I am on blog as stating that dietary fat, in common with carbohydrate, is stored in the aftermath of a meal. If you did not store your dietary fat it would sit there in your chylomicrons until you were as hyperlipaemic as a diabetic on an ADA approved low fat diet. All fat which is not used for on going metabolism must be stored. It may take a few hours to clear chylomicrons but they do get cleared. Mostly in to adipocytes.
EDIT: There is an update on this post here.
Okay, let's look at the Grey and Kipnis (GnK) 1971 paper.
If you take a human like ET, who is maintaining a bodyweight of 142kg by eating 4,200kcal per day, you can adjust her macronutrient ratio to pretty well whatever you like and she will remain weight stable, provided you insist that she always consumes 4,200kcal/d. Insulin will plummet on a high fat diet and this will release necessary fatty acids from adipocytes. These FFAs, the Spawn of Satan, will be both released and used at an increased rate. But will she lose weight? Of course not. She will just re-pack her adipocytes with the extra fat from her fixed, 4,200kcal, low carbohydrate diet. Many people, myself included, can maintain weight stability on a low carbohydrate diet for years.
There's a nice paper about fat accumulation under low insulin conditions on my hard drive. It happens. I will post about it when I feel like it, it looks interesting.
There was one participant in the GnK study, RP, who refused to comply with the study protocol. That's a 20% non compliance rate. She under ate and lost weight. We get no information about her caloric intake at any stage. We know relatively little about her diet (ie sugar vs starch) before the study. We have no idea what sort of carbohydrate was used in the study diet. The only information we have about which phase of the diet gave the weight loss is this graph:
But we certainly have a failure of compliance in this study where an obese subject refused scheduled food and subsequently lost weight. That's worth remembering.
Now let's look at hypocaloric conditions in the same paper. DB, SM and DM were put on to 1,500kcal/d (Keysian starvation) from 2,200kcal/d, 3600kcal/d or 3,800kcal/d respectively. They, err, lost weight. They lost weight pretty nigh on linearly over 12 weeks whether their fasting insulin was 40microIU/ml or 15microIU/ml, produced by adjustment of their carbohydrate intake from 240g/d, down to zero and back to 240g/d.
NB I am perfectly willing to accept these results as they stand but just as an aside; none of the individual records shows any suggestion of a weight shift related to to glycogen depletion/repletion on these changes in carbohydrate intake. The LC phase included zero carbohydrate. The HC version of 1,500kcal provided 72% of calories as some sort of carbohydrate, ie 240g/d. Maybe even Weight Watchers depletes liver glycogen following an overnight fast... A bit odd but probably irrelevant.
Back to the results. The caloric intake was fixed and low. Fat was stored in the LC/HF group and accessed easily because insulin was low. Under high carbohydrate intake calories were stored mostly as glycogen and glucose was metered out to avoid hypoglycaemia. Any fat lost by the lower-but-not-zero rate of lipolysis under high insulin levels was simply not replaced.
Just eat 1,500kcal/d and you will lose weight. Eat more than 1,500kcal and you're a pig.
The study was designed to get exactly these results.
But, out of only five subjects, one obese person became a food refusenick. Various studies have had similar compliance problems, with obese participants refusing food. Let's look at some of them.
I knew there had been a paper by Krauss looking at lipoprotein subgroups during weight stability on assorted carbohydrate intakes. It didn't measure plasma insulin but, if we accept anything from GnK's work, I think we have to accept that under weight stability we can dial fasting insulin by adjusting carbohydrate intake. At least between 4% and about 72% of calories.
Krauss looked at diets composed of 54%, 39% or 26% of energy from carbohydrate, with a bonus group on 26% carbohydrate and (gasp) 15% of total calories as saturated fat.... These folks were instructed to maintain weight stability. This quote had the LC brigade, myself included, giggling if not rolling around in the aisles.
"Despite our effort to maintain constant weight, the 26%-carbohydrate, low-saturated-fat diet group lost more weight than did the 54%-carbohydrate group during the stable-weight period. There was also a trend for a greater reduction in percentage body fat with the lower-carbohydrate diets (P < 0.02, analysis of variance)."
The numbers are in Table 2.
My browser squishes the table, these are the numbers that matter, simplified. Remember, everyone was supposed to be weight stable:
Some of these numbers made p<0.05 or even <0.02, shrug. What is more interesting is the trend in accidental weight loss. Oh and look, the sat fat group didn't lose the most weight, just the most fat. I like that.
My take home message is that the lower the carbohydrate intake (and it is reasonable to assume the lower the fasting insulin) the harder it is to consume enough calories to maintain the obese state. It's possible, but not easy.
Then there is this study looking at the HPA stress axis under fixed calorie low carbohydrate or medium carbohydrate diet conditions. I'll just look at weight and insulin because the changes in the processing of cortisol are about as lucid as Krauss' early papers on lipoprotein changes due to dietary saturated fat. It seems reasonable to assume things improved on LC, otherwise any deterioration would have been headline news. This is a crossover study, the same people did a month on low carb and a month on medium carb, in random order. This makes the results tables somewhat unintelligible but it still comes close to replication the 1,500ckal section of GnK's paper.
Under weight stable conditions fasting insulin was 16.6microIU/ml on 57% carbohydrate. Under LC (4% carbs) conditions, on a fixed 2000kcal intake insulin dropped to 7.3microIU/ml. Weight loss was 7.2kg in 4 weeks. Eating 2000kcal of which 35% was carbs gave 4.7kg weight loss on a fasting insulin of 9.2microIU/ml. After correction for water shifts under LC there was exactly the fat loss accounted for by a caloric deficit of 66kcal/d. This was, oddly enough, exactly the caloric count of the food REFUSED from the 2000kcal provided during the LC phase........... Which they had been asked to eat. Obese people refusing part of a 2000kcal ration.
These folks where in a residential diet study. They consistently refused food they had agreed to eat during the "fixed" caloric intake phase, but only if the macronutrient ratio lowered insulin. As an aside the insulin level on LC was statistically significantly lower than on weight stability but the drop on medium carbohydrate was not. I would argue that the difference between either 7.3microIU/ml or 16.6microIU/ml and 9.2 microIU/ml is biologically significant even if p is > 0.05.
The original report details the menus and a battery of psychological test. There is a mass of information in this study from Aberdeen. As we all know, people mostly seem to get depressed and stoopid on LC diets. In this instance they just stopped being hungry!
Here is one of the best quotes, from the results section:
"The 3-d maintenance diet was designed to 1) neutralize the ketogenic state and replete liver carbohydrate stores and 2) to return hunger to baseline levels— equivalent to the maintenance period 1, before ad libitum feeding—recognizing that a carryover effect from the weight-loss phase existed. This design is particularly relevant for the subjects who were given the LC ketogenic diet first and then the MC nonketogenic diet."
"to return hunger to baseline levels......" I like that. Hunger on the ketogenic diet is not at baseline levels, it is lower. Just supplying MORE calories INCREASES hunger, so long as the calories have carbohydrate at 57%. Hungry and weight stable or less hungry while losing weight. I really like that.
Then a brief quote from this paper, also a weight loss rather than weight stability study, but the quote is too entertaining to leave out.
Fasting insulin was 11.6microIU/ml and 14.4microIU/ml at 3 and 6 months under ad libitum calories but progressively less stringent carbohydrate restriction. Under rigid calorie restricted low fat eating it was steady around 18microIU/ml.
"Based on dietary records, the reduction in daily caloric intake was similar in the two groups. For the greater weight loss in the very low carbohydrate group to be strictly a result of decreased caloric consumption, they would have had to consume approximately 300 fewer calories/d over the first 3 months relative to the low fat diet group (28). Although the inaccuracy of dietary records for obese individuals is well documented (31, 32), it seems unlikely that a systematic discrepancy of this magnitude occurred between groups of subjects who were comparably overweight."
We know that obese people always under report their caloric intake, just ask any obesity expert. Why on earth should this particular group of obese people consistently over report their caloric intake? That's not what fat people do.
You could rephrase this to speculate that the LC group either ate and "used" an extra 300kcal/d or became pathological liars who exaggerated their food intake by 300kcal/d, presumably to wind up the experimenters. Ketosis does make you stoopid and depressed, why shouldn't it make you in to a practical joker too?
Is anyone seeing a pattern of people (or rats) refusing food under reduced insulin conditions?
In the real world people eat when they are hungry, because they are hungry. They don't drink fixed caloric intakes of mysterious liquid formulations from researchers who's rat models are based on either sucrose or vegetable oil.
Can people actually gain weight on high fat diets? Of course they can. You can accumulate fat without elevated insulin. But you are much less likely to gain weight if you are not hungry.
I note that Chris Voight was not on a fixed calorie intake and was not hungry while he lost an impressive amount of his excess weight. I think his fasting insulin was low and he was performing lipolysis at an impressive rate.
Let's make this clear. Fasting insulin determines weight loss. The effect is primarily through reduced dietary caloric intake secondary to lipolysis-mediated access to adipose tissue calorie stores.
Overfeeding in excess of preferred calorie intake breaks the system. GnK simply disabled the mechanism of appetite control by fixing caloric intake. Fine to prove a point. It's this sort of research that has got us where we are today.
NB I think this decrease in hunger probably only occurs in obesity. For those of us who have adopted a LC eating pattern without the need for weight loss (and still have little excess fat) there are clearly other factors coming in to play, as there will be when a previously overweight person approaches target/ideal weight, what ever that might be.
Peter
170 comments:
I had been losing weight on my low carb, high fat diet eating on average 1400 cals. Then my normal routine was halted due to shoulder surgery (my dominant side) and the several weeks long rehab; my loss stopped cold, though I remained in ketosis the entire time. I had to cut the fat and calories to get the weight coming down again. Of course, I'm in my sixties, though moderately active, but age tells regardless.
Hmm, just opposite experience - nearly one year ago in February I had a Cheilectomy surgery on my foot (heavy girls like my shouldn't be involved in a high-impact cardio). Before the surgery I eat close to 100 gram of carbs a day (mostly because I couldn't refuse myself some fruits - I have a small but productive garden in Florida ) and had been stack of a weight-loss plateau for 2 years after initially loosing 20 lb doing low-carbs. After the surgery I went on the ketogenic diet and lost by now 9 lb. Since I didn't count calories, it is not a very good comparison with the nancam's experience, but...
I have a question for you,Peter. You mentioned that it is more common for obese people to lose weight on LC through low hunger, but normal-weight people usually maintain their weight because there are some other mechanism in place. It is so common, that on LC obese people loose 20 lb than stop and in order to move forward they have to modify something (go more LC, or introduce IF, something..) Is it possible, that after loosing 20 lb , the "other mechanism" typical for normal weight people, start to function?
It is really funny how people try to find problems where there arent any...Insulin inhibits lipolysis. Less insulin, more lipolysis. If you eat less than you expend you lose weight. If you have low insulin but are in a positive caloric balance, FFA are re-esterified. Ultimately, wether on a HFLC or a LFHC, if you are in a caloric deficit, you will run on the fat stored in your ass.
The "real" metabolic advantage of HFLC diets is the resetting of satiation pathways. Yes, Voight lost weight and spontaneously ate less calories with only potatoes. But it was probably more because of the foods he STOPPED eating than what he ate. Food's palatability also influences spontaneous caloric intake. That you can lose weight and reduce hunger during an all potato diet does not prove anything. Your body gets tired of eating the same all sh*t over and over again.
Eat fat, lose fat and store fat. That is what the body is designed for.
Seems like sustained cholecystokinin release is the major satiety advantage of a high fat diet. One can simulate this to some extent with a low fat, high fiber diet, since the fiber delays the lipid uptake. That's pretty much the only way to not suffer from ridiculous hunger levels on a low fat diet. For some reason, in rebelling against high carb/low fat, most eating a paleo-ish diet go high fat/low carb/low fiber. The best diet for satiety, in my opinion and experience is high fat/moderate carb/high fiber. I define moderate carb as that carbohydrate level which is sufficient to replete glycogen stores without exceeding saturation point, or at least not by much. It's highly variable by individual and is influenced by the presence of anaerobic exercise. CCK is elevated for a very long time, ghrelin is sufficiently depressed due to the presence of the carbohydrates. In addition to fiber slowing the uptake of lipids, which slows stomach emptying via CCK, the added bulk triggers the mechanoreceptors of the stomach sooner and for longer.
I of course don't recommend biologically inappropriate levels of fiber like what we see recommended by medicine/conventional wisdom, but adding a tray of raspberries to my breakfast increases the satiety from my bacon and eggs far beyond what would have occurred if I had eaten the calories of the fruit simply as more meat and eggs. I could be an anomaly, but both myself and my GF have repeated this experiment back and forth and it continually yields similar results. The same occurs by adding vegetables of some type to lunch/dinner. Whether this a "healthier" eating mode is another matter, but if one is principally concerned with the reduction of adiposity, I firmly believe that the addition of fiber to a high fat/correct carb diet is advantageous.
The fact is that most nutrition researchers know almost nothing about proper scientific methodology.
For a start the laws of thermodynamics are theoretical conventions and only apply to ideal closed systems. They don't apply to rats or humans living in the real world.
I live in a subtropical climate. This means I get up to 1000KJ (238KCal) per hour of energy from solar radiation (assuming an albedo of 0.8) whenever I'm outside. Just wearing a black rather than a white t-shirt will have a massive effect on my energy balance.
The energy values of foods are obtained by bomb calorimetry (burning dried food samples in pure oxygen) which bears very little relationship to actual metabolic processes. Glucose and fructose have totally different metabolic pathways but both are assigned the same energy value which is totally nonsensical. Even food components which are not metabolised, such as cellulose and lignins, are mistakenly assigned an energy value when calorimetry is used.
The caloric values of fat, protein and carbohydrate are only estimated to one significant figure which makes metabolic studies meaningless. A 2600KCal diet and a 3400KCal diet are in fact both 3x10^3KCal diets.
It is time that nutrition researchers hired some chemists, physicists and statisticians to show them how to conduct proper experiments.
Travis,
That's interesting as I actually have the exact opposite experience. As Tessan commented in Peter's last post, as soon as I start eating carbs, I keep eating until I am physically uncomfortable (and even still have an urge to eat). Otherwise (usually cream or marrow), I simply become satiated, without any discomfort.
Without lots of fat, it seems hard for me to keep from losing lean mass (I've never really seemed to add fat)--I do [Olympic] weightlifting but no "cardio."
I think there is a completely different response to carbs when they are eaten in an isolated state instead of in the context of a fatty meal. I think our goal should be to delay the uptake of fat with fiber and the uptake of carbs with fat/protein. As such, I always try to eat a few quite large meals with no snacking whatsoever.
That was a spectacularily nice way to present that info.Usually at least 50% of what you say goes over my head.Thanks for the clarity.
Just to be clear, there's nothing wrong with getting fatter on a high-fat-LC-paleo diet, right? As long as those extra calories are Good Calories, there should be no problem. If, in between healing myself with food, getting enough carbohydrates per J. Kwasniewski, eating the full spectrum of WAPF foods, and my own indulgence with high-fat foods I've gained a stone of body fat, am I any less healthy than had I not gained that fat? Excess calories or not, I'd expect my insulin levels to be low, and my cholesterol levels to be high and healthy. As long as I'm eating a high-fat/paleo diet, fatter is healthier, right?
Peter,
You just don't get it.
People eat less on low carb diets because low carb foods just aren't as palatable as high carb foods. Insulin has nothing to do with it. People "have a right" to stay lean while eating palatable foods like donuts rather than unpalatable foods like steak. Don't confuse the issue with references to basic biochemistry. (sarcasm)
Hi Petro, great post.
“After correction for water shifts under LC there was exactly the fat loss accounted for by a caloric deficit of 66kcal/d.”
This is kind of off topic, but I ran the numbers and came up with ~181.5 kcal/d. There was a 66 kcal/d difference in food intake; how did you get a 66 kcal/d difference in fat loss? (if it was due to those "water shifts under LC," how are they corrected for?)
Thanks,
Bill
Don,
I disagree that low carb foods are less palatable. I enjoy low carb far more since the high carbs trigger unpleasant, insatiable cravings. Cravings lead to mindless eating of sugar/starch food that we may or may not get that much pleasure from; hence that almost immediate regret most people will experience after eating such foods. Low carb foods taste great, but since they don't drive us to overeat, we don't. And, we don't have the bizarre over attachment to food that many people do who say the can't live without pasta or bread or sweets.
Nancan, Don was being sarcastic.
Peter, your conclusion agrees with the data. It is just as hard to keep overeating (overfeeding studies) as it is to keep undereating (semi-starvation studies). Homeostasis, controlled by hormones and stuff ike chylomicrons, literally dictates how much food we eat. For example, the more chylomicrons shuttle fat to fat cells, the less you have for every other cells, the more you will eat to compensate.
When you're growing fatter, you don't actually overeat in the classical sense (eat more than hunger warrants, gluttony), you just eat more to compensate (you are more hungry). To compensate for what? For what your hormones are telling you to eat. And when you stop growing fatter and stay at a stable, but fatter, weight, you don't overeat, you just eat what your hormones tell you to eat to maintain homeostasis. If that's more than the other guy, then maybe it's because you're fatter than the other guy, and we all know that a bigger system requires more energy than a smaller system, don't we.
It's kind of ironic that you'd say you're a calories kind of guy, but then proceed to use chylomicrons to make your point. Every other calories kind of guy just use the First Law of Thermodynamics. Just saying.
Peter said...
I think that it might be a good idea to state here that I'm a calories-in calories-out sort of a person.
You've done it now! You're going to get "Colpo'ed". ;-D
I like posts (like this) where you explain your thinking clearly.
Regarding the situations of stubborn fat on those who aren't obese (anymore), I was wondering if this could be still due to small insulin increases due to things we aren't thinking about, such as caffeine, cephalic insulin responses (maybe you work as a restaurant chef or pastry shop, etc.) or eating late at night, which ruins your circadian-controlled naturally low insulin (Taubes mentioned this too in GCBC).
In individuals whose metabolisms are already compromised due to a lifetime of the SAD, these small insulin rises over time (and we are more sensitive to them as well), and therefore can add up to stall you in losing those last few pounds.
Subborn fat? See lipohypertrophy/lipodystrophy. Do an image search on google.
Sue, thanks for pointing that out. One shouldn't blog sleepy. There is an old joke in these parts that we don't get irony in Pennsylvania, maybe not sarcasm either--at least at bedtime. Sorry Don.
To Gunther's point, I'm near my goal weight and have wondered if there is a type of fat cell that is more resistant to give up its stores to protect the body from the ravages of starvation. I did a 30 day water- only fast 8 years ago, and weight dropped a pound a day until about Day 23, then in the last week I lost only a couple pounds. I was maybe ten pounds overweight when I began. Naturally, I regained the weight at about the same pace.
A very interesting article about how lab animals become fatter when crowded even when diet and exercise levels are unchanged.
http://www.scientificamerican.com/article.cfm?id=does-this-collar-make-me-look-fat
So for those us on a VLC diet who are looking to lose a little weight but have stalled, what is the best way to lower fasting insulin levels?
@ Lucas
You wrote:
"It is really funny how people try to find problems where there arent any...Insulin inhibits lipolysis. Less insulin, more lipolysis. If you eat less than you expend you lose weight. If you have low insulin but are in a positive caloric balance, FFA are re-esterified. Ultimately, wether on a HFLC or a LFHC, if you are in a caloric deficit, you will run on the fat stored in your ass."
There is a paradox in this reasoning.
Insulin inhibits lypolisis. High carbs keeps insulin high. Thus, caloric deficit with HC won't be allowed to induce lypolisis.
So with LFHC, rather than "run on the fat stored in your ass", you'll run on the protein stored in your muscles by turning in into glucose, which is a very well known problem with conventional calories-restricted diets: lean mass loss instead of fat loss, in varying proportions depending on the composition of the diet and the invidual.
A lot of LC dieters know that they can loose chiefly fat and not much muscle thanks to LC, because low insulin means easier lypolisis (less inhibition of lypolisis), thus limiting the need to turn to muscle mass as a source of energy.
This is old news, BTW, and I'm really wondering how such a simple and well documented thing may keep on being "forgotten"...?
(follow up to my previous post.. ;-))
So coincidentally, I think that studies comparing diets, when focusing on WEIGHT loss without providing the actual FAT loss, mean abstolutely nothing: one can loose a lot of weight by dieting just through muscle mass conversion to glucose, without loosing much fat. That's what happens with many of these high-carbs, low-fat, calories-restricted diets.
"Weight loss" comparisons are a scam. That's FAT loss,and fat loss only, which should always be focused on.
That's why I particularly liked Peter's article, and how he giggles from the weight loss vs. fat loss comparison. :-) It brought a smile to my face too!
Cheers from Belgium :-)
@ Lucas
You wrote:
"It is really funny how people try to find problems where there arent any...Insulin inhibits lipolysis. Less insulin, more lipolysis. If you eat less than you expend you lose weight. If you have low insulin but are in a positive caloric balance, FFA are re-esterified. Ultimately, wether on a HFLC or a LFHC, if you are in a caloric deficit, you will run on the fat stored in your ass."
There is a paradox in this reasoning.
Insulin inhibits lypolisis. High carbs keeps insulin high. Thus, caloric deficit with HC won't be allowed to induce lypolisis.
So with LFHC, rather than "run on the fat stored in your ass", you'll run on the protein stored in your muscles by turning in into glucose, which is a very well known problem with conventional calories-restricted diets: lean mass loss instead of fat loss, in varying proportions depending on the composition of the diet and the invidual.
A lot of LC dieters know that they can loose chiefly fat and not much muscle thanks to LC, because low insulin means easier lypolisis (less inhibition of lypolisis), thus limiting the need to turn to muscle mass as a source of energy.
This is old news, BTW, and I'm really wondering how such a simple and well documented thing may keep on being "forgotten"...?
My two posts got mixed up. Second first, first second. Sorry about that :-)
Hi Peter.
I'd say that I pretty much agree with your post. Insulin and caloric deficit are not mutually exclusive, ie, low-insulin could enhance fat loss on a caloric deficit or, looked from another perspective, a caloric deficit could enhance fat loss if someone has low insulin level.
I have only one question for you. For the sake of it lets make thing black and white.
What do you believe is the most important thing to do, in order to achieve weight/fat loss
a) be in a caloric deficit (your insulin level does not matter much)
b) having a low-insulin level (it does not matter much if you're in a caloric deficit or not)
Again, in real life, I don't believe they exclude each other, but if you could fix only one to have a weight loss, which one would you fix? Calories or insulin?
The way I see it is that, as you stated, insulin inhibits lypolysis, but more lypolysis does not equal more oxydation. It still has to be matched to energy expenditure. In that case, calories would be the most important factor. That's my point of view and it could be wrong.
I'm just wondering if you agree to some degree with it, because reading your post, I get the idea that you do.
Thanks for your time.
"Is anyone seeing a pattern of people (or rats) refusing food under reduced insulin conditions? "
What about the psychological issue that success breeds success in humans? Losing a few pounds can increase motivation.
Also, while low carb/insulin reduces the desire for food--or rather carbs make people constantly crave more carbs, but I note on the blogs I visit that we are also past masters at finding ways to get them via cheese, nuts, etc.
Great post Peter, nice insights.
The two first paragraphs are priceless. Next time I find myself replying to someone who accuses you of having a "flawed" insulin based hypothesis while missing the point of calories in, calories out, I'll just link to this post.
John
This post reminds me of Lex Rooker's experiments on himself. He'd been zero carb for two or more years and decided to shift to a higher percentage of fat over protein while maintaining constant calories. He gained weight. But after a while he could not keep eating that much because he was too full (even after taking up jogging), so he dropped about 200 calories. He also noticed that his glucose spikes after eating were lower; he noticed that glucose correlated with the amount of protein he ate (remember, this was all zero carb -- he eats nothing but raw meat and suet). Assuming his insulin was also lower, this corroborates Peter's theory that insulin is correlated with hunger. He had very high ketones in his urine the entire time he was on the higher fat procotol (4 months). The ketones dropped back to his baseline as soon as he went back to the higher protein/lower fat protocol (still zero carbs). Interesting stuff.
Galina L, this is why I'm interested in Stephan Guyenet's ideas on set point. In the average obese person it is very likely that chronic hyperinsulinaemia simply stops the body weight dropping to a normal weight, ie you cannot drop to your set point. But if you have been up to 200kg and are dropping back to some sort of set point, will it be the 60kg you perhaps would have stabilised at as a normal adult on real food or something higher? ItsTheWoo, who has commented here in the past, has done this and has to count LC calories unless she injects leptin. Other than that it's down to counting carbs and calories for some... And what shape is their liver in????? Probably matters.
Bluetooth.enabled, yes, that's exactly how I see it. The big unknown is people like me at low BMI. Does LC protect me from the high all-cause mortality associated with low BMI? I hope so!
Don, oh bugger. I knew I was doing something stoopid. Must be a donut deficiency!
William, the results tables are a total mess. Look at table 1
http://jcem.endojournals.org/cgi/content/full/92/11/4480/T1
Start weight is 111.1 kg, n=17. HF-LC end weight is 101.7. But the start weight for the LC arm is some of the folks from baseline plus the folks randomised to MF-MC who had already lost some weight. Arghhhh! And ditto for the start weights of the MF-MC phase/arm.
If you go to the first paper from the same study and look at
http://www.ajcn.org/content/87/1/44/F5.expansion.html
the actual weight loss curves both start at about 109kg.
So you can't check the math...... I did mention the results table was a bit naff! The insulin levels will be fine as these probably stabilise in just a few days after after diet change then don't budge much.
Lucas, yes, no transfats for a start....
Travis, it's hard to eat meals of real food without some fibre creeping in. I can live with that.
john, I've overdosed on fat occasionally. An hour of queasiness does not encourage a repeat episode.
Martin, I would agree. In particular post prandial insulin might well partition food away from metabolism, never mind fasting insulin slowing its release. There's a limit to how much you can put in a post....
Gunther, there's a ton we don't know. If you trawl the GnK rat paper they used aminophylline to over ride fasting induced pancreatic glucokinase downregulation. Aminophyline is a drug related to caffeine and theophyline in coffee and tea. Atkins said go decaff......
nancan, well you gave me a giggle. As did Don
blogblog, methinks stress=cortisol=insulin resistance=hyperinsulinaemia?????
efalke, count protein (you can go as low as 40g/d but I usually run at about 60g/d) as well carbs, consider exercise. I know nothing about the minutiae of exercise but the impression I have is that walking is good, running is bad and moving heavy objects is good...... Oh, I said consider exercise, should have said use some! Not to burn calories but to increase insulin sensitivity. Ultimately check calories.
Frank, I'll comment later in reply to this.
John, I'm interested in understanding what is going on. When the data convince me that low fat is the way to go I'll be right there. That would be science. I'm particularly interested in unsuccessful LC eating but hard data is impossible to get. Clearly it happens.
Gordon, as you say, interesting.
Peter
Sorry for all the probable typos, one handed, one fingered......
wiz.public, the Glasgow paper got weight loss with elevated fasting insulin, accompanied by a deterioration in every other measured parameter. I'm guessing lots of muscle loss and a little pot belly growth!
http://high-fat-nutrition.blogspot.com/2010/06/fsa-in-glasgow.html
Peter
Ah Frank, now there is a question.
Without caloric deficit (and I want uncoupling proteins, sleeping metabolic rate, spontaneous movements, etc, etc, etc, everything, accounted for) there will be no weight loss.
But, in real life, if I could only alter just one, it would be insulin.
I would expect no weight loss but I would expect improved health.
What else matters?
Peter
John and Travis,
I'm "sensitive to carbs" I guess. I can easily eat a truck load of pasta floating around in butter. If I eat a rib eye steak instead of spaghetti, I eat like a normal person. With the carbs I can't eat normally, without them I can. But I need some good quality protein with every meal.
I have a lot of experimenting to do, and the weight loss is not my main objective, yet. A lot of things that I have read here on Peter's blog and in his replies to comments make sense to me in my situation. I need to get as far away from all grains as I possibly can. Illustrating this point is for example that sugar (fruit, muscovado in tea, occasional ice cream) does not trigger anything. But oh does wheat! And rye. Barley, I guess. Over eating, candida, joint pain, tiredness, cognitive fog... Thank you, Peter, for explaining it so simply that even I understand.
Peter,
Thanks for the link to your article about the Glasgow paper, I hadn't read it yet. Now I have.
I'm with you, I'm also betting on the belly :-)
"But, in real life, if I could only alter just one, it would be insulin.
I would expect no weight loss but I would expect improved health.
What else matters?"
Well said.
When I went for low carb / high fat (mostly saturated) about a year ago, initially it was for weight loss, which worked wonderfully (I lost 38 pounds). But now I'm sticking with it for the dramatic improvement in my health! :agree:
Hi Peter
We're definitvely on the same page then.
Thanks for your answer.
Peter, do you know about cloprostenol sodium salt injection?
Thanks, I see Peter. So on a paleo diet, fat loss and a low BMI would not be beneficial, at least no more beneficial that fat gain.
Then it seems that so many are mislead into believing that weight loss is the desired goal of high-fat/paleo eating. People are brainwashed into believing a low bodyfat/BMI is synonymous with good health, and mainstream paleo helps convey this message. Why do the paleo blogs and books not proudly display men "after" photos at 23% body fat instead of 10%, who knows.
So if fatter is healthier when paleo, then weight loss or a low BMI isn't really worth that much.
If fatter is the product of years of chronic hyperinsulinemia, how is it any healthier than years of chronic hyperinsulinemia?
I had an easier ride than Woodoo. During my life my body had different set-points. The last one was established after my last failed pregnancy at 40 years old (a have one child, just in case if somebody worries about me). It was 172 lb, I am 5'6", pear-shaped. According my med. records, fasting blood sugar then was 92 - 93 mg/dl. Between 45 and 46 I gained 26 lb, while exercising more then before and eating according Dr. Weill's advice(limited sat.fats and red meat, whole grains,fruits, veggies + soy products). My fasting BS became 99 mg/dl, frequent infections, worsening of migraines, allergies, leg edema, terrible mood swings, hungry all the time even more than before. My family doctor prescribed me a diuretic and said I was just getting older. In a way, he was right, just didn't know that LC could be some help.I never had an abnormal lipid profile or BP higher that 115/65. Probably, a lot of exercise was helping in that.
After starting LC that edema was gone in a day, I started to loose weight slowly and stopped after magic number of 20 lb. My body quickly forgot its setting point of 172 lb and decided to be 178. Still better than 198. All my health problems got better on LC, but I need the ketogenic level of a carb restriction in order to control my migraines and to be completely flue-free. Allergies are also better. You warnings about staying in ketosis almost all the time left me worried, but my choise is between a better health now and some danger later in life. Now my weight is 169 lb and I continue to loose very, very slowly and sort of curious to find out when it stops. For the record - I am 50 years old now. I know , the big hormonal change is around the corner. Suppose to be some changes.
Frank,
Good question to Peter.
Peter...
Uncoupling proteins, BMR, brown fat, spontaneous exercise -- Do you believe these are hormone induced and regulated (outside of insulin)?
One of the first studies that tripped Taubes into the calories in ≠ calories out theory was an experiment on ovariectomized rats who immediately gained fat. (birth control does this to females stupid enough to take them, incl ph*rmac&%$sts) *ha*
-G
Wizzu, yes health benefits kick in very rapidly on many fronts, often well before any significant weight loss. You do have to be a little careful about attributing the changes to changes in insulin though. This could easily be a simple biomarker for dropping trans fats, excess fructose and a host of other things which happen accidentally when you low carb... Or it could be simple insulin. Or hyperglycaemia. Or.
Frank, OK
Martin Levac (and bt.e). Horse and cart. Obesity on the SAD is a marker of chronic hyperinsulinaemia. Lowest all cause mortality on the SAD occurs at a BMI around 27, Dr Briffa collects these observational studies, there are about four of them. They do not include populations biased by Schwarzeneggers or their ilk.
Weight gain from LC is possible with low (normal) insulin levels. What is the ideal BMI on LC? Who knows, but I see no reason that eating a real food diet to achieve a BMI of 27 should be any worse than using the SAD. A BMI of 20 is catastrophic on the SAD. Is it on LC? Again, who knows...
cloprostenol, I had no idea it is "a potent inhibitor of rat adipose precursor differentiation". It sounds like it would keep rats slim and bring forward the onset of type 2 diabetes, certainly in rats fed a diabetogenic diet.
Galina L, interesting. Even on full ketogenic high sat fat, gluten free eating my wife gets migraines still. Keeps me reminded that I certainly do not have all of the answers.
G, I think insulin is a massive over ride on a whole stack of control systems, both hormonal and direct autonomic innervation. The most superb, intricate watch can be broken with a cheap hammer...
Peter
Maybe those studies look only at SAD-eating populations. And maybe the method by which they get below 27 BMI is what makes them sicker, not the BMI itself. In populations where the SAD is the norm, caloric restriction would also be the norm to get below 27 BMI. Caloric restriction causes all sorts of bad things like emaciation and neurosis.
I would prefer to look at specific cause of death rather than all cause. This would tell us, for example, if getting below 27 BMI kills us through suicide or malnutrition or deficiency, while going above that kills us with diabetes, heart disease and cancer.
I'd also like to see that data compared to populations that eat a traditional diet.
Thanks for the reply Peter! :-)
(BTW I guess that you guessed that wiz.public and Wizzu are the same person.. ;-))
You wrote:
"This could easily be a simple biomarker for dropping trans fats, excess fructose and a host of other things which happen accidentally when you low carb... "
I didn't mention that I was already eating in a health-conscious manner before going LC. I avoided all high GI/GL foods, all sugars, wheat flour, trans fats of course, pasteurized cream and butter, milk, industrial products etc...
For some, I guess it would be enough to have great improvements in health, specially those on the SAD.
But insulin resistance and easy weight gain runs in my family. Big time. You don't wanna know.
Only when I went VLC (by supressing high carbs vegetables, fruits and legumes) did I start to loose weight and have better health... and I got even better and lost even more weight, when I replaced butter by ghee, and cut on cheese and cream.
So I eventually assumed that the insulin explanation was the right one (since cream, cheese and even butter still have some insulinogenic properties). My fasting insulin dramatically dropped, BTW, as did my triglycerides.
But I'm still open to different explanations, of course. Nothing is ever so simple. Personally I like to think that drinking green tea and eating lots of coconut oil also helped with the fat loss. But maybe that's just silly prejudice from too much Internet read. ;-)
Keep up the good work here. I love your blog. It's great food for thought.
We do have some answers i.e.
Getting fat (3) is good (1)
in your own words,
Being fat is good for you.
Yet if you read most paleo blogs the topics of discussion are commonly on how to lose weight, or so-called weight loss success stories. Why aren't there more articles on how to get fatter and healthier on a high-fat diet?
"Obesity" on a high-fat/LC/paleo diet would not be chronic insulinemia from SAD diet, so where's the issue in a BMI >= 27.
Anyway thanks for the enlightening article and responses.
Peter, I am especially bothered by all the people who refer to 1500 cal/day intake as starvation. It simply is not for a woman. Indeed for many of us that is not much lower than maintenance. Mark Sisson has a sample menu over on his website that amounts to around 2500 cal/day and he says that he doesn't eat everything on that sample every day. That's a lot less than some people think they should be able to eat without gaining weight.
Minnesota starvation experiment was half the calories and almost no protein or fat. That's quite a bit different than just about any responsible CRD.
Also if one pokes around low carb discussion boards like Jimmy's they will see that most of the women who report intake are consuming fewer than this amount.
I realize you're being somewhat sarcastic there, but eating more than 1500 isn't being a pig, but 3000 certainly is.
Peter, do I understand you correctly here. Eat today to lower fasting insulin tomorrow so you eat less the next day?
Is your position that insulin induces hunger?
Let's make this clear. Fasting insulin determines weight loss.
I don't see the data supporting any such claim.
Low carb diets tend to lead to spontaneous reductions in intake because of the satiating effect of protein. There are so many studies on this I don't know why anyone (not you specifically) questions this. I'm convinced the reason CRD's fail for most women is that 15% protein in a 1200-1500 cal diet is just insufficient to satisfy hunger.
Up the protein, and women lose weight without even trying:
http://carbsanity.blogspot.com/2010/04/high-protein-diet-induces-sustained.html
bluetooth.enabled wrote:
""Obesity" on a high-fat/LC/paleo diet would not be chronic insulinemia from SAD diet, so where's the issue in a BMI >= 27."
Quite right. But it won't necessarily be a good thing either. Biology is full of mysteries.
The focus should rather IMO be on the amount of *abdominal* fat, and the triglycerides levels. If a high BMI is not accompanied with these two evils, I'm willing to bet that this high BMI is, indeed, benign and innocent.
But it's still to be demonstrated, that it's actually possible to obtain such figures with LC/HF "overeating".
We are in left with conjectures, I guess.
CarbSane wrote:
"Low carb diets tend to lead to spontaneous reductions in intake because of the satiating effect of protein."
Oh my. Simplistic explanation IMO. Even sounds like a blanket statement.
What about the satiating effect of fat?
What about the fact that people on the OD don't seem to eat more protein than those on the SAD?
Galina: it could be that a food you're comsuming may be triggering your headaches. You didn't mention what carbs you are eating. Common culprits are grains, dairy, eggs, nuts, high sulphur foods (garlic,onion), sulphites (from grapes and wine) and cocoa (my trigger). Try an elimination diet by excluding the foods you eat one at a time for a week or two and see if the headaches disappear. Best of luck.
If protein was the thing that caused spontaneous reduction in food intake, then why did Stefansson report never being satisfied on a lean meat diet? It's not the protein. It's the fat.
Insulin causes satiety in the brain. So how does lowering insulin by lowering carbs suddenly cause greater satiety and thus spontaneous reduction in food intake? It's not the insulin. It's the insulin resistance. Just like a diabetic type 1 is extremely insulin sensitive, and a diabetic type 2 is extremely insulin resistant, the level of insulin determines insulin resistance, yet insulin resistance can affect insulin level. The point is that as insulin drops, cells grow more insulin sensitive, thus the effects of insulin are that much more potent. So, if insulin is made more potent, it's made more potent as an anorectic in the brain.
Here's one study that shows that it's the fat, not the protein, that causes greater satiety, and thus spontaneous reduction in food intake:
http://forum.lowcarber.org/showthread.php?t=402590
Something to think about. If the low carb group did in fact eat less than the high carb groups, and ate the same % of protein, then they ate less absolute protein. If protein was the satiety determinant, then they should have been more hungry, not less.
Special thanks to Martin Levac for fighting misinformation with far better arguments than I came up with. :-)
@Wizzu: If memory serves, it's in part III of this BBC documentary where they test this:
http://carbsanity.blogspot.com/2011/01/must-see-tv-for-those-suffering-from.html
Also, I don't have the link at the moment, but if you Google Holt satiety you should find the study. Fats don't seem to fair well on a calorie-for-calorie basis.
@wizzu and Martin: http://carbsanity.blogspot.com/2010/04/high-protein-diet-induces-sustained.html
I'm not saying it's solely protein, but for most that's exactly what it is. Not satisfied on lean meats w/o carbs - is anyone surprised?
Insulin is not an evil hormone, it is insulin RESISTANCE that leads to all the problems. Low fasting insulin correlates with sensitivity to insulin and body weight.
If someone does not lose weight or get to a relatively normal weight on low carb, their fasting insulin will probably remain high.
In Shai, the diabetics that had lower fasting insulin at 2 years with comparable weight loss to LC were the Mediterranean (highest reported carb consuming) group.
Instead of people changing their diet to suit their poor insulin sensitivity, they should be increasing their insulin sensitivity.
See http://nigeepoo.blogspot.com/2011/02/insulin-resistance-solutions-to.html
and
http://nigeepoo.blogspot.com/2010/12/eat-less-move-more-solutions-to.html
@Carbsane
You said "not satisfied on lean meat without carbs". You are inducing that the lack of satiety from a lean meat only diet is due to the lack of carbs. Stefansson reported that eating about 250g of fat per day would take care of that lean meat problem. Care to speculate on the effect of an equivalent amount of calories from carbs?
@Nigel
Exactly. But what if the cause of insulin resistance is what you eat? I think that's the case for most of us.
wiz.public:
This is the third time I try to post my response. Two times before it vanished. LBM loss is related to protein intake, not HFLC per se. You can have minimal LBM loss during calorie restriction with a relatively large proportion of carbohydrates in your diet as long as your protein intake is a little higher. If you include resistance exercise you are set up. You can find studies like this on PubMed:
http://jcem.endojournals.org/cgi/content/abstract/89/6/2717
"The LF group better preserved lean body mass when compared with the LC group; however, only the LC group had a significant decrease in circulating insulin concentrations."
There is more than insulin for weight/metabolic control. Does it play an important role? Obviously. But it is not the evil hormone everyone says. Did you know that insulin is anti-inflammatory? The problem is not insulin per se, but the trigger for hyperinsulinemia, ie. hyperglycemia. You can find a more elaborate explanation somewhere in the text here:
http://www.ketotic.org/2011/03/ketomyths-ii.html
Can somebody tell me who ever said insulin was evil? No? Then could you all stop saying that?
When you say insulin is not evil, are you saying we shouldn't blame insulin? If you say we shouldn't blame insulin, then you probably want to blame calories? If evil is a function of blame, then you're saying calories are evil?
So obesity is just one big fight between the forces of good and evil?
Are you all fucking retarded? Stop saying insulin is not evil. You just look stupid.
@Martin:
Chill out.
"When you say insulin is not evil, are you saying we shouldn't blame insulin? If you say we shouldn't blame insulin, then you probably want to blame calories? If evil is a function of blame, then you're saying calories are evil?"
Yes, we should not blame insulin. We should blame hyperglycemia and pathological IR.
@Wizzu
Why a simplistic explanation could not be good? Why does it have to be complicated? The satiating effect of protein are not to be demonstrated any further. Don't you believe that carbs > insulin = obesity is extremly simplistic too?
@Lucas
Right on for everything that you've wrote.
@Wiz
You can easily find many weight loss studies on pubmed, in the obese IR individual, whereas lost-weight with a high carbs diet, lowish protein diet, is usually 75% fat, 25% protein. The idea that an IR person would lose only muscle mass on such as diet is, i'm sorry, but complete nonsens and i'm not aware of any study which found this to be true. As Lucas said, you just need to up you protein around 25-30%, do resistance training, and in the newbies, it's actually possible to gain muscle mass while losing fat even on a higher-carb diet.
@Martin Levac
Well, it's clear that insulin has gotten a pretty bad reputation lately. It's making us fat. It's bad, bad, bad. So we're just portraying this by calling it evil.
@all
I'm personally trying to reconcile different point of view, and even if I might be consider dogmatic in that I believe that calories are important, i'm far from denying the role of insulin and other hormone in bodyweight regulation. I simply believe it does not all come down to this. And I don't believe LC is optimal for everyone. Some studies have found it lower thyroid function, and that in training individual, it worsen the cortisol : testosterone ratio. Some studies find it negatively affect mood. Why not just consume carbs but at a place where there cause the less trouble, ie, post workout, and be lower carbs on non-training days. That's the best of both world, if you ask me. And it seems by now that about everyone agree that it takes a caloric deficit to achieve weight loss, upping protein and doing resistance training would do a job at maintaining muscle mass, and lowering carbs could enhance lipolysis. I'm hoping this is making my perspective a little bit clear, and i'm always open to consider that i'm wrong. I just need strong argument and less hostility :) I'm guilty of doing it, too, sometime...
@ Frank
I thought simplistic meant overly simple, not just "simple"? Maybe I'm wrong since english is not my mother language.
Of course something can be simple and true. But that's totally beside my point: CarbSane was using the protein argument in a very specific way, which is what I called "simplistic", i.e. to explain the process by protein intake and protein intake alone:
CarbSabe wrote:
"
Low carb diets tend to lead to spontaneous reductions in intake because of the satiating effect of protein."
I maintain that is an overly simple explanation as to why some loose weight on LC, which was CarbSane's take on the question in (her?) post.
It's not even a one-fits-all explanation for the loss of hunger from LC.
For many individuals, the cravings from eating high GI/GL carbs is a totally sound explanation.
Please consider that picking words (here simplistic) and taking them out of the context of the discussion is not a good idea if the goal is to have a constructive one.. :-)
"The idea that an IR person would lose only muscle mass on such as diet is, i'm sorry, but complete nonsens and i'm not aware of any study which found this to be true. "
?? It's the second time you make me say what I didn't... please let me quote myself:
wiz.public wrote:
"lean mass loss instead of fat loss, in varying proportions depending on the composition of the diet and the invidual."
Please consider taking the time to read with more attention before judging my comments... ;-)
@Peter, It happened that during my Electroencephalogram test in Moscow I had a migraine and it was found out that during the migraine attack I had an abnormal electrical activity in my brain typical for epilepsy. Sort of an epilepsy without any seizures . I also feel weird during migraines - spaced out, very clumsy. So, the neurologist prescribed for me a very low dose of anty-seizure medicine, together with magnesium supplements and periodic courses of Cerebralizine injections. After taking the anty-seizure medication for several months, I came across the information about using ketogenic diets for epilepsy and decided to give it a try. It worked for me to the same degree as the medicine. It doesn't eliminate migraines completely. I still have it, much less frequently (1 -0 a month instead of 3 - 4), less debilitating (I can do something instead of laying in bed 3-4 days and vomiting to the point of being dehydrated),it lasts now 1-2 days instead of 3 - 4 days. It is correlated mostly with a certain phase of my hormonal sickle(I am a female). Before I could get an attack as a result of emotional distress or if I couldn't eat when I was hungry. Hunger it a non-issue now, and being upset doesn't cause migraines any more. But I have to be consistently in ketosis especially during and around the time of my period. Somehow that small amount makes a difference.If your wife knows when her migraine likely occurs, she may also try to cut on some starcy food and see how it affects her.
When I was a teen and started to have migraines, my neurologist in Moscow used to prescribe to me 10 - 15 magnesium injections every other day 2 times a year . I remember that it worked. Probably , it is not looking smart to advise anything to a doctor, but you may consider it for your wife.
@ Blogger rpineau_..
Thank you for your advice. I eat no grains. Who knows, may be, by eating low-carbs, I eliminated some trigger. My neurologist from Florida told me to avoid caffeine completely. It sort of helped a little bit, but on LC I could reintroduce tea and coffee back
@CarbSane, your comments about protein reflect your inability to read the methods section of the Aberdeen study. Go read it.
Your concept of insulin resistance shows your complete lack of understanding of either LC eating or not eating at all. These are intensely insulin resistant states, utterly physiological and are associated with reduced appetite, especially in the obese. Insulin resistance is only a problem when some idiot comes along and tells you to eat carbohydrate while in that insulin resistant state.
Insulin is a satiety hormone, in the correct model. I would have thought you would have known this. You also need to realise its effect in an intact animal is quite different, especially as blood glucose drops. Reducing insulin does not suppress appetite, accessing stored adipose calories does.
I have explained in great detail why your interpretation of Axen and Axen's work is completely incorrect.
Your paper by Grey and Kipnis tells us nothing except how to get the result you want.
I made a great mistake when I first came across you, having been forwarded the 2010 Axen paper. I thought you simply needed to have the physiology and pathophysiology explained and you would adjust your point of view.
I was completely incorrect in this, but don't worry, I think my current opinion of you nowadays is probably less mistaken.
Please desist from putting up worthless papers in which you have failed to comprehend the flaws. I have only limited enthusiasm for posting about such inanity.
Peter
Hi wizzu,
Quite right. But it won't necessarily be a good thing either. Biology is full of mysteries.
Well why wouldn't it be, Getting fat (3) is good (1), unless we're disputing this.
I agree, getting fat and obese on the SAD is not necessarily good.
The focus should rather IMO be on the amount of *abdominal* fat, and the triglycerides levels. If a high BMI is not accompanied with these two evils, I'm willing to bet that this high BMI is, indeed, benign and innocent.
For a high BMI on a low-insulin, high-fat paleo diet, is there any reason for us to suspect that a high BMI would be accompanied by these?
But it's still to be demonstrated, that it's actually possible to obtain such figures with LC/HF "overeating".
As we have read on this blog, excess dietary fat can be stored, rats and humans can be overfed, so why not.
Even if we can say an obese BMI >= 27 might not necessarily be the healthiest, the images of what's considered success plastered on paleo blogs trends more toward the < 15% BF range than 15% - 25%. Whatever sells, I guess.
Martin Levac said...
@Nigel
Exactly. But what if the cause of insulin resistance is what you eat? I think that's the case for most of us.
I think that it's a combination of diet and lifestyle that fills cells to overflowing with glycogen.
Populations that eat the right amount of unrefined starchy carbs (Kitavans with their tubers, Asians with their rice etc) and are active enough to burn them, don't over-fill their cells with glycogen.
Populations that eat too much refined grains (bread, pasta, cereals etc) & fries/chips, drink too much sugary crap and sit on their asses/arses all day, do over-fill their cells with glycogen.
@gunther gatherer RE stubborn fat: you may want to read this article:
http://www.leangains.com/2010/06/intermittent-fasting-and-stubborn-body.html
Hi Peter,
"These are intensely insulin resistant states, utterly physiological and are associated with reduced appetite, especially in the obese. Insulin resistance is only a problem when some idiot comes along and tells you to eat carbohydrate while in that insulin resistant state."
I think this physiological fact is causing most of the confusion. Most folks, especially low carbers, are convinced by the idea that insulin resistance is always a bad thing. If low carbers/paleo's experience difficulties, they are often told 'there's probably still some insulin resistance going on'. I never miss Robb Wolf's podcast - I'm not so much into heroes anymore, but I respect the guy tremendously - and I've heard him saying this several times. On the other hand he is aware of physiological IR, for he advises carb exposure pre OGTT in order to avoid being diagnosed as a diabetic.
Many scientists see an insulin sensitive state as optimal, because it is associated with absence of most things we don't want. They use insulin sensitvity as a health parameter. The obvious question - sorry for asking it again - is: is the insulin resistance seen in low carbers really totally benign? Are you sure there's enough insulin signalling left to sustain optimal health?
In Lindeberg's small paleo trials with CHD-patients and diabetics, the paleo's have way better insulin sensitivity than the 'mediterraneans', despite a lower carb intake. So these folks do paleo (pretty low carb), but maintain or improve glucose tolerance.
What do you mean, confusing ;-).
The idea that a calorie is a calorie is an outdated myth.
The assigned average energy values of fats, proteins and carbohydrates is nothing but a crude approximation based on calorimetry with no real connection to what actually happens in the body.
Two so-called "isocaloric" diets may in fact provide totally different amounts of energy when metabolised.
American Journal of Clinical Nutrition, Vol 42, 769-777, Copyright © 1985 by The American Society for Clinical Nutrition, Inc
Whole body oxidation of dietary fatty acids: implications for energy utilization
PJ Jones, PB Pencharz and MT Clandinin
Whole body oxidation of dietary stearic, oleic, and linoleic acid was measured in males consuming a test diet of normal foods at a level commensurate with energy requirements for 16 days. Labeled stearic, oleic or linoleic acid was consumed with the breakfast meal on either day 8, 11, or 14. Breath samples were analyzed for total CO2 content and 13CO2 abundance. Breath enrichment of 13CO2 after ingestion of labeled substrate was calculated over background 13C abundance with diet only and expressed as fraction of substrate dose absorbed. Fecal excretion of labeled and diet fatty acids was determined for pooled stool collections. Stearic, oleic, and linoleic acids were separated from fecal fat extracts and combusted to determine 13CO2 enrichment over background. Both dietary and labeled stearic acid were less well absorbed than either oleic or linoleic acids. At hours 7-9 after ingestion of the labeled breakfast, significant differences in percent of absorbed dose excreted in breath were observed between all three fatty acids. Significant differences were observed in apparent amounts of labeled oleate, linoleate, and stearate oxidized after 3 to 9 h. This difference in fatty acid oxidation challenges the assumption that dietary fat is oxidized at a rate independent of its long chain fatty acid composition.
Digestion, absorption and energy value of carbohydrates
http://www.fao.org/docrep/w8079e/w8079e0k.htm
blogblog said...
The idea that a calorie is a calorie is an outdated myth.
The assigned average energy values of fats, proteins and carbohydrates is nothing but a crude approximation based on calorimetry with no real connection to what actually happens in the body.
Two so-called "isocaloric" diets may in fact provide totally different amounts of energy when metabolised.
This proves what, exactly?
That counting calories is a waste of time? Yes. I've been saying this for years.
That you can basically exercise as much gluttony as you want as long as you're eating fat and protein*? No. Only a Taubes nut-swinger believes in fairy tales.
*Ref: 8 minutes 8 seconds into http://www.youtube.com/watch?v=sKIhYQZuLZ8
For folks wondering about the importance of fat loss per se, Stephan posted on fat distribution some time ago. In summary, peripheral fat is good, but encasing your organs in fat is bad. Nephropal has posted on the hormonal activity of ectopic fat in the past, too, if you're interested.
http://wholehealthsource.blogspot.com/2008/12/peripheral-vs-ectopic-fat.html
@ Nigel
Two so-called "isocaloric" diets may in fact provide totally different amounts of energy when metabolised.
This proves what, exactly?
a) There is a metabolic advantage to certain types of diets.
b) Appetite suppression is not the only mechanism that causes weight loss in LC diets.
c) It helps explain the "Kitivan Paradox" where people eat unrefined "high carb" traditional diets with few health problems. It shows:
i) they are not getting anywhere near as many calories from carbohydrate as claimed. ii) they are also being subjected to a much lower glucose load than estimated and iii) they are producing large amounts of volatile fatty acids via colonic fermentation.
That you can basically exercise as much gluttony as you want as long as you're eating fat and protein*? No. Only a Taubes nut-swinger believes in fairy tales.
Taubes is correct.
You can eat as much fat and fat and protein as you like and not get fat.
You can't get very fat on a strict VLC diet because there is no mechanism to store excess fat. Fat can only be stored in adipocytes which requires elevated insulin. This insulin surge doesn't happen on a VLC diet.
Habitual VLC dieters are also highly insulin resistant making fat storage far more difficult.
Gluconeogenisis occurs strictly on demand so there is never enough glucose to stimulate excess insulin production.
What happens to this excess energy?
Most of it is wasted as excess heat (up to 4000Cal/day. This is equivalent to just over 3kg/week of fat loss.
An adult male has about 2m2 of surface area. If the skin surface temperature is 36C radiant heat loss is 192W when the ambient temperature is 20C. 192W is equivalent to 3960Cal/day.
http://hyperphysics.phy-astr.gsu.edu/hbase/thermo/bodrad.html
It is observed that grossly obese people are most common where the climate is hot (eg Pacific Islands, West Africa and Mexico) or central heating is present.
The Lewis and Clark expedition members ate virtually nothing but fresh meat - up to 4kg per day for months - without getting fat.
Combine heat loss with increased activity and increased musculature and it is easy to understand why you can eat huge amounts of fat and protein only and not get fat.
Again in reference to the stubborn fat loss issue for the non-obese, I was thinking that any high-carb binging that occasionally occurs while doing VLC could be causing much more fat gain than under "normal" conditions due to the physiological insulin resistance the VLC state causes. Wouldn't a donut for us cause far worse consequences than in someone on the SAD? This may be where the weight loss stall occurs. Just a thought.
It's funny that Kwasniewski would rather have one binge on high carb than high protein. But Taubes would probably want you to binge on protein. Taubes states that anything that makes you fat will cause diseases of civilization, but Kwasniewski is devoted to lowering insulin as much as possible for the same purpose.
So who do you side with here?
@Melchoir
Insulin resistance is not a disease. It is a parameter. It may be appropriate or inappropriate, depending on the dietary context and the ORGAN we are referring to.
Being IR in the context of high carb intake is bad, in the context of fasting it is absolutely necessary.
The disease part. IMO, is determined most by the relative IR of the nexus organ of these metabolic disturbances - the liver. If liver IR at a given glucose load is too high as a result of insults from the neolithic agents of disease, etc, inappropirate hyperinsulinemia may result, driving fat storage and in turn causing adaptive knock-on changes in IR in other organs in order to adapt to the higher insulin levels - muscle and brain especially.- this state is what is indicated by high fasting insulin - hence the predictive value of this parameter.
Matt Stone - with his theory of "healing" diabetes by increasing carb consumption - is confused by this as well. Increasing your whole body Insulin sensitivity with carb overfeeding while you steadily gain fat might be a sign of a flaw in the theory.
Saying "Insulin resistance" means as little as saying "weight gain" - neither has any meaning without context. Either can be appropriate or inappropriate.
blogblog,
"You can eat as much fat and fat and protein as you like and not get fat.
You can't get very fat on a strict VLC diet because there is no mechanism to store excess fat. Fat can only be stored in adipocytes which requires elevated insulin."
Not true. For one, the body does have mechanisms to move fats into adipocytes sans insulin. I forget the enzyme, but it exists.
For another, VLC tends to help keep insulin low, but it is not a guarantee. Imagine the scenario where the liver is producing glucose through gluconeogenesis, and the pancreas is producing insulin trying to manage the resulting blood sugar. What if the liver ignores the insulin signal and continues to pump out glucose? This is in the absence of dietary carbohydrate.
Peter has previously posted well on the topic that the circulatory system is not a buffer for calories. The liver, adipocytes, and muscles all buffer calories. Releasing those calories to be used where they are needed is a somewhat complicated process. This concept that this or that particular diet will always do this or that to some circulating system really trivializes the amazing orchestra of systems that nature has produced. And it overlooks the variety of ways that this complicated system might go wrong when a part of it is damaged.
(All that said, I GENERALLY agree that it's HARDER to gain weight on VLC. Insulin is powerful. My primary reaction is to your black & white statement on the topic.)
Nigel, what's pathological IR? What's the cause? It doesn't just get here on its own, something causes it. Could it be that there's a substances, non-caloric, that causes IR? Does it matter if it was caloric? Why should it, it's not about the calories. What if it was some protein in grains or something?
Why do we feed grains to cows anyway, to make them leaner? Nah, to make them fatter. Wagyu beef? Soy fed. Angus beef? Corn fed.
The Kitavans don't eat lots of carbs. I've never heard anybody give a convincing explanation why Kitavans should be immune to over 300g of carbs per day their entire lives. Can you give us one? The Asians don't eat lots of rice. Stop portraying those populations as if they did. It's like the Kitavans are the poster child for the exception to the carb hypothesis. I'm telling you they're the poster child for those who just don't think.
How can the Kitavan be immune to over 300g of carbs per day their entire lives? They are not active like the sugar workers. They are no more active than any other traditional population. As for Asians eating lots of rice, you're all confused as to which population eats lots of rice, and which suffers from that consumption. Stop mismatching data.
300g of carbs. That's 1/3 lbs of glucose/fructose dammit.
Actually Nigel, you can believe that eating as much meat as you want won't make you fatter. Why am I so sure? Because just like semi-starvation, you can't keep overeating it no matter how tasty it is for you.
Because to grow fatter on nothing but meat, you'd have to overeat, and not just eat more to compensate. When you eat more to compensate, you satisfy a physiological need. When you overeat, you surpass a physiological need. Both of these are controlled by hormones. As we know, hormones is what drives obesity, not calories.
Remember the overfeeding studies done on prisoners? That's not a fairy tale. Where do you get your fairy tales anyway?
Nigel wrote:
"That you can basically exercise as much gluttony as you want as long as you're eating fat and protein*? No. Only a Taubes nut-swinger believes in fairy tales."
You're blowing the Taubes quote out of all proportions, apparently just for the sake of having an apparently rational argument to diminish Taubes' (hard) work...
Do you have anything remotely consistent to criticize Taubes, or are you just in it for pleasure and, maybe, a personal agenda?
Besides, I personally know several individuals who can virtually eat as much as they like, up to twice what I eat, without EVER gaining weight. (As you can guess, it makes me mad as hell ;-)).
What's so difficult, then, in believing that it's possible to eat huge amounts of fats and proteins and not gain weight? I have no problem in believing that myself, because whatever theory it contradicts, observation tells me that it's entirely possible.
Who cares about the beauty of a theory when actual observation constantly contradicts it?
But whatever. It's pretty obvious that you'll obviously always find something to criticize Taubes. And blow it out of all proportions.
I can't wait for the next episode of your sacred war against us, the looney "Taubes nut-swingers".
Shoot your shot, I have my funnel on. :biggrin:
@Martin: If a person wants to maintain weight, there's only so much protein they can process (OK so now I'm seeing higher theoretical limits than I previously remember - let's say roughly 250-almost 400g = 1000-1600 cals) after that they have to get energy from somewhere.
So when a normal weight person eats just lean protein they're gonna be hungry! They need more energy.
It doesn't matter where that comes from fat v. carbs from an energy POV. I'd say getting it from certain starches is equal and may well be superior to getting it from some fats.
Lipolysis does not equal fat burning folks. That is beta-oxidation. Excessive lipolysis w/o burning the fat means ectopic deposition and elevated circulating free fatty acids. This is not a desired state. Don't believe me? Read all of the studies from none other than the fat metabolism experts interviewed by Taubes himself.
I think it is a dangerous myth that insulin levels per se correlate with health. It would surprise many I'm sure, but insulin is a vasodilator, antiinflammatory and possibly anti-atherosclerotic. How can that be what with hyperinsulinemia being so closely correlated with MetS? Because it's the insulin RESISTANCE.
If you lower fasting insulin, you are likely healthier because that means you've probably improved your insulin sensitivity. But if you're doing it with low carb, I think it's fair to say at least that the jury is still out on that.
WOW Peter. You told me!
I actually do know that insulin is, if anything, an appetite suppressing hormone - although my gut feeling on that is that it's not a big player in that regard.
YOU say: Let's make this clear. Fasting insulin determines weight loss. And discuss reduced appetite/intake when insulin levels are presumably lower. So I asked - politely - for you to clarify if I got that right.
In return I get this nonsense about how I can't read and should desist posting on my blog.
Sheesh. Now it's my turn to say I'll blog on what I want! Sorry it offends you so to have to explain how G&K don't fit your hypothesis.
Oh, dear. I see that reading comprehension in some of you Taubes nut-swingers has reached an all-time low. Lack of carbs, perhaps? ;-p
I emphasised the words some of above for a reason. Words mean things. The absence of words also means things.
If Taubes had said "Some of you can apparently exercise as much gluttony as you want as long as you're eating fat and protein.", I would have not bothered quoting him. However, he put his low-carb foot in his mouth by leaving out those three important little words.
RE Kitavans & Asians: What is a high-carb diet? Is it one with a high percentage of total calories from carbs, or is it one with a high absolute amount of carbs? Try reading Diet Percentages: Part 2
In fact, read every article on that site. Then, some of you wouldn't come across as complete idiots who have no idea how the human body works. "Insulin is the fat-storage hormone." Oh, puh-lease!
My "Colpo'ed" comment near the beginning of this thread was a reference to how Anthony Colpo went from being the darling of the low-carb community to a whipping-boy, when he pointed out that low-carb diets were great but calories still counted. I don't intend to end up like him and waste my precious time arguing with idiots like some of you.
So g'day! (as Colpo might say)
CS and Nigel, this is starting to degenerate into the same arguments as in Peter's last post. We get that you don't buy the insulin-for-fat-loss argument, and that for some reason you really hate Gary Taubes.
Now you're just hogging up the comments with provocations, insults, poorly read studies and idiotic diversions. You're contributing nothing to this blog and it's getting quite old.
If you're both so right, then go write a book about it. But is it not clear to you yet that you're making fools of yourselves here?
CarbSane wrote:
"Try reading Diet Percentages: Part 2
In fact, read every article on that site."
Thanks for the link, very interesting articles.
You could have done without the insults, though... which sadly demonstrates a lack of maturity, rather than a superiority in knowledge or insight. Too bad, since your input isn't all hogwash, I must say. You just sound well, not much compelling, because of a dislikable attitude. Contrary to.. say... Denise Minger, or.... Gary Taubes.
(I'm running for cover now, LOL).
@Nigel:
You lecture us about the meaning and importance of words. Fine. In return, I'd like to turn your attention to the meaning of sentences, and context. Do you have any idea of what "blowing things out of all proportions" mean? And what it implies? Because frankly, you seem to have no idea...
"Taubes said that you can pig out on fat and protein and still stay lean, which is BS, so Taubes is a fraud" "He said it and it's BS so he's a fraud" crrr "He said it and it's BS so he's a fraud" crrrr "He said it and it's BS so he's a fraud" crrrr "He said it and it's BS so he's a fraud" (repeat ad nauseam).
You think we didn't get it the first 50 times? :-)
Or something's stuck somewhere? Jammed? Lack of oil, maybe? ;-)
Ok, I'm gonna stop playing "who's smart" with CS and Nigel now. Too time-consuming, I'm behind schedule on my daily pigging out on butter, lard and yolks. I've even had a big serving of -yikes- endives. Carbs! I miss my all-time low. Damn. *LOL*
Pun, irony and even mild sarcasm fully intended. :-)
@blogblog
Thank you for the first reasonable estimation of how much energy can be burned by the body as heat.
It makes sense as I have noticed that I can no longer sleep under the covers and I'm constantly warm when eating 5000 calories a day.
@Peter
If my understanding is correct when fasting insulin is low it encourages lipolysis. Furthermore, some people keep spontaneously enter mild ketosis on fasts as short 8 hours (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995232/). Clearly calories in must equal calories out must be true at some level, but I find that it is very difficult to actually estimate the parameters of this equation directly. For example, it seems that leaner folks have an easier time generating ketones (and thus they're literally urinating excess calories).
Have their been any scientific attempts to measure calories lost via urinated ketones and increased thermogenesis when overfeeding on LC (or high-fat/moderate protein if you will) diet?
Also, I understand lipolysis != fat burning and ketosis != lipolysis.
The connection I want to make is that people who are leaner seem to have livers that are extremely opportunistic about coverting acetyl-CoA into ketones. It seems this happens even when citric acid cycle intermediates are not necessarily being used up by gluconeogenesis.
What are the most important factors that mediate the citric acid cycle? I presume the body and more importantly the brain must have some signaling mechanism to upregulate production of ketones even in the prescence of an active citric acid cycle (i.e before glycogen is depleted).
One more thing to add on to my last comment-- how do you measure the calories out of the acetone escreted via respiration and sweat?
@Matt
Few quick questions.
You realise that 5000 calories is quite a lot. Even if you were very muscular, you're daily energy expenditure might be around 3000kcl, not considering activity level, but you said in the other thread that you're not very active. Is there anywhere I can see a sample menu of what you eat? 5000kcal is about what a heavy weight bodybuilder (200 pounds more) eat to gain weight.
In the Gourmand rat thread, you talk about being able to eat 5000kcal and not gaining weight. I'm curious because when Eades putted number onto the metabolic advantage of LC, he talked about 100 to 300 calories at most. I'm always perplex when I hear people say that they can eat 1000-2000 calories more than their basal requirement and not gain weight.
I'm pretty sure Colpo presented data for ketones in the urine and thermo on LC. It was trivial, if I remember well. I'll try to find back the reference.
@Matt
re: thermic effect of food
The role of energy expenditure in the differential weight loss in obese women on low-fat and low-carbohydrate diets.
http://www.ncbi.nlm.nih.gov/pubmed/15598683
http://www.geekbeast.com
One of my favorite meals:
http://www.geekbeast.com/2011/01/16/dinner-january-15th-2011/
Pictures for the first 35 days... I got overwhelmed near the end of the quarter. I'm going to keep this up until around April 19th when I get my bloodwork done and then I'm cutting calories back to 2000 - 3000.
When I say I'm inactive I'm being slightly misleading. What I really mean is that I don't do (chronic) cardio. My ORM in squat is 500 and I lift very heavy with almost no rest for about 30 - 45 minutes once to twice a week. I have found that my overfeeding even on workout out days tops out around 5500 calories. At that point just looking at food is revolting.
For a detailed description of my eating rules see http://www.geekbeast.com/the-experiment.
I'm about to post before and after shots. By my calculations, I'm looking at a 2000 calorie surplus per day for about 45 days. If calories in = calories out, there are 90000 unexplained calories (not counting the 15 lbs of weight loss).
Thanks for the link. I started laughing uncontrollably upon reading the abstract: The differential weight loss is not explained by differences in REE, TEF, or physical activity and likely reflects underreporting of food consumption by the low-fat dieters.
It's not the diet-- it's the obese that can't accurately report what they're eating. When all else fails appeal to caloric amnesia.
Again, my question still stands-- how much energy is someone in ketosis giving off via the acetone in their sweat and breath, via ketones in their urine, and via thermogenesis.
The thermic effect of food is obviously a component, but I'm wondering about things like black adipose tissue that also burn energy and give it off as waste heat.
Carbsane, I forget where I read this but I remember the topic. It was a researcher who forgot to cut the insulin drip in one of his laboratory dog's leg for a few months. I think it was Taubes that mentioned I read it from first. Anyway, when he realized what he'd done, he decided to see what the effect was. It turned out that the insulin drip leg was completely blocked by atherosclerosis, while the other leg was just fine.
So, based on that tidbit, insulin is directly atherogenic. It explains how we die of heart disease after years of chronic carbohydrate poisoning, and thus years of hyperinsulinemia.
Furthermore, insulin is vaso-constricting. Although maybe not directly. It's complicated but down the line insulin causes other hormones to do their thing and one of them is adrenaline. Guess what adrenaline does to the vascular system.
Nigel, the data on the Kitavans and Asians that is always cited is all observational. Show me a single study where they actually tested those diets.
Scratch that, show me a single study where they compared a true high carb diet that emulates the Kitavans' and Asians' to a true low carb diet that emulates Atkins or something like that.
Extrapolating observational data is one thing, extrapolating hard data from clinical trials is another. For credibility, I prefer the latter.
Matt, so how plausible would you rate those claims that it's possible to grow fat by eating 5000 kcals of meat? Not much I bet. Yet so many just go ahead and make those kind of claims all the time, firmly holding on to their dear ideas about calories.
On another forum, I remember one guy who tried to maintain weight on 3000 kcals of nothing but bacon, cheese and some other meat. Anyway, he already knew his maintenance calories was 3000 kcals on a mixed diet. He failed to maintain on that test diet. His starting weight, 280 lbs. It's almost unbelievable that he could maintain that weight even on a mixed diet of 3000kcals but that's what he said and I'm inclined to believe him since he was an experienced bodybuilder and heavy weight lifter. He also reported having gobs of energy and wanting to train all the time. During that month, he lost about 9 lbs.
Somebody might ask how that's even possible considering he knew his maintenance calories and ate that much. Maybe he lied. Or maybe it's just not about calories.
Did you follow the Colpo/Eades debate on metabolic advantage? In there, I think you'll find your answer to the question of how many calories are spent on ketones excretion. If I'm not mistaken, the difference was something on the order of 100 kcals per day.
Matt, something to think about. Heavy weight lifting stimulates growth hormone secretion more than any other exercise. I don't know how much more but growth hormone is powerful. Maybe more so than whatever calories are spent during exercise. So even if it's only a little more than baseline, it could still have a significant effect on fat accumulation and offset the effect of a caloric surplus. GH is commonly used to shed fat in bodybuilding circles to great effect.
There's also the effect of heavy weight lifting on insulin resistance. Insulin resistance might also have a significant effect on fat accumulation. It does for classic obesity anyway. IR > insulin > fat accumulation. Taubes talked about this.
ed wrote:
"Not true. For one, the body does have mechanisms to move fats into adipocytes sans insulin. I forget the enzyme, but it exists."
Would you happen to be referring to ASP? In this case, as far as I know, ASP is regulated by... er... insulin.
> PMID 9034195
> PMID 8492712
@Matt
That's interesting. I'll follow you experiment to see what comes out.
re: the conventional explanation for underreporting.
Why are everyone looking at researcher and MD as if they are all complete idiot? They know a thing or two about nutrition and physiology, don't you think? Under or over reporting might really be the real explation - or not. But it's getting tiring to see everyone claiming that nutrition researchers and MD are clueless idiot. I don't think the jury is out yet on the mechanims behind LC and GCBC is only one book, one interpretation of the research by one individual. There are other very clever individual who don't buy into it, and there's probably good reasons to this.
You should read the article by colpo, trying to leave all the hostility aside and stick to the fact as objectively as you can that he presents.
http://anthonycolpo.com/?p=94
http://anthonycolpo.com/?p=99
As Martin Levac said, ketone etc would amount to something around 100kcal hence why Eades was talking about a 100 to - at the most - 300 kcal of metabolic advantage. And i'm curious. If one of the proeminent metabolic advantage guru says it's around 100-300 kcals, how come you think you can manage to have a 2000 kcal metabolic advantage? As Colpo say in his article, you realise that 2000kcal is mostly 2-3hour worth of exercise, right? Simply by lowering carbs the body would be able to burn that much of energy? From an evolutionnary standpoint, it does not make much sens that the body would have wasted so much precious energy on a high-fat meat diet.
Fasting insulin and weight loss.
How about fasting insulin and fat tissue size? I'm not talking about how much fat is in fat cells. I'm talking about how many fat cells.
Lipodystropyhy/lipohypertrophy.
This is the basic idea. For equal fasting insulin, two fat cells will contain twice the fat as one fat cell. And, insulin determines how many fat cells.
For somebody who has twice the fat cells as another, how would he go about achieving the same body fat %? If it's through caloric restriction, he'd have to eat less. To stay lean forever, he'd have to eat less forever. If it's through carbohydrate restriction, he just couldn't do it. That's because the whole idea of carbohydrate restriction is to return insulin, and pretty much every other hormones, to normal. Yet paradoxically, carbohydrate restriction could still result in a leaner state than caloric restriction, even if fatter than half as many fat cells.
But here's the kicker. The more fat cells, the less we'd have to eat for equal body fat %. So how much less would we have to eat if we had 5x fat cells?
After 40 years of high carbs and hyperinsulinemia, that's the whole problem.
@Wizzu
In the first paper that you quote, the author says
Insulin increased ASP production up to 2-fold (208% +/- 18%, P < 0.01). However, the most profound increase in ASP was generated by the addition of chylomicrons to the cell culture medium. Chylomicrons (CHYLO) obtained from postprandial plasma increased ASP production in a time- and concentration-dependent manner, producing up to a 150-fold increase in ASP at the highest concentration of CHYLO tested (500 microg triacylglycerol/mL medium (P < 0.001)).
So, insulin increase it about 2 fold, and postpandrial chylomicrons increase it 150 fold. Postprandial chylos seem to have a much much stronger effect on it's activity.
Frank wrote:
"You can easily find many weight loss studies on pubmed, in the obese IR individual, whereas lost-weight with a high carbs diet, lowish protein diet, is usually 75% fat, 25% protein. "
Interesting. But I didn't find the studies you mention. I mean, I did find similar ones, but only with rats or mice. I'm not a believer in proportional extrapolation of animal results to humans...Care to help somehow? Some references?
This is for the benefit of CarbSane, Nigel and anyone else (eg most nutrition researchers) who doesn't understand basic biochemistry.
1) Carbohydrates are a class of chemicals with the general formula (CH2O)n where n=>2.
2) Some carbohydrates are partly or totally indigestible eg starches and cellulose.
3) Carbohydrates are assigned an arbitrary energy value of 4Cal/g. This is based on calorimetry not metabolic studies.
4) The actual metabolic energy value of a particular carbohydrate is always under 4Cal/g and may be as low as zero.
5) The actual caloric value of a carbohydrate rich food depends on how it is cooked, how much it is chewed, the gut bacteria present and a host of other factors.
A Kitivan eating 300g/day of sweet potato "carbohydrates" is not getting anywhere near 300g of glucose or 1200Cal of energy. They are getting about 200g of partly digestible starch, 60g of fibre and less than 100g of sugars - mostly as maltose. The 1-2% sucrose in their diet is barely going to affect their insulin levels.
I'm pretty sure that Kitivans couldn't handle two litres of Coke and a couple of Mars bars for dinner any better than the average westerner.
What about that Swedish overfeeding trial? Wasn't there a huge difference in how much weight the subjects gained? And how easily they lost it? Or was that the US prison overfeeding thing? I imagine there'd be a difference also wether someone's body was "force fed" regarding apetite (insulin? Leptin?) Because of some other issues (maybe food addiction, eating for comfort) rather than sinking insulin levels? The difference between suction and pressure, if you like.
@Martin
I won't say its impossible, but it would be pretty hard. In fact, the reason I drink olive oil/macadamia oil/heavy cream is two-fold. The first reason is that it helps me hit the 5000 calorie over-feeding goal. There seems to be muted satiety with olive oil The second reason is that its far more affordable than eating a 2-lb grassfed leg of lamb every evening.
@Frank
As a person who has struggled with weight my entire life, I'm hyper-sensitive to what I eat. I can't speak for the folks in that study, but why would only folks on the low-fat diet under-report their food consumption? With regards to this specific study I sincerely doubt that the high fat people as a group were accurate while the low fat people were cheating and not telling investigators about it.
I read through Colpo's points. He lost me when he started ranting about caloric deficits. I've trained for the STP (208 mile cycling event), a half-ironman, an ITU triathlon, and a couple of other centuries. I have tried counting calories and limiting to 2000 (or less a day). At one point, I tried only drinking two to three cups of skim milk for about two weeks and quit when I started gaining weight. Colpo is the naturally lean asshole who kept telling me to eat less and workout more. I took it to the extreme ( I was commuting to work by running 4 miles every day). I have never weighed less than 230 lbs until this February.
All that aside, I think the calorie restriction crowd has some good points, but they're so focused on weightloss being a lack of self-control in eating that they miss out on another important part of the picture. Now that I've restored my metabolism to some semblance of normal, I can eat sweet potatoes, sourdough, and a bunch of other stuff as long as don't eat too much of it-- without putting on a bunch of fat.
Prior to this point, I was one of those calorie restricted obese rats that was starving while my adipose tissue built up.
One other thing I should mention is that I was doing daily fasts from midnight to 7 - 8PM.
With regards to your point about evolution-- why would the body store fat that it has to carry around when fat is plenty and accessible? It would make much more sense to opportunistically dispose of it. Again, I'm not the expert here, I'm just doing my best to synthesize something that works for me.
Correction I said when I started gaining weight on the milk diet-- that should have read when I didn't lose any weight. Remarkably, I didn't feel that hungry or miserable while on that diet. I simply remember thinking this is rather bland, but I don't remember feeling like I was starving.
Interesting in the context of satiety and protein.
Now, I'm on research kick since I managed to get UW full text access at home.
http://www.nejm.org/doi/full/10.1056/NEJMoa0808718
Interesting given that BAT was demonstrated to play a role in mediating thermogenesis and weight in rats.
http://www.nature.com/nature/journal/v281/n5726/pdf/281031a0.pdf
@Wizzu
Sorry about the sarcasm. The endless to-ing & fro-ing with blog-blog & Gunther gets a bit old after a while.
P.S. Can you please post clickable links? I use the
^a href="url"*text^/a* and bold HTML tags.
Note: ^ represents the less-than character and * represents the greater-than character.
Cheers, Nige.
Wizzu,
Yeah, that's it.
Look, I'm not saying that insulin doesn't have an effect. I'm saying that you can store fat without eating carbohydrates. Dietary carbohydrates are not a required trigger for fat storage.
From your first reference,
"Insulin increased ASP production up to 2-fold." "However, the most profound increase in ASP was generated by the addition of chylomicrons to the cell culture medium."
That chylomicrons are far more powerful triggers of ASP than insulin would seem to make this a reference to contradict your point...?
CarbSane,
Seems like the conversation has moved on, but I thought I'd try a little here.
"Lipolysis does not equal fat burning folks."
Well right, but it is required. It is not sufficient, but it is required. It's like saying, just your fuel pump working doesn't mean your engine will run. That's true. But the engine sure won't run if you can't get fuel out of the tank.
I would think that nobody would contest the idea that adipocytes are very much "calories in, calories out." ASP and LPL move fat in to fat cells. HSL moves fat out of fat cells. If the net flow is in, adipocytes get bigger. And vice-versa.
So the next question is, what influences ASP, LPL, and HSL?
ASP is mediated by chylomicron concentration. LPL by insulin. So we have two mechanisms for moving fat into fat cells.
HSL is inversely mediated by insulin.
If you want fat out of fat cells, you need lower insulin, as compared to higher insulin.
Help me out here. Do you contest that fact?
"I think it is a dangerous myth that insulin levels per se correlate with health."
"If you lower fasting insulin, you are likely healthier because that means you've probably improved your insulin sensitivity."
If you lower fasting insulin, you are likely healthier because you've improved fasting blood glucose. High blood sugars are directly damaging throughout the body.
Not to mention the fact that, as we all agree (right?) you won't be able to access your body's rich store of valuable calories -- all that luscious fat in those fat cells -- with high fasting insulin. (When I see an obese person complain about being painfully hungry, I imagine their high fasting insulin depriving them of all that valuable energy they've been saving up over the years. It's a shame to die of thirst right next to a lake, for lack of a drinking straw.)
High insulin with insulin resistance is a problem. Low insulin with insulin resistance is not a problem. Thus, insulin resistance isn't the issue, it's the insulin. Duh. :-)
Well even that's not right. As Dr Kurt said -- and I hope you take his message to heart, because without understanding it, you have little hope of progressing, grasshopper -- insulin resistance is only meaningful in context: which organ, which blood glucose level, which fatty acid level. It's not a one-dimensional axis.
@Wizzu
Just look at any weight loss study out there and tell me if you can find one where the group on high-carb lost mostly no fat and only muscle mass, or if you can find a very big difference inbetween the groupe. Considering that carbs are "protein saver" if one is to go on a high-fat, medium to low protein diet with a caloric deficit, I really doubt that he will maintain most of it's muscle mass.
I had no specific study in mind while saying this, but i've certaily read a few weight loss study and i've never seen a study where participant on a high-carb group where losing a large proportion of muscle mass and a small proportion of fat mass, even in varying degree.
http://www.ncbi.nlm.nih.gov/pubmed/12043107
http://www.ajcn.org/content/63/2/174.abstract
http://ukpmc.ac.uk/abstract/MED/8968851 (more muscle mass lost here in the LC diet)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC333231/ (more fat mass lost here in the higher carbs diet)
http://www.ncbi.nlm.nih.gov/pubmed/1858694
Anyway you can find much more by yourself i'm sure :) I'd like to see the study where obese individual don't lose much fat on a high-carb diet and lose a lot of muscle fat.
Frank, I don't think carbs are protein savers. They induce insulin resistance especially once glycogen is replenished. As insulin resistance rises, protein (rather amino acids) have a harder time getting in for the same insulin level.
What is a protein saver is ketones. They stimulate what's called chaperone mediated autophagy. A sort of protein recycling system where junk protein, those that are glycated for example, is brought to the cell surface for dismantling. This in turn prevents or slows down lean tissue catabolism. And reduces AGEs by the same token.
blogblog, that was my argument all along. Kitavans don't absorb anywhere near 300g of carbs per day. I doubt it's even 100g. I'd believe 50g.
Everybody seems to forget a critical aspect of our diet. It's all fortified with some essential nutrient or other. Rather, it's deficient without that fortification. Vitamin C, D, A, K, iron, B12, calcium, you name it. Every single one of those essential nutrients is intended to prevent a deficiency of some kind. If you really want to compare a high carb diet to a low carb diet, take away that fortification. I promise you, we'll start seeing rickets, scurvy, and all the other things we tried to eliminate with that mass fortification of deficient foods like grains for example.
We must also consider that in spite of all that fortification, we still grow fat, sick, weak and probably stupid. And treat all these things with ever growing continuous medication and hospitalization. We have medicalized our health level and longevity.
Frank, I think that from a natural selection standpoint, it would be very advantageous to have the ability to waste lots of fuel in a short time, as is possible by cutting the carbs.
As Matt alluded to, it wouldn't be smart to keep all that fat on our bodies if we can get it from that carcass instead. Nor would it allow us to survive an encounter with a stronger but slower predator. We'd have to have been fast. Not fat and slow and sick. That's another thing. As humans grow fat today, they also grow sick, and weak. That's not conducive to survival is it.
What about poop?
No, not the kind slung around as insults on the Internet, but the REAL poop. You know, the kind only monkeys sling.
Wikipedia tells me that about 7% of fat ends up being discharged normally, and up to 12% when a person has diarrhea. If a diet is higher in fat, does that percentage increase, or does it only increase in cases of disease?
Some fitness forums have posts advising people to see if their poop floats ... evidently evidence of higher fat level. Perhaps a survey comparing the relative flotation characteristics of feces in those advocating calories-in/calories-out vs. LC metabolic advantage should be conducted. That could settle the argument.
@Martin
Carbs are protein saver the first week at least, until one is fully keto-adapted. But there will still always be a need for some glucose in various tissues, especially in training individual, and protein will be use in gluconeogenesis if the basic need are not met by diet.
Well, let's imagine nomad tribe living in a nordic climat. First off, what make you think that they readily had access to a lot of food? Second off, keeping onto the fat seems like a good strategy in time of starvation. Wasting it in the urine and thermo does not make much sens, especially for individual who walk and move around so much. Well, that's all speculative from my part, but in time of non-food abundance, it does not make much sens that our body would waste 2000 calories a day in heat and ketones. Let alone that ppl would have access to 5000kcal worth of food.
Human have used tools to defend themselves and to hunt. We have never relied on any special physical hability such as being fast or powerful.
And Matt has not yet answered myself why he would have a 2000kcal metabolic advantage when it is supposed to be in the ballpark of 100-300 kcal, as claim by Eades in the comment section of one of his blog post.
Anyway, what strong evidence is there behind a metabolic advantage, else than speculative and theorical? The only study cite in support of it was with self-reported dietary journal. Does not make it invalid, but it will take a better design and reproductible result to prove that our fundamental understanding of energy measurment is wrong. And when one look at the bulk of the study done comparing the two, it's not so obvious that there is anything special about LC.
I've just cite a few study up there and none have reported any greater weight loss from going LC, else than probably water weight loss. Some have even reported better result in the LF/HC group.
Again, i'm open to change my view, but not based on speculative mechanisms about the second law of thermo, ketones, BAT, uncoupling protein, etc, etc. I want study comparing the two diet, with strong design (most notably, matched protein and caloric intake controlled, energy expenditure measured) and I want the metabolic advantage to be obvious in many of these studies.
Frank and Martin, discussing whether there is a metabolic advantage to LC is missing the point of Peter's post. The point is that if insulin is low, you can now eat your own bodyfat between meals. Hence your appetite goes down, as well as the frequency with which you need to eat. Taubes mentions as well that any metabolic advantage of LC eating wouldn't be that significant in terms of extra calories burned.
LC doesn't magically burn fat in a thermostatic manner. No one is claiming that. It just lets you finally use the "food" you're already carrying before you have to eat exogenous calories.
I never claimed to have a metabolic advantage. That term got inserted, because I'm a low carb advocate and I'm overfeeding on a large number of calories.
When I started this experiment, I had never even heard of the term "metabolic" advantage. My original idea was that someone who is IR could fast and only consume fat calories. In a state of insulin resistance this would essentially trigger "carb" starvation in insulin resistant tissues as the lower levels of insulin would be insufficient to replenish glycogen (not impossible just a lot more difficult). Thus by inducing ketosis, I would increase my insulin sensitivity and force my metabolism more towards the fat end of the spectrum. As it was, I clearly wasn't burning fat.
With regards too feces-- that's an interesting point. However, it goes back to there's a ton of different variables on the calories in side of the equation and there's a ton of different variables on the calories out side of the equation.
Assuming calories in equals calories out, tracking all those variables across multiple people would be infeasible. I did see James Krieger mention that some biophysicist had a computer model that given some diet could predict weight change accurately, but he didn't provide any further references.
I'm also not saying that I'll look like Anthony Colpo or Martin Berkhan eating 5000 calories a day. That requires genetic luck and a significant calorie deficit.
One last thing, if diabetics can waste away eating uncontrollably where is their "metabolic advantage" coming from?
Great blog post.
I want to go a bit further - as a low carber, I've found that over time I am more sensitive to carbs. Understanding this might bring about why some people can tolerate carbs and not get fat - instead they get energy. While some of us get high BG and high insulin and if we restrict food we get tired and end up less active and thus less calories out.
That insulin increases hunger and thus increases calories in is helpful - but there is even more going on that needs to be figured out.
What controls the ability of some people to get energy from carbs and others fat?
Frank said"
Well, let's imagine nomad tribe living in a nordic climat. First off, what make you think that they readily had access to a lot of food? Second off, keeping onto the fat seems like a good strategy in time of starvation. Wasting it in the urine and thermo does not make much sens, especially for individual who walk and move around so much. Well, that's all speculative from my part, but in time of non-food abundance, it does not make much sens that our body would waste 2000 calories a day in heat and ketones. Let alone that ppl would have access to 5000kcal worth of food.
Modern humans didn't evolve in a Nordic climate with food shortages. We evolved in subtropical savannah climate where food was essentially unlimited and very easily obtained.
It should always be remembered that modern environments are nothing like paleolithic environments which contained a vastly greater abundance and variety of animal life.
@Martin
blogblog, that was my argument all along. Kitavans don't absorb anywhere near 300g of carbs per day. I doubt it's even 100g. I'd believe 50g.
The Kitivan studies reek of junk science. These people are very short and very slender but supposedly eat a lot of calories and do very little physical activity. The logical conclusion is that they are a) eating fewer calories b) less carbohydrates and c) are more physically active than claimed.
My preferred explanation is that they are converting a lot of their sweet potatoes into SCFA and farts via colonic fermentation.
Kurt,
Thanks for your insight. The idea that a (very low carb induced) glucose intolerant state might be OK as long as there is no hyperglycaemia and hyperinsulinaemia creates huge cognitive dissonance in my head, but I'm working on it ;-).
There is still the question why one low carb diet creates 'insulin resistance' (the very low carbers failing on an OGTT), while the other low carb diet increases insulin sensitivity (Lindeberg's paleo trials). I thought the exlanation was that Lindeberg's paleo menu was relatively high carb (included some tubers), but then Barry Groves pointed out that it was actually pretty low carb.
Ergo: other things than macronutrient composition, meal frequency and total energy intake determine if a low carb diet block or enhance insulin signalling.
Lindeberg's paleo groups eliminated all grains, legumes, dairy and added fats (and of course added sugar).
@Martin:
http://carbsanity.blogspot.com/2010/11/insulin-is-anti-inflammatory-and-anti.html
http://carbsanity.blogspot.com/2010/07/vascular-functions-of-insulin.html
It's not insulin levels that count most, it's sensitivity to appropriate levels.
@Melchior: Simple ;-) Lindeberg's Paleo diet was relatively "high carb"
http://www.cardiab.com/content/8/1/35/table/T5
I would ask all engaged here a question: Define diabetic for me.
If by diabetic you mean hyperglycemic, VLC is a "cure"
If you define it as normal beta cell function, VLC is not and may actually cause diabetes, or at least contribute to its progression in those genetically predisposed.
@Wizzu, ASP is not regulated by insulin. It can be stimulated by it, but it is stimulated primarily by chylomicrons, aka dietary fat.
If folks believe our ancestral evolutionary diet is VLC/VHF, and humans likely had periods of feast and famine, what sense does it make for:
(1) An inability to store excess fat in the absence of carb for a "rainy day", or
(2) Futile cycling/uncoupling/whatever off any excesses rather than storing it.
ASP is described as the most potent agent of esterification. Not by me, but Taubes' own sources.
Carbsane:
If folks believe our ancestral evolutionary diet is VLC/VHF, and humans likely had periods of feast and famine, what sense does it make for:
(1) An inability to store excess fat in the absence of carb for a "rainy day", or
(2) Futile cycling/uncoupling/whatever off any excesses rather than storing it.
There is very little evidence of famine in any HG group except Inuits. Humans are the most versatile species and HGs are extremely unlikely to starve unless they live in a totally barren region.
There is a very good reason to "waste" body fat - it becomes oxidised during storage. The more calories you eat and the more fat you burn the less time the fat is stored.
Eating large amount of real food also ensures that high levels of nutrients are obtained regularly. Some nutrients such as water soluble vitamins can't be stored.
Lindeberg is a total idiot.
His "paleo" diet is high carbohydrate, low fat, has very little meat and contains alcohol and fruit juice.
http://www.cardiab.com/content/8/1/35/table/T5
No HG society ever studied obtained less than 50% of calories from meat. Even the "semi-vegetarian" Kalahari HGs traditionally ate 500-800g per day of meat.
@Melchoir
It is well established that we adapt to CHO content by changing our insulin sensitivity. What determines if you are inappropriately insulin resistant or if you are pre- diabetic ( very poor glucose tolerance) is precisely whether you have insulin sensitivity that matches your CHO intake appropriately. If your usual intake is very low, it is appropriate for you to have higher IR than if your CHO intake were higher. Otherwise you would get hypoglycemic at the drop of a hat. Similarly, a HC eater that is pre-diabetic may have WHOLE BODY insulin sensitivity better than his friend who eats VLC at a given point in time, but if his IS is not enough to handle the CHO load he eats at each meal, he is sicker than the VLC eater even though he might handle a 50g bolus of starch quicker on an OGTT test - at one point in time and without any changes in the way they eat beforehand.
Insulin resistance is not a disease state unless it is failing to match the macro ratio of the diet.
VLC eaters just failing OGTT is not a sign of pathology, it is a consequence of normal physiologic adaptation to low CHO intake. It take at least several meals to get back to the high CHO tolerant state. If you are diabetic, you can't get there due to beta cell damage etc. (And by the way, the idea that VLC can kill your beta cells because NEFA does not fall after a low CHO meal is bollocks)
"The idea that a (very low carb induced) glucose intolerant state might be OK as long as there is no hyperglycaemia and hyperinsulinaemia"
That is the idea exactly and it is normal physiology.
Those who say the IR Is the disease are totally confused. IR that allows hyperglycemia and hyperinsulimia and even NEFA elevation when glucose is abundant - is the disease state.
NOT all IR in all organs under all conditions.
How much do we know about ASP? Is it a recent discovery?
"Galina L, interesting. Even on full ketogenic high sat fat, gluten free eating my wife gets migraines still. Keeps me reminded that I certainly do not have all of the answers."
I don't want to be off topic, but did you try Magnesium supplementation ?
MgS IV cures even clasters for some people (the only other effective treatment for some people that I know being LSD).There is research somewhere in PubMed, to lazy to dig it up.
My wife gets frequent migarienes and 1-3g of Mg-Citrate usually stops it in next 20 minutes.
The other thing that helps to many people is Niacin - B3. The extra plus you get is improved HDL and less depression if you have it.
@ majkinetor
Yes, I use magnesium citrate supplements daily 400 - 600 mg a day, never tried to stop migraines with with 1 - 2 gram of it, will try next time. I thought it may cause an upset stomach.Is it a problem for your wife? I intend to get some magnesium suitable for injections when I go to Russia for summer. In USA everything requires a prescription. I should try niacin. I don't have a depression. Being in ketosis puts me in a wonderful mood. It is like being constantly happy without over-excitement. Thank you for all your suggestions.
Peter wrote: "Can people actually gain weight on high fat diets?"
I overate fat & protein (3500 cals/day @ 5'8" 150) while restricting my carbohydrates to some green vegetables for almost two weeks and I hit a weight gain plateau early on: I could only gain 3 pounds on my whole chickens & coconut milk cans binge. I kept a food log and counted my calorie intake so it isn't a case of underestimating the quantity I ate. I tried reaching 4000 calories one day but my stomach refused that extra coconut milk can, I just couldn't drink it. What surprised me was that I didn't have stomach or digestion problems during the experiment. At times I thought I was going to throw up but I didn't.
I also lost weight overeating in a similar fashion: I had eaten too much cake and french fries, put on 8-9 pounds, so instead of doing just a zero carb phase to get back to my usual weight I decided to experiment overeating on zero carbs which I did for 3 days and I still lost weight: 2 pounds per day for two days and on the 3rd day 1 pound.
If I can sit on the couch and watch movies all day long while I overeat fat and protein and still lose 5 pounds in three days it means something other than the wilful caloric deficit is at work.
More people should try overeating experiments like the ones I did. They'd be surprised at the results.
(and like 'Matthew' above I don't know what is this 'metabolic advantage' supposed to be or how it works if it works. What happened to me as I described it is real, the how exactly biochemically it happened I don't know but it looks like there's such a thing as a bodyfat set point.)
@Michael,
I've been eating about 3500Cal/day VLC for five years and haven't gained any weight (I weigh 77-78Kg). Even with force feeding of around 4,000Cal/day for several weeks I've never gained more than 1-2kg. The extra weight usually disappears in a week or two when I revert to 3,500Cal diet.
The most interesting thing is that my weight doesn't vary by more than 1-2kg regardless of activity levels or calorie intake as long as I stick to VLC.
Carb Sane said
"If you define it as normal beta cell function, VLC is not and may actually cause diabetes, or at least contribute to its progression in those genetically predisposed."
I'm quiet interested in that side of things from a familial perspective and ask if you would elaborate on this please.
It seems at odds that NOT burning out your beta cells through overuse would be a bad thing.
Lionel, CS has an extensive blog and you can puzzle at her ideas as much as you like there, but please don't encourage her twaddle here. Thank you.
Peter
I tried to gain fat on VLC and it worked. I ate full-fat cheddar and mayo with every meal, and in some amount of weeks, I gained about 5 pounds. Perhaps I was underweight before? Perhaps all the n-6s in the mayo had some sort of bizarre metabolic effect? Maybe it was the dairy? In any event, the fact that I was VLC didn't stop my body from putting on those pounds. (And returning to non-mayo and non-dairy eating has not taken the weight off again.) I was skeptical at first that I could put on some fat without carbohydrates, but alas, it worked. Has changed my view, for sure.
Katie, really? Some might say that's quite impossible and it defies a lot of theory.
Don't feel bad about gaining 5 lbs of fat though, Getting fat is good (1). Remember to eat your fish oil!
The carbohydrate hypothesis does not say we can't grow fat by not eating carbs. It says hormones control fat tissue, and carbohydrates disrupt those hormones to promote excess fat accumulation.
Removing carbs from the diet does not automatically restore hormones back to normal. It merely removes the single most potent cause of this disruption. The rest depends on those hormones and whatever damage was done with years of chronic carbohydrate poisoning, and the resulting hormonal pressures on fat tissue, and any other tissue affected by this through the years.
If fasting insulin is the primary determinant of fat balance, it's only so within the bigger picture of all determinants such as fat tissue mass, lipolytic hormones like growth hormone and insulin resistance for example. If fat tissue mass was made bigger physically (more fat cells) and not just through increased fat content for example, then returning fasting insulin to normal will only bring total body fat mass back to whatever it is now, and not to whatever it was then. If growth hormone is now lower than it was, then this will also affect overall fat mass.
It does not refute the idea that fasting insulin is the primary determinant of fat loss, it just tells us there's more to it than just getting insulin back to normal and the fat out of fat cells.
@Katie,
of course you can gain a few kilos on a VLC diet - especially if you are underweight.
However it is very hard to become very fat on a strict VLC diet.
BTW mayonnaise is not always LC.
My apologies Peter. As you say, an extensive blog and I am suitably puzzled by most of it.
Sumo trainers have perfected the art of getting people very fat quickly. How do they do it? By consuming 20,000 calories per day consisting mostly of refined carbohydrates (noodles and rice), moderate protein and beer. The sumo diet is very low in fat by percentage.
(Former)sumos typically suffer serious health problems including diabetes, hypertension, heart, kidney and liver disease and usually die before age 65.
@Sue: I don't want to contribute "twaddle" here, but, no, ASP is not a new discovery. A ton of research has been done to demonstrate that it stimulates glucose transport into adipocytes in an insulin-like fashion, is a potent regulator of esterification in response to chylomicron (dietary fat), etc. If you're interested, I have a dozen posts on my blog (as of time of this comment) on ASP. http://carbsanity.blogspot.com/search/label/Acylation%20Stimulating%20Protein%20%28ASP%29
@Lionel: Yeah, do please not encourage my twaddle here. Encourage, instead, wild conspiracy theories to divert from the fact fasting insulin has nothing to do with weight loss.
@Edward: The notion that fatty acids are somehow "locked away" and inaccessible to the obese for fat burning is an enduring myth, but a myth nonetheless.
However, because of the increased fat mass, total NEFA delivery to the circulation is increased in obesity. Furthermore, if ‘lean body mass’ (including skeletal muscle and liver) is used as the denominator for NEFA turnover, then NEFA delivery to the consuming tissues is clearly increased in obesity. The ‘insulin resistance’ of adipose tissue lipolysis may be particularly relevant in relation to the delivery of NEFA in the postprandial period. Despite high plasma insulin concentrations in response to a standard mixed meal, obese subjects fail to suppress NEFA release from adipose tissue at a time when it is completely suppressed in lean subjects.
Fasting insulin has nothing to do with weight loss?
For the 5th time, CS: how are your brilliant revelations working for you? I will keep asking you that until you go away. You really should be ashamed of yourself giving health and weight loss advice to readers which NEVER WORKED FOR YOU YOURSELF.
You have your own blog and we all can go there if we want a laugh. There is no reason to crowd up this blog by posting your trash here.
Sucks for you that you are still fat after years on LC, LF and whatever else. Unfortunately that is not the rest of the world's fault. Time to grow up.
Run along now.
@Martin: Fasting insulin and weight loss.
How about fasting insulin and fat tissue size? I'm not talking about how much fat is in fat cells. I'm talking about how many fat cells.
Insulin's action on adipocytes has been described as protective in nature to assure appropriate sequestration of fat to the appropriate tissue (fat). As fat cells grow they lose insulin sensitivity, meaning HSL is suppressed less, and NEFA are released in larger amounts. NEFA stimulate basal insulin secretion from the pancreas - apparently to compensate for this. The fatter we get, the more NEFA released but the less sensitive the adipocyte to the action of insulin. Thus fasting insulin tends to correlate best with exactly what you're wondering about: amount of fat tissue!
@gunther: Ultimately my weight (and I'm not "fat" anymore bud) is irrelevant to what the research shows, right?
GnK's study demonstrated just that. Peter linked to my blog and folks here had a go at me, so I don't see my responding here at all inappropriate or "hogging" anything. Perhaps you should get a blog of your own to express yourself rather than getting off on hypocritical criticisms of folks like me, all the while posting as "gunther gatherer" around the web.
I'll give you kudos for at least creating a persona so that folks can recognize you around the web. It's better than the legions who go by "anonymous" and can't even be bothered to open a free blogger or similar account so folks know who they're talking to about the net.
@gunther: Ultimately my weight (and I'm not "fat" anymore bud) is irrelevant to what the research shows, right?
GnK's study demonstrated just that. Peter linked to my blog and folks here had a go at me, so I don't see my responding here at all inappropriate or "hogging" anything. Perhaps you should get a blog of your own to express yourself rather than getting off on hypocritical criticisms of folks like me, all the while posting as "gunther gatherer" around the web.
I'll give you kudos for at least creating a persona so that folks can recognize you around the web. It's better than the legions who go by "anonymous" and can't even be bothered to open a free blogger or similar account so folks know who they're talking to about the net.
"Ultimately my weight (and I'm not "fat" anymore bud) is irrelevant to what the research shows, right?"
You either don't understand the research or you simply don't want to, because you're still overweight and you're angry about it. This much is obvious from your own blog posts and bio. So you're going to blame LC and all of its advocates because you failed for whatever reason.
I know it's not fair that it's working for others and not you. A responsible adult would admit it and try to exercise in addition to LC, but you don't. You blame the science itself and anyone who reads it.
If you had lost all the weight you wanted to lose on LC, the internet would never have been plagued with your presence. Once again, grow up.
@All, just a request, please do not encourage CS. Gunthter, there is nothing you can do to someone who will not see. It's fine by me for her to do as she wishes and it's fine for anyone to follow her line of thought, if they are able. Let them go, that's their problem. My simple and embarrassingly over dumbed down explanation clearly has no effect. No need to stress.
Peter
Peter, I'm very disappointed in your responses here. You linked to my blog, you let folks have at me in your comments, played along with the "humor", and intervene now to prevent your fans from encouraging me to challenge your post here.
All because your posts don't support your contention that fasting insulin ultimately determines weight loss and I dared point that out on my blog.
Gunther, I'm not mad at LC or dissatisfied with my weight per se. I am concerned that LC has taken me to a rather attractive size with some disturbing changes in my weight distribution and ultimate weight.
But please, if you want to have at me, do Peter a favor and "man up" and post directly to me on my blog.
blogblog said...
@Katie,
of course you can gain a few kilos on a VLC diet - especially if you are underweight.
However it is very hard to become very fat on a strict VLC diet.
BTW mayonnaise is not always LC.
Agreed. My "heavier" self is still skinnier than my carb-eating past self. (I was normal weight to start with, but became skinny, skinny, skinny eating lots of VLC calories. I was skeptical that my weight gain plan of mayo and cheese would work, but dairy protein being what it is, I thought I'd give it a go before heading for the carbs. I was maybe around 20-40 carbs a day during that time--sometimes less than 10.
I don't think I could be obese eating this way. But I did discontinue the cheese/mayo experiment because it started to be more than I wanted coming back on. I am too vain to continue....
Katie, yes vanity is a harsh master/mistress. My BMI is 20ish and I'm really hoping that I'm not looking enjoying the all cause mortality seen in observational studies at this low BMI on SAD based diets. Time will tell...
Peter
@Katie,
Dr Lutz said that thin people usually lost weight initially on a VLC diet but later gained weight.
Carbsane, you totally missed the point. I'm not talking about bigger fat tissue due to increase fat content, I'm talking about bigger fat tissue due to more fat cells.
Think of it this way.
All other things equal, two fat cells will contain twice the fat as one fat cell.
Everybody is stuck on the notion that obesity is solely a matter of how much fat is inside fat cells. So everybody is focused solely on how to get that fat out. So everybody is confused when they regain weight after having lost so much and then returning to their previous diet, or reach a plateau after having been so fat for so many years prior.
Is any of you confused about lipohypertrophy due to injecting insulin in the same spot for years?
Seriously. Can one of you get unstuck for a moment?
What if losing weight meant not only getting the fat out, but reducing the number of fat cells? Does cutting calories/carbs result in a reduction in the number of fat cells?
Why are women generally fatter than men? Is it possible that they actually have more fat cells? But why are girls and boys equally lean before puberty? Is it possible that they haven't yet gone through the process of adipocyte differentiation due to sexual hormones?
Hormones do not only determine how much fat is inside fat cells. They also determine how many fat cells there are.
@Martin,
even traditional Inuit women tended to get moderately fat in middle age.
blogblog, I don't understand where your argument comes from. It's like I'm talking about car engines but then you say "oh yes, but you gotta watch the clown cuz he's fast as a duck".
Are they fatter because they have more fat in their fat cells? Or are they fatter because they have more fat cells?
Can somebody just get out of their head for a moment and make the goddamn distinction between fat, and fat cells?
Thank you.
Martin,
Check out the [free] full text of http://www.ncbi.nlm.nih.gov/pubmed/17433128
Note the differences in adipocyte number vs size in the different diets. There's other cool stuff too--big differences in leptin, liver weight, liver trigs, and insulin.
Peter would probably have better idea of what's going on, as I have almost none.
@Martin: Forgive my confusion. We most definitely get fat both for the number of fat cells and how much we store in each cell. It seems that the number of fat cells is determined sometime by early adulthood but we have adipocyte turnover. Insulin does stimulate differentiation of pre-adipocytes to mature fat cells. Smaller/younger adipocytes are more sensitive to insulin than older/inflated ones. There is a class of diabetes drugs (forget which) that cause weight gain by stimulating insulin-promoted fat cell proliferation. Aesthetically not what most want, but metabolically protective. Then their's GLP-1 analog Byetta that stimulates insulin production but causes weight loss especially in the fattest of diabetics.
Obviously there's something other than insulin at play here!
If I've still missed what you're getting at let me apologize in advance for twaddling about.
Martin definitely brings up a good point. Adipocyte hyperplasia is probably more of an issue than hypertrophy. I would think that it is easier to shrink the size of a cell than it is to do away with the cell all together.
John, it's a lovely paper.
The thing to note is that rancid deep frying oil consumption is associated with impaired insulin secretion from the pancreas. These rats were chronically hypo insulinaemic and, not unsurprisingly, could not deal with glucose.
The utterly hysterical aspect is that chronic hypoinsulinaemia, even on an adlib diet providing 50% of calories from corn starch, produced slim rats! Very slim rats.
Ha ha ha bloody ha.
I think it's debatable whether there are prostaglandin analogues blocking adipocyte formation or whether this is simply secondary to chronic hypoinslinaemia. You might be able to do the same with diazoxide. I'd have to Pubmed that, no time now to chase.
Of course it might be just that the rancid fat diet was unpalatable to hypoinsulinaemic rats, omg, another fit of giggles!
Or maybe oxidised frying oil contains a chemical which makes rats count calories and sneak off to the gym in the middle of the night. Just fantastic. More giggles.
I love it! You've made my evening. Many thanks.
Peter
@Martin
As far as I know, hyperplasia can't be reversed.
I'm relieved. I thought I was going crazy and nobody else understood the problem. I'm happy to see that's not the case.
Anyway, Justin, that's the problem. Once we've created more fat cells, how do we convince them it's time to die cuz we don't need as many anymore?
Actually, how do we convince pre-adipocytes to stay where they are so that they don't replace the old ones, nor add to the existing number, to ultimately reduce the total number?
If there are hormonal mechanisms that can increase fat cell number, there must also be hormonal mechanisms that can decrease it.
"My preferred explanation is that they are converting a lot of their sweet potatoes into SCFA and farts via colonic fermentation."
@ blogblog: very well-put!
To emphasize the point I may as well pose, for those who believe an observational study above all else, a couple questions:
1. Knowing that the ruminants eat grass what do you think they metabolize on - carb or fatty acid?
2. How do you think the law of unintended consequences would apply to someone who lives in a temperate (or colder climate) where higher endothermic output is necessary (thermogenesis or high expression of uncoupling protein - however you choose to call it) and tries to imitate someone else living in an island whose attire constitutes a mere loin cloth?
Eat carb if you want but don't pretend that it will do anything to extend your healthspan.
@Martin,
I have no idea why older Inuit women got fat on a VLC diet. It is just an observation by Stefansson.
I'm fairly certain that adipocytes can even survive fatal starvation.
@JohnN,
Cattle eating natural pasture are on a VLC diet with ~2% carbohydrate. Dairy cows often develop quite "severe" ketosis during pregnancy and lactation.
JohnN,
I am seriously thinking that the obesity epidemic may be due more to to central heating and the global adoption of western clothing designed for cool climates rather than diet.
Obesity is far more common in hot climates eg Polynesia, Mexico, southern USA, Australia than cold climates eg Japan, Korea, Finland.
Hi Peter, have you encountered any good research which identifies variability between healthy individuals in their degree of insulin response to food, and therefore maybe also basal insulin levels? ie. Can two very similar and healthy young individuals have a significantly different insulin response to the same meal, and perhaps also have different basal insulin levels? I listened to an interview recently where Prof Robert Lustig identified some individuals as what he called "hyper-secretors of insulin". If this variability in insulin response does exist it will likely predispose the higher insulin producer to over-eating?
Thanks Lou
Peter,
THANKS ;) I couldn't see your blog (or mine) in China, just back...
Insulin and IR (insulin resistance) are so primitive, primordial and 'utterly essential for survival' as you said. I get it!! For fat loss (or maintenance of lean muscle), we would prefer IR on the adipose level (I think) -- keep the energy in free circulation and prevent long term storage in the adipocytes (but insulin sensitivity elsewhere).
-G
Frank, Nice to see you back!
This is finally jiving for me...also, every state that puts fat on women is a state to promote survival for BOTH mom and baby or future baby:
--high estrogen (pregnancy)
--estrogen dominance or progesterone deficiency (PCOS and menopause and birth control -- result, infertility where perhaps environment not conducive to support birth)
--starvation (study: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T88-3VXJHBB-9&_user=10&_coverDate=04%2F30%2F1996&_rdoc=1&_fmt=high&_orig=gateway&_origin=gateway&_sort=d&_docanchor=&view=c&_searchStrId=1712170238&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=8cfb434b50a9fa919d3f6cf93f9957e4&searchtype=a)
--(and for MEN, MOOBIES where xenoestrogens fake fat into adipocytes)
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