uncommon with starvation diets. This is why anorexia is a really bad thing.
___________
the context of this discussion was relatively short term electrolyte loss.
cardiac arrest in the end stages of anorexia nervosa happens because the heart muscle has lost too much functional mass to continue working properly. electrolyte imbalance can occur for these patients but it's not the main thing precipitating their deaths AFAICT.
NOTHING to do with electrolytes ... discussing anorexia nervosa in this context here is non sequiturial.
> Which has a greater effect on hunger: hypoglycemia or the famous satiety effects of insulin?
__
what bentleyj74 wrote
∵ hypoglycemia[0] → and ∵ some sound logic → and ∵ some more sound logic → and ∵ even more sound logic → ∴ Taubes®© Truth®©, QED
[0] which hypoglycemia - the one where when asymptomatic peoples' blood glucose is tested for something unrelated to diabetes or hunger, the tests come back with very low glucose - that hypoglycemia?
Sanjeev, do you have access to the full text? I don't see anything precluding anorexia, and hypokalemia is a symptom of bullemia. I just think it's beyond premature to attribute this to a low carb diet, when there are far more likely candidates.
> about your up to the second science knowledge
didn't claim MY knowledge is up-to-the second, just that Taubes is at least 5 years and probably several decades behind.
THAT WAS MY POINT - thanks for emphasizing, punctuating and exclaiming it for me ... I'm NOT up to date I've never claimed to have done "three PhDs worth of work", or even a 2-year associate diploma's worth but when I can easily find more current and more balanced than someone who HAS claimed that it makes me wonder about those PhDs
this appears to be where you got the idea from my claim:
> If you don't keep up with science, science leaves you behind
Which is not the same as claiming MY knowledge is state-of-the-art and up-to-the-second
> but here's a puzzler for you
not so much
> -not to disturb you in the middle of your chortling, smirking and guffawing
No worries mate, you didn't
I don't have the text, and as you point out, bulimia IS a good candidate because from my reading cardiac arrest in these patients is more indicative of electrolyte problems.
I didn't write that anorexia is precluded, I was adding a bit of info along the lines of "if you hear hoofbeats when on the Serengetti, it's probably Thomson-gazelles, zebras, impalas, topies, buffaloes, Grants-gazelles, giraffes and less likely to be horses than if you were in North America".
> electrolyte imbalance can occur for these patients but it's not the main thing precipitating their deaths AFAICT
> I didn't write that anorexia is precluded
Anorexia Nervosa, that is
@Alex: the entire text can be read here with a (free) Medscape login
http://www.medscape.com/viewarticle/442894_print
There is next to no additional detail of this unfortunate girl or her diet. The bulk of the article is a discussion ONLY and I'd suggest one that has already decided to condemn this kind of diet -- without necessarily being specific as to what "this diet" is... they just know it is BAD!
They admit to not knowing WHY she suddenly died but build an house of straw anyway. The ketone discussion being just one example as they go on about how Ketones MIGHT do this that or the other WITHOUT having even established WHAT her ketone levels were... a simple enough test that can even be done at home these days.
They do however accept that there may have been more going on than was known "It is also possible, although no such history was obtained in this case, that associated problems such as bulimia, anorexia, and diuretic or laxative abuse can cause or potentiate electrolyte losses in such patients."
Here is the pertinent section discussing ketones... and yes I accept that if she were on a calorie-restricted diet her ketones could have been high (her blood pH was on the acidic side at 6.89 -- but surely they have to rule out cause for this other than ketosis?) that still does not justify the lack of this simple test.
"Restriction of caloric intake to less than the basal needs results in the catabolism of protein and glycogen stores, which have a high water content, leading to a diuretic effect with the loss of free water and electrolytes. Ketone bodies undergo urinary excretion with a cation to maintain electrical neutrality, resulting in the additional loss of cations, including calcium, magnesium, and potassium.[11] When compounded by inadequate intake, deficiencies of these cations may ensue. Caloric restriction is not generally recommended on most low carbohydrate diets, including the Atkins diet, further emphasizing the dangers of using these diets without strict adherence to their recommendations." BUT again these comments do NOT directly relate to this case but formed part of a general discussion only.
This is a sorry story to be sure but I see no convincing reason in it to find it or the idea of a low carbohydrate VERY scary unless I had an axe to grind ;-)
@Alex,
the comment from Frank G. on The Scribble pad blog http://itsthewooo.blogspot.com/2012/07/their-hysteria-is-incriminating.html contains more information
"For anyone interested to read further, the full article can be read here with a Medscape login (free) http://www.medscape.com/viewarticle/442894_print
But here are few snippets to balance the shock-horror anti-LC bias :-0
"Abstract
We describe a 16-year-old girl who had sudden onset of cardiorespiratory arrest while at school. She had recently attempted weight loss using a low-carbohydrate/high-protein, calorie-restricted dietary regimen that she had initiated on her own. During resuscitation, severe hypokalemia was noted. At postmortem examination, no other causes for the cardiac arrest were identified. Toxicologic findings were negative. The potential role of the dietary regimen as a contributing factor to the hypokalemia and subsequent cardiac arrest are discussed."
In short: they don't know WHY this poor girl collapsed and died suddenly... sad to say it happens from time to time BUT just because they can't figure out why, does not excuse them building an house of straw.
The remainder of the article is a "discussion" ONLY with no substantial evidence for any cause and effect in this case.
Notably they concede that "Postmortem and toxicologic examinations revealed no apparent cause for the death."
and
"Caloric restriction is not generally recommended on most low carbohydrate diets..." although they fail to acknowledge that recommended low-carb diet are high-fat not high-Protein -- but if she was calorie restricting (how severely?) that may be neither here nor there.
another snippet "It is also possible, although no such history was obtained in this case, that associated problems such as bulimia, anorexia, and diuretic or laxative abuse can cause or potentiate electrolyte losses in such patients." hmmm... not to play on a stereotype but a teenage girl desperate to lose weight, taking diuretics or laxatives without her mother's knowledge... possible or unlikely?
I am most upset that this reflection of the pressure put on teenage girls by advertising etc... which has led to so much suffering, is being perverted to try and scare people away from what they could find to be an healthy way of eating.
And my overall response to this shock-horror tactic from the anti-LC brigade is courtesy of the British comedy duo Mitchell and Webb... http://www.youtube.com/watch?v=tCzh0KDW8YQ"
"All diets which cause weight loss do so because calorie intake goes down."
gunther, what are you basing this statement on? This blog post is on an article that measured the metabolic response for different diets and it would seem that different diets certainly seem to affect the metabolic rate.
Dan, you have arrived late to this blog. Stephan has discussed how there are obviously many metabolic pathways that lead to weight loss and weight gain. That was the point of the clip I linked and my comments about Jimmy Moore. There isn't just "take out sugar" or "take out fat", and that solves the problem.
Given our evolution as omnivores having to survive through drought, flood, feast and famine, I don't think it could be any other way.
All diets, whether LC, LF, fruitarian, bland diet or whatever, make the subject lose weight because they ingest less calories. Stephan has mentioned this several times. And we've seen from all the fat LCers that the increased resting energy expenditure doesn't really make a difference to them. They are still ingesting way too many calories, or maybe Stephan would say their bodies have lowered their resting metabolic expenditure because their setpoints are still too high, or maybe that they never went down at all during the diet.
I don't think there's any serious discussion anymore among diet and nutrition professionals about how humans lose weight. The question now is how to do it long term.
But this is all barking up the wrong tree. I don't think resting EE in isolation has much to do with long-term weight loss or gain. Otherwise according to the study results, you'd see lots of fat vegans and fruitarians and that is almost never the case. And meanwhile we know there are many fat LCers...
Sorry Dan, just to be clearer than above, my whole point was that if resting EE really mattered for weight loss, all vegans (HCLF diet) would be fat and all LCers (more or less HFLC diet) would be skinny.
(I realize they didn't even really study vegans, just a refined laboratory LF diet, but veganism is quite HCLF for comparative purposes.)
But we see in real life that this isn't the case, and is actually moe the reverse, so the conclusions of the study and are pointless and knowing REE of one diet over another gets us nowhere.
@Galina
Sorry to have alarmed you. I think this is real, though. Gunther gatherer says he was 'pissing his bones down the toilet' on LC, which is a polite way of saying this diet depletes minerals.
I cannot agree with you that a ketogenic diet is a normal human way of eating. If it were, people eating it would not need supplements. Both you and Wooo take magnesium, and the case of the girl who died suggests it may be necessary.
A recent paper (2010) tells us how the ketogenic diet probably works. It's the same process as hormesis, by which a small amount of something toxic generates a protective response against large amounts of the toxin.
'..The mechanisms underlying the efficacy of the ketogenic diet (KD) remain unknown... Here we present novel data suggesting that consumption of a KD initially causes production of low levels of ROS [reactive oxygen species], which may serve a redox signaling role, thereby activating one of the major cellular detoxification pathways, the Nrf2 pathway... With respect to Nrf2 activation in the liver, our results strikingly parallel those of acetaminophen [paracetamol] toxicity studies in which liver GSH [glutathione, an important antioxidant] is depleted, concomitant with nuclear translocation of Nrf2... Thus, the health effects of chronically depleting liver GSH need to be addressed in future studies of the KD. ..'
http://www.ncbi.nlm.nih.gov/pubmed/20594978
In other words, we don't know what happens in the long term, but it doesn't look that good.
Jane,
This Rat-Fed diet consisted of:
"The KD was comprised of 78% fat and 0.76% carbohydrate, while the control diet was 5% fat and 65% carbohydrate."
This would provide 4.56 gms CHO on a (human) intake of 2400 kCals/day.
On the basis of this Rat Study, you are unduly Risk Averse.
Life is just TOO short, and while Keynes says "In the long run, we are ALL dead", I prefer the Eagles "You can go the distance / We'll find out in the long run."
http://www.youtube.com/watch?v=DI_rkZIuHzw
Slainte
> 2) Double labeled water has not been fully validated for use in obese subjects. The reason is that they seem to sequester the isotopes creating a bias in the results. I could totally see diet playing a role in the level of sequestering.
_________
I'd like more information on this but my google search terms appear inadequate.
Links or cites please, to experiments documenting the obese sequester the relevant isotopes.
I'm taking courses @ a university with a top notch medical school so I may be able to get citations no matter how obscure.
Energy expenditure in lean and obese subjects
http://ajpendo.physiology.org/content/261/3/E402.short
@Jane,
I based my opinion that a ketogenic diet is ONE of normal ways for humans to eat on the reading about the experience of Vilhjalmur Stefansson.http://en.wikipedia.org/wiki/Vilhjalmur_Stefansson and on some logical thinking that during periods of ice age groups of people supposed to have to survive at long periods by sustaining themselves only on animal products. I am one of individuals who eat organ meats and bone broths, not only stakes and chicken breasts as sources of meat. I also eat vegetables(some root ones as well)and small amount of milk products and eggs .
You didn't particularly alarm me, it is just that I don't understand what kind of advice you try to give me. Sure, you don't want me to drop everything I am doing only because of some blog comments that may sound alarming for an anxious type of person. You sound like an intelligent human being, and I think you just want me to watch for possible health issues and take my magnesium because you don't think avoiding grains and getting you nutrients mostly from eggs, meats and LC veggies is healthy. I had my liver enzymes tested couple years ago, I don't remember exactly why, probably my doctor just included it in a long list of things that was tested during routine blood test. Soon I will have a bone density scan because it supposed to be done at my age.
There are a lot of wrong LC diet advise going around, it is a small surprise many complain on their inability to loose weight and feel healthy. It is not rare to notice some dieters on forums who try to loose unwanted pounds by eating more butter and/or an abnormal amount of meat and snacking on lc nuts and Atkins bars. When people just follow some set of rules instead of self-observation, it is harder to modify your diet in order for it to fit personal needs, it makes life more stressful and socially isolated. As a result many rebel against meaningless rules (like forbidding your children ever have a birthday cake because sugar is a poison) and go into an opposite camp just out of spite for their previous one then declare that all you need is eating "real food". Sometimes it is enough for many after LC period of eating, but it is not my case.
gunther, what do you think the primary reason is for people starting a lc diet to begin with? is it their ethical opposition plant consumption? now, why do you think vegans become vegan? because they'r trying to lose weight? telling us that vegans are thinner than low-carbers (which seems anecdotal at best; i know a lot of fat and/or doughy vegans) tells us nothing about how they got this way. that's like saying diet soda must cause obesity because all a lot of fat people drink it. seems you're confused about causation...
When it comes to body weight, the best quality science we currently have tells us that the body completely has a mind of its own.THis is the most curent top quality research.
The reason for this being that Dr. Jeffrey Friedman, Dr. Rudolph Leibel and Dr. Michael Rosenbaum run this research back and forth dozens of times. To say they are extremely thorough would be an understatement. Their work alone is enough to compleyely discredit Innternet salesmen and hearsay.
I remain a dietary agnostic as Dr. Friedman is. Very large studies for many , many years ( very long term, not short term) are needed to settle this issue about the composition of diet being particularly fattening. In people, the answer remains unknown.
This metabolic advantage issue is like asking "what cheese the moon is made of." It is a distraction- largely on the Internet.
We need to study HOW the body is fighting back forcing regains ( DESPITE the continuing of healthful behaviors) and what to do about it to understand it better.There are many things it does which are undiscovered tricks.
We need to know WHY the body THINKS the obese state is the perfectly normal state. This is what is going on in severe obesity as Dr. Leibel most recently has shown. That is BAD news.
Without these insights into the body's weight regualtion systems and fat mass defense systems the problem of obesity would truly be hopeless.
Weight maintenance is the HUGE issue with obesity .
With this insight treatments - new EFFECTIVE treatments can eventually be devised for once, discarding recommendations that science has shown do not work well.
As Dr. Friedman saisd "eat less move more " is NOT a given. It has been a failure largely. At BEST- at very best Friedman said that the nostrum "eat less, move more" is a RESEARCH QUESTION.
Paul,
You're right that not all vegans are thin and not all LCers are fat, I'm just making a point about REE and how it's obviously not the only thing causing weight loss or gain.
Paul,
So most vegans choose that diet for reasons other than weight loss -- so the implication is they self-select from a leaner population. Most go low carb for weight loss so self-select from a fatter population. Fair enough ... but if the EE data are accurate (which I doubt) or would remain different once one becomes adapted to the diet, then the longer someone has been a vegan the fatter you would expect them to become, right?
And yet vegan advocates, who've been eating that way for decades are demonstrably leaner than LC advocates. Some of that might be that more of the low carbers are formerly obese, but why don't the vegan "pre-obese" get fat?
I don't know any overweight vegans. Veggies are a different story, you have a lot of those who are ovo-lacto and this subset tends to be more susceptible to fattening. And then it's possible to be a SAD vegan or veggie if one drinks sugary beverages and coconutty confections and chocolate.
Evelyn,
Yes, the "doughy-er" vegans I know all eat significant amounts of fat in the form of chocolate, nuts, coconut and vegetable oils. Tofu, "not-dogs" and other vegan frankenfoods are pretty high fat too.
I cannot find any fat long-term fruitarians on the net. And I have really looked.
Stephan and you have both mentioned more than once that dietary fat seems to favor bodyfat gain, while carb intake seems to do the opposite. In fact I think the conversion from carb to bodyfat is so inefficient that you only get about 30% of excess carbs made into bodyfat.
Think about it: a tablespoon of olive oil has more calories than the whole salad combined. Throw in an avocado and nuts, then eat some chocolate or coconut cream for dessert, and sure you can still get fat.
I think a very low fat vegan diet would be very effective for weight loss. I know because I've basically been doing this for the last 3 months and I'm stuffing myself just to keep my weight. But I avoid the high fat foods mentioned above.
I'm not recommending this for anyone nor am I militantly anti-meat or anti-LC. I'm just throwing this out there so others might see that maybe they're sabotaging their weight loss with foods they think are innocuous or even healthy.
I think Dr. Esselstyn is a very nice man who is dedicated to patients.
However, his claim about reversing heart disease is suspect. Here is why. As Dr. Steven Nissen has pionted out coronary angiography is outdated technology and misses a TON of plauqe. You c an have little to no narrowing but huge plaques in the wall of the artery- as Dr Steven Nissen's lecture pointed out. Science now knows that coronary disease is not a disease of the lumen, but rather, the vessel WALL.
The technology of IVUS was not around back when Dr Esselstyn did his study. Those patients never went through the IVUS, which could have spotted what coronary angiography missed- which could be a ton.
If you want to know IF yuo have CAD, narrowing of the arteries will NOT tell you because you can have no narrowing but VERY SIGNIFICANT CAD.many patients were sent hom with a fine health, yet had HUGE palques in the walls
Science is a LONG, LONG, LONG way from knowing the optimal diet. We are ALL taking risk with ou dietary decisions. We need to learn much more about cellular biochemical operations to answer that question.
Here is Dr. Nissen's detailed lecture abuot how coronary angiography misses a TON- which used to be on my blog:
Promoters of low carb, high carb, vegan and the pink people eater diet etc. are all groping in the dark.They are all making money. Dr. Fuhrman is just as much of a huckster capitilizing on things. He is far too sure- 100 % certain etc.
Too little is currently knwon about nutrition.
NO diet has currently. Zero evidence. Dr. Nissen admits this.YOu can improve symptoms but it is NOT a cure.
We know *some* things. Eating anti- oxidant rich is likely very beneficial. The evidence points to making fruits , leafy greens, vegetables,seeds nuts the bulk of the diet. The current knowledge suggests not lettign meat crowd out the fiber and anti-oxidants of a vegetable rich diet etc.
Dr. Nissen is world renowned.He has scientific integrity and spoke up about Avandia.
http://www.youtube.com/watch?v=1N0bstymScU&feature=relmfu
* No diet has been shown to actually reverse heart disease. Symptoms can imporve and outcomes- but the disease itself cannot be reversed from DIET alone.
For some reason this did not take above.
Eric said...
"3) If the REE was so different for the LVC group why wasn't the findings corroborated by a change in weight over the 4 week period?"
Richard Nikoley published a response from Dr. Ludwig to a similar question (http://tinyurl.com/6qcdc8k):
Richard Nikoley: "...if they ate the same calories, had the same physical activity, maintained the same weight loss throughout, then how are the 300 daily calories accounted for if not in additional weight loss beyond the initial loss? ...."
David Ludwig, MD, PhD.: "... 4 weeks isn't long enough to translate a 300 kcal/d difference into statistically significant weight change, especially when one considers that body weight normally fluctuates by a kilogram or two through the course of a week, based on differences in hydration status, the time of the last bowel movement, etc. We'd need 6 months to reliably see this effect. Nevertheless, there was a slight, and not statistically significant difference in the hypothesized direction, with body weight highest on the low fat diet (data included in the results section)."
In other words, given more time, Dr. Ludwig thinks the LC subjects would have lost significant weight. Despite that, he doesn't recommend the LC diet and instead recommends the low-glycemic diet that produced less weight loss but what he said were better numbers for CRP and cortisol (all of which he discusses in this interview: http://onpoint.wbur.org/2012/07/05/new-research-on-carbs).
I don't know whether Dr. Ludwig's expectation is correct or not re: longer-term weight loss and I'm not promoting his view, just sharing what he said that might help answer Eric's question. Based on the On Point interview, it does seem like Dr. Ludwig thinks that carbohydrate are more fattening than fat (and the study report hinted that this where it stated "The low-fat diet produced changes in energy expenditure and serum leptin42-44 that would predict weight regain" and "In contrast, the very low-carbohydrate diet had the most beneficial effects on energy expenditure"), and this may help explain why he hasn't reacted strongly to the media treatment.
Ludwig's focus appears to be on overall health, rather than maximum weight loss, and in the interview he did attempt to explain why he doesn't like the LC diet on that basis, though he didn't address the media's lack of emphasis on that. Even the online summary of the On Point interview gives the impression that the study was promoting the LC diet, rather than the intermediate-carb, low-glycemic diet that it and Dr. Ludwig actually promote (which I'm not advocating).
You can fatten mice and make them obese simply by transplanting the gut microbiota from an obese mouse into thin, sterile mice. The thin sterile mice now become obese with NO CHANGE AT AWHATSOEVER in diet OR activity levels.
Mice are VERY similar to humans genetically. They are excellent model organisms especially in relation to obesity and heart disease. The gurus do not recognize the value of mice. Some scientists even call them litle furry humans.
To the Internet gurus it is "all about calories." They display a 1st grade level of understanding of this complex phenomenon.
We have enough evidence to declare the simplistic caloric hypothesis dead. Calores are only one factor among dozens, upon dozens ,upon dozens in regard to obesity.
Razwell has it right, I have just seen so much real life evidence that suggests the body has its own agenda.
I know a girl from my neighborhood that still has a perfect female figure at 31, she eats junk, drinks quite a bit, smokes, and has had TWO kids. Although her face is showing signs of aging, she still has the body of a teen.
Razwell, I've heard about the gut microbiota transplant studies too. I'll grant you that it's not just about calories ingested but what your body (or gut bugs) DO with the calories that matters.
There are lots of horses around here where I live. They are all absolutely jacked with muscle and no fat whatsoever on an all-hay diet, just standing there all day munching. There is something we are all missing.
Yes Jacko... you're missing the fact that horses are herbivores! LOL
Not only are horses herbivores, grass and hay are relatively low carb.
Horses will have severe reactions, including colic (the leading cause of death among horses) and laminitis when subjected to sudden intake of feed with high carb foods content like grains or rapidly-growing spring grass. Horses overfed on high carb feeds get fat, just like cattle do. And, just like cattle, they develop ulcers. Diabetes among grain-fed horses is not uncommon and almost unheard of among grass/hay fed horses.
@Gunther: The gut microbiota transplants in mice validate CICO! Rodents have a functional cecum which looks kinda gross (remember I used to cut these critters open for a living) and is a pouch after the small intestine designed to ferment otherwise undigestible fibers and such. They rely on hindgut fermentation for calories ... not so much as ruminants, but moreso than humans (it is thought our appendix is a vestige of the cecum). Sterile mice get no nutrition from these fibers, populate their cecum with "bugs" and voila!
So far fecal transplants in humans have elicited at least temporary improvements in glucose homeostasis, but not weight loss. They are apparently very helpful in eradicating cases where the bad bugs have taken over and you just need good bugs to edge them out.
Awesome observations, gunther and Kindke. :)
Very perceptive.
CarbSane, the simplsitic "calories are everything" hypothesis is down and out. There is enormous evidence against it.
Try to inquire , rather than defend failed hypotheses. This is undoubtedly bad for business of gurus who swindle people with fat loss books.
The mice studies do NOT validtae caloric hypothesis at all. They are in DIRECT contradiction.
You could learn A LOT from Urgelt. The simplsitic claoric hypothesis was dead even in 2008. about science.
The gut flora mice experiments open up a completely NEW ( and desperately needed) hypothesis in the pathology of obesity.
Both Dr. Gordon AND Dr. Seeley have said this in the article.
This research opens up NEW windows. It is an exciting time, not a time to defend the failed claoirc hypothesis. It is time to move on.
I do not udnerstand your emotional attachment to a failed 60 year hypothesis and always defending it when it has been contradicted many times by experimental evidence.
One puzzling thing Dr. Ludwig said in his interview was that US fat intake as a % of calories decreased from 42% in the 1960s to 30% today, which differs substantially from the USDA numbers Stephan showed at:
http://wholehealthsource.blogspot.com/2011/08/carbohydrate-hypothesis-of-obesity.html. I have also seen LC advocates claim that fat consumption has gone down. I found that Dr. Eades cited National Health and Nutrition Examination Survey data here http://www.proteinpower.com/drmike/weight-loss/a-toxic-environment/ (the data source is here http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm). It shows kcals from total fat decreasing to 32.8%, which is close to the 30% figure Ludwig mentioned, so that might also be his source.
Is the USDA data better because it tracks what was sold rather than what people report in surveys, which may be unreliable?
Agreed, Total Daily Energy Expenditure (TDEE) is a measure of daily consumption of energy. It is composed of your Basal Metabolic rate (BMR), which is the energy you use up just staying alive and the energy you use doing everything else (walking, talking eating and exercising). By the way I am Dorothy of California Health Plans.
@Phil
USDA data is unreliable, because it measures what was sold not what was consumed. Imagine what happens when people eat more from a fryier than from then pan: they buy much more oil but consume around the same amount, may be a bit more, may be a bit less. In any way, not all the fat you cook with lands in your guts, a lot is lost.
I think even Stephan had an entry on that from several years ago.
Razwell and Evelyn,
Looking forward to more studies on gut bugs. It does look like an untapped well of info there. Not sure how it's practically applied though. This is the main problem with all these isolated studies.
Phil,
The data discrepancy between Stephan and Ludwig needs some definitive (and objective) explanation. It could singlehandedly settle the debate between low carbers and low fatters right now about what's been causing the obesity rise.
Though then we have a different problem: if we're eating more carbs now than ever before, a low fatter can say we're actually getting less calories since the conversion to bodyfat is only 30%. If we're eating more fat than ever before, a low carber can reply that insulin is therefore lower than ever before, hence less conversion to bodyfat.
Either way, why is obesity going up? It's got to be about the overall calories, regardless of carbs or fat.
Hi, gunther
Dr. Jeffrey FRiedman addresses the skewed numbers about obesity. ONly 26,000 people a year die annualy from obesity related complications. That is a far cry from the completely false 400,000 number due to CDC computer mistakes.
When we measure a continuous trait like body weight using a fixed threshold ( e.g. BMI 30 and over is obese) there is a disproportionate increase over time of the number of people who exceed this.
There's no question obesity is a problem today. But there is no epidemic. The actual data shows since 1990 we are only about 7 to 10 pounds at the most heavier . Thin people are exactly the same and have held steady. The biggest difference is only seen among the obese. Dr. Friedman acknowledges though that the extra 7 pounds or so is a problem.
Obesity has been with us since at least 23,000 B.C. People are more sensitive to it now and njotice it due to the scare mongering. It is ture that there are more obese people today but it is exaggerated by using a faulty dioagnostic tool (e.g. fixed threshold the over it under it BMI of 30 thing for a continuous trait)
There is a very good documentary on overfeeding called " Why Thin People Are Not Fat on YOuTube. Dr. Leibel is featured explaining things. This Asian guy hardly gained anything and almost all of it was msucle. He looked betetr at the end of the study. Others gained a lot. People who particpate in these studies who have obesity and diabetes in their familt usually do not lose all of the weight fast like the others.
Overeating is bad, but it is not the true cause of obesity. Manuel Urbe has soemthing going on drastcally different. I ocudl try my best but I oculd never be 1,000 pounds. My body woudl put the squash on it. I would estimate with a deliberate extremely poor lifestyle I could be 300 to 350 tops- and that is after many years of it.
Urgelt opened my eyes to all of this. Urgelt understand science extremely well. he also enjoys Stephan;s blog. it is the only blog he reads because he warns me that Internet syhsters who are not genuine scientists never admit vast unknowns.Human physiology is mind boggling complex.
Dr. Friedman hopes everybody who is able leads a good lifestyle to stay at the lower end of our setpoints- about 8 to 10 pounds less. That seems achievable lon gterm . But that is all any scientiost can ask of anybody.
True severe obesity is a complex phenomenon for whcih te unknowns are far greater than any knowns.
Best Wishes,
Raz
@Galina
'..I don't understand what kind of advice you try to give me..'
Perhaps this will clarify things. If a ketogenic diet is a normal human way of eating, the traditional Inuit diet must have been ketogenic, right?
'.. the Eskimo on his usual dietary shows no ketosis ...On fasting he develops a ketosis, but only of mild degree compared to that observed with other human subjects'. ..'
('Studies on the metabolism of Eskimos', Heinbecker 1928)
Gunther, In an interview with Ian McCarthy Alan Aragon - I think the one where they discuss Lustig/Stanhope on "60 Minutes" talked about some recent data showing obesity rates in the US have stopped rising. Whether this is a short term pause until they resume an upward trend or start going down somehow is anyone's guess. They have plateau'ed though
Jane, I believe the Yupik & Inuit who eat near zero carbs (those not now living in cities and consuming massive amounts of KFC and Coke) are in ketosis most of their lives.
ON a ketogenic diet one is always in ketosis but may stop showing ketones in the urine ("ketonuria").
IOW any "metabolic advantage" from ketone losses in the urine disappear. This happened to me. Near the start of Atkins I regularly registered purple on ketostix and within 2 years I rarely went above light pink despite being more strict.
PS - Gunther, IMHO there are people worth getting in a discussion with and others ... not so much. Please be kind to your own future self & spare his sanity.
@LeonRover
Yes, that diet was pretty extreme. But it did find out how ketosis works. My position is that ketosis is unnecessary because the benefits, which are apparently due to protection of mitochondria, can just as well be obtained by increasing the ratio of manganese (protects mitochondria) to iron (damages mitochondria). A high-iron diet can cause manganese deficiency, because iron transporters get down-regulated and they are also used by manganese.
Sanjeev, the paper I linked says this:
'In his analysis of the ketogenic and antiketogenic factors, the
balance between which seems to determine the appearance or
non-appearance of ketosis, Shaffer (1) has considered the Eskimo
,dietary, using the data reported by Krogh (2). According to his
.analysis the metabolism of the foodstuffs contained in the Eskimo
dietary would not be expected to cause ketosis, because the calculated
antiketogenic effect of the large protein ingestion was somewhat more than enough to offset the ketogenic effect of fat
plus protein.'
They ate enormous quantities of meat, and this was converted by their very large livers into glucose, so they had no need for ketones.
Gunther:
I'm not sure that your understanding of fiber's effect on enterohepatic recirculation of hormones is correct. It is quite unlikely that the sequestration and elimination of hormones attached to fiber is beneficial.
The percentage of meals during our evolution that were mixed, (i.e. containing meat and fibrous things) would have been much lower than what we consider normal today. Simply eating fiber without fat wouldn't result in biliary secretion of these hormones. If one were to only eat fatty meat for a meal there would be near complete reuptake of the hormones. If there's one thing we know about evolution, it's that it is a process that favors efficiency. It would be energetically wasteful to excrete hormones in this way.
The purpose of enterohepatic recirculation is actually a lot more interesting. These conjugated hormones are meant to interact with microbiota, get modified, and reabsorbed. There are forms of hormones that [healthy] individuals absorb in that manner that actually cannot be manufactured otherwise.
Sure, fiber will pull estrogen out of the system, but it will also pull out progesterone, testosterone etc. As such, it would not be a reliable method to reduce estrogen dominance. Has your diet from the last 3 months affected your testosterone levels (which might be measured by proxy via perceived libido)?
Wow, great article, I really appreciate your thought process and having it explained properly, thank you!
familyplanningoxnard
I had gone through it thoroughly its really worth to spent time on it and i really got to know a lot more from it .
Leech Therapy
I would like to post this video from Urgelt of YouTube on how to protect yourselves from Internet website claims and shysters. They have scientific SOUNDING sites, preying on the masses:
http://www.youtube.com/watch?v=Ec72CMCbCuQ
I have no biases with regard to diet. My own diet is center of the road. Research is suggestng there is a metabolic advantage ( I have zero problem with that), but I don't think it will amount to that much. In other words, I don't think it is the solution ( or even a major factor) to obesity most likely. I could be wrong.
I really believe the battle of the diets so popular on the Internet is just like asking "what cheese is the moon made of?" Everybody then discusses if it is American, Provolone or Swiss.
We have the ask the right questions in science. Only then will we get the something closer t the truth - or "less wrong." This is what made Issac Newton , Albert Einstein and Richard Feynman so amazingly great.They had an immense talent for this.
Science does not stand still. It is a perpetual work in progress with ALL knowledge being tentative ONLY.
To sum up my main message: There are many self serving liars at large. They are everywhere. If a source of information on the Internet does not admit to consdierable uncertainty and vast unknows, it is not a scientific source of information. Stephan's blog is the only blog I bother to read, because he sells nothng and is an authentic researcher.
All dietary decisions are a minefiled through which we all tread. We need to know FAR more than we currently do to know what the optimal diet. More research into cellular biochemical operations will help this. We know *some* things.
Consider this: Even if you know the correct mushrooms to eat in the wild, you could pick some that a deer pooped on and die.I bet this happened to many of our ancestors.
If an Internet guru is making a claim that the world's reputable, genuine scientists cannot do, then that is a HUGE RED FLAG.
Stephen--As always you have hit on all the important points. Although diet composition and fat storage is a complex matter, the brain seems to call the shots when it comes to fat storage.
We also believe that certain dietary elements can adversely affect brain function. The combination of excessive fructose mainly from sugar and HFCS and high glycemic carbohydrates mainly from grains seem to be the primary triggers of food induced brain dysfunction. We now call this condition Carbohydrate Associated Reversible Brain syndrome or CARB syndrome. People with CARB syndrome can develop up to 22 brain dysfunction symptoms that interfere with their ability to function. They also seem to store more excessive fat even when they lose lean body mass from under-eating. Learn more at http:carbsyndrome.com.
BTW, Body Mass Index has been shown to not in any way correlate to mortality.
1.
Those propounding the idea that obesity is unrelated to the brain on the basis of gut flora, can they please elaborate why they view it as such?
The reason I'm asking is because it is pretty established that the gut flora itself impacts brain development and beahvior.
http://www.scientificamerican.com/article.cfm?id=the-neuroscience-of-gut
I do not see how one can legitimately separate the issue of obesity being from the body and not the brain through gut flora, when the connection between gut flora and brain development and behavior seems to be established.
2.
Further, this article also clearly establishes the relation of gut flora to the utilization of certain vitamins, such as B6.
3.
I would also like to comment on the point regarding fecal transplants. A fecal transplant would generally only provide long-term benefits for obesity, if the food pattern changes pre-fecal transplant. The primary reason for this is that diet also alters the ratio of bugs, so going back to the same diet when one was obese would shift the gut flora back to the ratios that may pre-dispose a person to obesity.
4.
Also, it is often missed amongst the Paleo-prononents when arguing about traditional diets, that these people were not as 'sanitary' as we are today, and were not prescribed anti-biotics which, through constant bombardment in today's society, totally disrupting their gut flora.
Further, their infants were not introduced to formula instead of breast milk, while the baby's digestive tract and immune system is developing and in it's infancy and so on.
5.
It's all about the UTILIZATION of calories by the body, meaning one can find a synthesis between the idea that is the quality of the food, as well as the 'CICO', as well as gut flora, as well as the brain.
Nobody, in these diet discussion seem to point to the issue that their weight could have been influenced by how their parents raised them when they were young, from the perspective of:
1. Formula feeding vs. breastfeeding
2. Whether or not their parents gave them antiobiotics aplenty during their infancy, and into their childhood
As Dr. Ayers points out, these radically alter the gut flora, impacting the immune system, leading to chronic inflammation.
Another interestoing point, though it is speculative, is tonsillitis. Tonsillectomy, which is a common procedure, has a relation to weight gain.
The fact that tonsillitis is rather common would seem to indicate some issues in how the immune system deals with foreign antigens. It is well worth to note that the gut flora is the primary method upon which the immune system learns to deal with foreign antigens, but the tonsils are the first line of defense.
http://pediatrics.aappublications.org/content/123/4/1095
"Children who undergo (adeno)tonsillectomy are at increased risk to develop overweight in the years after surgery."
So one can see how the immune system could trigger obesity as well.
http://bytesizebio.net/index.php/2010/04/25/obesity-the-role-of-the-immune-system/
@Jane,
I didn't mentioned Inuits at all(and your link didn't answer my question about your advice), what I said was that big groups of people had to be able to live on animal products for a long time during human evolution. Vilhjalmur Stefansson and members of his expedition had such experience. As I remember from my reading, when V.S. and one of his team-members participated in the study in a New-York hospital about the healthiness of his all-meat diet, the complaisance with the diet was checked by ketones in urine.BTW, I am not aiming for deep ketosis all the time because I don't want my liver to be too efficient with producing glucose, I commented about it on Hyperlipid blog.
As I understand, your diet consists of whole grains and milk products. It is good it works for you, I don't think it will be the case for many.
Asim, Sapolsky's talks on toxo and other viruses/parasites may also interest you ... the long running theory of toxo causing schizophrenia for example
http://www.edge.org/documents/archive/edge307.html
I heavily discount any parental impact on adult humans except in cases of severe abuse/neglect.
Peer group pressure/acceptance/standards IMHO far outweigh parental effects in most areas. The most obvious example of this is the development of accents in immigrants' children - peer group effects far, FAR outweigh anything the parents can do.
Despite living in very different lifestyles and living in very environments , these international samples of monozygotic twins reared apart looked almost exactly like their other twin as far as body fat and body weight. Even the spots storing the fat were the same.
This is some of the best quality science out there that the Internet gurus ignore completely. This is Dr. Friedman's , Dr. Leibel's and Dr. Rosenbaum campaign- to educate the public , other scentists as well as doctors that obesity is a BIOLOGICAL problem with the genetic componsnt being massive. The individual either has a BIOLOGY to be leaner or fatter.
I work out but I am not naive enough to falsely believe my workouts are the reason I am 6'2" 160 pounds. It is BIOLOGY. I am an ectomorph by nature. But I do not do shady things like Internet gurus who are lean and try to make MONEY scamming gullible people who read their sites.In fact, I HATE that I cannot seem to get "big guns." I will never get the arms of a guy like MIke Tyson.They are too stringy and long. Randall Cunningham will not either.
MIke Tyson, Lance Armstrong, Emmit Smith, Randall Cunningham. All these athlete have very different builds.
They are not "paragons of virtue", or better than anybody else. THey look like they do to BEGIN WITH. The workouts only midly enhance it more. Lance Armstrong would look silly tryng to bulk up like MIke Tyson. If he did even achieve it , it most likely would not last and it would not look right on him. Tyson carries lots of muscle very well. MIke Tyson is a classic endomorph with obesity running in his family. No surprise with the anti- depressants ( these drugs act on the neural circuitry that regulates weight) , family history and lack of boxing that he balloned a few eyars back.
Look at all of the fat amateur marathoners every year. No professional marathoner is fat because they LOOKED like that to begin with- lean- that is why they went into the sport. Same with sprinters. They are jacked and naturally muscular to begin with-much more so than marathoners.
Professionals in any sport are gifted physically to begin with.
The heritability and genetic component of obesity is absolutely massive. It is more than ANY other condition studied by science= with the *possible* exception of height alone. And height barely surpasses it. They *may* be equal.
Wishing your build one way or another is not going to change much. An individuals' biology is in control ultimately. If the public realized this they would not pay for all of these cheesy fat loss books filled with false promises and false hope.
True obese people have odds against them that are extremely strong- biology is powerful. An ectomorph losing weight has no idea hwo hard it will be for a person with true medical obesity and a family history. The palying field is not at all level- it is dramatically bumpy.
THis is why a metabolic advantage focus is a waste of time.It is good to investigate , but COMPARED to OTHER things that are more important, it can be a distraction.
I love the taste of low carb myself. I have nothing against it.
Gut hormones,GENES ( there are over 400 genes directly involved in body weight regualtion) gut microbiota , complex neural circuitry. We will eventually figue out how this feedback loop talks to each other.
The weight regulation system has many components but the brain is key, so far as science can tell. Obesity science has tremendous uncertainty.
It is convenient for playing an opinion ping-pong, there is almost always some research done to support any point of view. Here is one of several to support my opposition to eat grains, especially with a lot of fiber,
"Decreased Absorption of Calcium, Magnesium, Zinc and Phosphorus by Humans due to Increased Fiber and Phosphorus Consumption as Wheat Bread."
http://jn.nutrition.org/content/106/4/493.short
@Galina
'..I didn't mentioned Inuits at all(and your link didn't answer my question about your advice)..'
I am not giving you any advice, Galina. It would be inappropriate for me to do so, especially on Stephan's blog.
If you remember, you were telling me a ketogenic diet is a normal way for humans to eat. I am trying to point out it isn't. If by a 'ketogenic diet' you actually mean a diet high in animal products, that's different.
It is my belief that the wellbeing experienced by many people on an Atkins type diet is due to the relief of not having to count calories and to eat as much animal fat as they like. I know how this feels, because I LOVE butter and cheese and whole organic milk, and being able to eat as much as I like of them and not worry about getting fat.
But meat is another matter. The Inuit thrived on a meat diet, but this does not mean eating a lot of meat is a good idea today. Again, let me emphasise I am not giving you advice. I know you don't eat vast quantities of meat. I am merely telling you what I have found in the literature.
I know you don't like grains, and I am not suggesting you should eat them. I needed to tell you about my reasons for eating them, in case your circumstances change and you find yourself forced to eat them because there's nothing else. If you read the Financial Times every day like I do, you will be thinking about such things.
So Jane-
High fat and high carb concurrently, eh? Sounds fun. What did you eat yesterday?
@Jane,
It happened I didn't spent all my life in a stable environment, I witnessed the Soviet Union disintegration, completely empty store shelves, nearly complete lack of valuable money due to enormous inflation,when my son was born at 1992, I basically had no resources to live on at that time. I sold all vintage silver which happened to be in the family, moved with my mom and a new-born son into grandma apartment and rent out mine and mom's apartment to tenants, I also cooked for them for money. When stores are empty, black market is thriving, money is a help, but you need more of it. Good thing about crisis it doesn't last forever. There is no point to worry in advance about what to do when a crisis happens, a danger changes and mobilizes people, you will manage like the most. In 1995 me and my son moved to Canada where my husband got a job earlier.
As a result of my experience, I can tell, that the best way to provide you with source of food in case of food shortages would be growing potatoes on some piece of land, it could be even some clearance in the forest or a park, many did it in Russia. Grains are good only if you stored it in advance. I have some land around my house in Florida and a forest in a backyard. I would rather trap squirrels and opossums, our forest is over-populated with them. I am sure my American neighbors wouldn't compete for such resource. Squirrels are fine, when my son killed one with an air gun, I braised it, the taste was pretty good. However, I don't worry about a crisis, I survived a major one, I know I can do it again. The main thing to preserve it order to survive every challenge imaginable is your health.
@Travis
Breakfast: wholemeal bread with butter and honey + glass of whole milk
No lunch, no snacks, no drinks except a little water
Supper: wholemeal bread + butter and cheese, chunk of raw sweetheart cabbage, bowl of uncooked oatflakes with whole milk, fruit and nuts
I spend my days in a university science library, and I walk the 2 miles there and work without a break until 5, and walk back. My breakfast and my liver together provide me with enough glucose to keep me feeling - well, high, to be honest - all day.
@Galina
I think you're right about the potatoes. This really is the thing to do in a crisis.
During the past 20 years, there has been a dramatic increase in obesity in the US and rates remain high. In 2010, no state had a prevalence of obesity less than 20%. Thirty-six states had a prevalence of 25% or more;
Obesity in the US
@Travis,
It looks like there are more similarities between Jane's diet and mine than I thought before(I avoid grains and starches). I think that timing of eating and not snacking in many cases is as important as a macro-nutrient content because it addresses the same issue. I have the best lady-friend in Russia, like me and Jane she eats two times a day, first meal is a gruel made of oatmeal or buckwheat with milk , also some coffee, another meal without any limitations is in 6 - 8 hours later, with no snacking in-between, some unsweetened green tea as a drink. She controls her weight in check with her meal pattern, but she is naturally thin, before 45 she could eat whatever she wanted anytime, excessive hunger never was her problem. I think my diet serves me better because I don't get minor seasonal flues and infections, but she still does. It is a complete speculation , there are always personal variations.
@Jane,
a population in Russia developed some drill - in expectation of crisis they buy big amounts of salt, soap,matches, sugar and grains. Some regions survived for long periods just fine on own potatoes, fermented cabbage, onions, salted pork fat, wild mushrooms collected in a forest dried or preserved with vinegar and salt(great with potatoes), sunflower oil.
Remember, obesity is FULL of politics. Always remember that. There are very, very, very few valid surces of information. Dr. Jeffrey Friedman is one of the valid sources.
There is a supposed huge increase in obesity. These numbers are greatly skewed. Obesity is a public health problem, no doubt.
However, as mentioned beofe, ther is NO "epidemmic." Obesity has always been with us- since at aleast 23,000 B.C. People are MUHC more sensitized to noticing all of it now due to POLITICAL scare mongering.
Only 26,000 people die a year from obesity complications. This is nowhere near the 400,000 figure- whihc ws the result of CDC computer mistakes.
The obesity numbers are greatly exaggerated. This is due to a faulty diagnotic measure- the BMI. The BMI measures a CONTINUOUS TRAIT like body weight with a fixed threshold ( e.g. over 30 you're obese- under it you're not)
Obesity is a public health problem, but to put things BACK TO REALITY- we are only 8 pounds more today than we were back in 1990.
Another point I have noticed is that naturally thin people can eat A LOT.
What is the dfference between a thn person pigging out and an obese person pigging out? The latter i viewed with disgust by socoety while the former gets a free pass.
What is the difference between an obese person eating to satiation and "energy balance" vs a thin person doing the exact same thing?
I have witnessed this among friends who are both obese and rail thin. I have witnessed. obese people NOT eating too much- very modestly. No, don't ASSUME they are sexcretly eating. That is a commercial weight loss industry lie to save a failed hypothesis.
Science is moving us in a completely different direction that than the outdated and simplistic caloric model.
Remember ,all we can be in science is "less wrong." The uninformed Internet gurus misuse science. They use words like "prove." Their entire money empire rests on the faulty caloric model whose days are numbered.
Obesity is not a simple condition of over eaing, nor is it the passive accumulation of calories. To admit this recently gained sicentific knowledge would make the advice in fat loss books useless.
We need to find a long term treatment of obesity. This has eluded us. Gastric surgery STILL leaves patients OBESE- but less so.
The way it works is that it creates a favorable gut hormone cocktail( it also interfers with the INVOLUNTARY weight regulation system in a beneficial way) that scientists are currently tryng to replicate in a pill.
You could not get the same result by simply only eating 800 calories. That has been tried already and failed terribly.
Gastric surgery has incredible risk, and is FAR from perfect. A pill form would be a better option, of course.
As Paul pointed out much earlier, Stephan's statement about Taubes op-ed:
"It proclaimed triumphantly that "a new study suggests that carbs, not calories, lead to weight gain.""
is compeletely wrong. Taubes never said that. Stephan even puts it in quotation marks! Very unprofessional.
When I went to school, to make it clear one was quoting verbatim one had to separate and indent the quote. "in - line" quoting was almost always paraphrasing/summarizing
I don't know what the quoting rules are now, that's why I try to be clear by putting in "(paraphrased)" or "(summarized)" whenever I'm doing either.
But anyway ... Google refuses what I wanted to do here, so please imagine it;
<blockquote>If we think of Dr. Ludwig’s subjects as pre-obese, then the study tells us that the nutrient composition of the diet can trigger the predisposition to get fat, independent of the calories consumed. The fewer carbohydrates we eat, the more easily we remain lean. The more carbohydrates, the more difficult. In other words, carbohydrates are fattening, and obesity is a fat-storage defect. What matters, then, is the quantity and quality of carbohydrates we consume and their effect on insulin.
From this perspective, the trial suggests that among the bad decisions we can make <blockquote>
Here's a quote from Purdue:
"The primary function of quotation marks is to set off and represent exact language (either spoken or written) that has come from somebody else." And "Since you will most often use them when working with outside sources, successful use of quotation marks is a practical defense against accidental plagiarism and an excellent practice in academic honesty."
So clearly you should not use quotation marks when paraphrasing. Otherwise you risk seriously misrepresenting what someone else said, as Stephan did in this case. (I would think someone with a PhD who has written a lot of research papers would know how to use quotation marks.)
The rest of the quote from the Taubes op-ed that Sanjeev included is below:
"From this perspective, the trial suggests that among the bad decisions we can make to maintain our weight is exactly what the government and medical organizations like the American Heart Association have been telling us to do: eat low-fat, carbohydrate-rich diets, even if those diets include whole grains and fruits and vegetables.
A controversial conclusion? Absolutely, and Dr. Ludwig’s results are by no means ironclad. The diets should be fed for far longer than one month, something he hopes to do in a follow-up study. As in any science, these experiments should be replicated by independent investigators. We’ve been arguing about this for over a century. Let’s put it to rest with more good science. The public health implications are enormous."
thanks, looks like I need to forget what I remember from my late 70s style guide.
Hi Mary B,
You are incorrect, that exact quote was in the Sunday New York Times. I did not paraphrase. It was the highlighted summary quote, but it does not appear in the online version. Think before you start flinging accusations.
Clarification: the quote was in the print version.
I think Gary Taubes has mentioned that everybody has a personally "upper limit" for carbohydrates before they start packing on fat, and that we are all different regarding this.
I have noticed ,in myself, that if I go for a week eating lots of dates, white things, candy etc. I get a bigger belly a bit. This happens consistently. In other words, the bdoy fat around the abdomen increases. My weight does not go up that much at all, but my body looks worse.
My safe carbs are apples, greens, nectarines etc.
I do enjoy reading your blog sometimes, I have a blog I started called metabolic syndrome of course a blogger blog. I don't know about the arguments presented here, but I do know this, by decreasing my high gi carbs dramatically, taking a glucose tolerance factor, more sunshine without sunscreen, being careful to not wash my oils away to much to allow vita d to absorb,digestive enzymes and unlimited veggies fruit when I desire it, meats, I love dairy, hamburger, dark chocolate yummy! nuts when I want it, anyway since I have started to do this my a1c is falling, I am finally sleeping better (Not needing to get up and eat anymore) which was a problem for many years despite diet changes nad exercises supplements. I have more energy etc (this didn't happen overnight, not the story of I started this diet and lost 10 pounds the first month nonsense. the underlying nutrtional deficiency and metabolic dysfunction first before any weight can be dealth with, after all obesity is a symptom not a cause.
rose
Guyenet: "In Dr. Ludwig's paper and the accompanying editorial in JAMA, they made no claims about carbohydrate being more fattening than fat, and they didn't even broach the topic, because Dr. Ludwig's study is not relevant to the question. I would love to see Dr. Ludwig set the record straight on this, but unfortunately most researchers don't fight back when their results are abused in the popular media."
Ludwig is receiving funding from Taubes's NuSI group. That makes it even less likely that Ludwig would speak out against misinterpretations made by Taubes.
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