“A hypocaloric diet, whatever the proposed type, is an inadapted treatment to chronic disease, like obesity. All diets are inefficient on the long term. The weight loss is generally small, about 1-2 kg a year. The results are the same, independently of the type of diet, and the patient’s compliance is clearly the main key to succeed. About 80% of patients regain weight the first month following the diet, and only 1% can keep the obtained weight a year later. Nearly half of the patients involved in a diet program give up before the end. Finally, because of risks of macro and micro nutriments deficiency, certain diets are to be avoided and hypocaloric diet shouldn’t be proposed.”
~ from, Hypocaloric Diets: Which Ones to Advise/Avoid? Di Vetta V, Clarisse M, Giusti V.
Readers of this blog are, of course, not the least bit surprised by the above quote, as it is common knowledge within the larger Paleo community; conventional dieting fails miserably, and those currently engaged in conventional dieting are, for the most part, well — miserable. The 10,000-dollar question remains, however; why do these diets fail? Now, in my real-world, day-to-day comings and goings, I’m not much concerned with whether I’m hypercaloric or hypocaloric. I know that, by whatever mechanism is at work in my Paleo way of life, over the long-haul I’ll maintain single-digit body fat levels coupled with a stellar blood profile; my health will be excellent and my vitality vibrant. And all of this will come free of any feeling of depravity, gnawing hunger, rampant cravings or lethargy. I’ll have no need for a calculator or scale, nor will I ever be concerned with meal timing. I am a curious sort, though, and so I wonder: Am I, over the long haul, actually either ingesting fewer calories or burning more calories than in my pre-Paleo days? Is it a combination of the two? Or, does the total calorie content really not play that significant a role?
I know I’m not going to raise the eyebrows of any long-time TP readers by stating that, in my opinion total calorie ingestion plays a minor, short term role in weight control (body fat and lean tissue) when compared to the hormonal/enzymatic environment elicited by the ingestion of those calories. In other words, it’s the type of calorie ingested that trumps the amount of overall calorie ingestion.
Now, it’s obvious to the most casual of observers that caloric restriction below the basic metabolic rate (BMR) and total calorie expenditure will result in weight loss. But are all hypocaloric diets created equal? Again, TTP readers know the answer, but, for purposes of comparison, let’s take a look at this study:
Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The A TO Z Weight Loss Study: A Randomized Trial
Now, let’s have a gander at the recent Harvard study (Diets That Reduce Calories Lead to Weight Loss, Regardless of Carbohydrate, Protein or Fat Content) that I wrote about here.
Just what, exactly, is going on here? We seem to be getting mixed signals. If a calorie is truly a calorie, then what is going on with this Atkins group? Thanks to Chris, at Conditioning Research, for finding this apropo cartoon, from this very smart and witty collection.
The problem with scientific studies, though, lay in (1) the minutia and, (2) in the interpretation. And, as the above cartoon so very well illiterates, correlation does not necessarily imply causation.
Well, here’s the short version of my take on the issue
There is a dramatic shift to fat burning when insulin levels are low and/or not overly released with each caloric ingestion. Insulin immediately shuts down fat burning (the release of stored FFAs – free fatty acids) and begins the process of moving FFAs, and excess glucose in the blood stream into body fat. By comparison to a high carbohydrate meal, very little insulin is released by eating the TTP/Paleo way, and this slight rise in insulin will occur over a period of hours — not seconds or minutes as would be the case from eating the usual high carbohydrate, high glycemic-value, high total caloric load (all contributing factors) typical of the “normal”, western diet.
It is very clear to me that the bodily chemical processes (especially the action of insulin) that entail the digestion of all foods work via certain, distinct pathways, and knowing these pathways gives us the tools to knowingly adjust our diets which, over time (and which is clearly demonstrated by empirical evidence), can cause us to correctly assume what is optimal for our individual body types, and to allow ultimate control of our body composition. My contention is that that function of determining how a fuel calorie (glucose and fatty acids) will be utilized — whether stored as fat, or burned as energy in the muscles,or in the act of bodily repair/replenish — is carried out primarily by the hormone insulin via interaction with the enzyme lipoprotein lipase (LPL). It is interesting to note as well (though a bit of-topic for this discussion), that sex hormones also interact with LPL, which is why men and women gain/lose/carry body fat differently. It is insulin, though, that acts as the primary gatekeeper, the traffic cop, so to speak, in the ultimate partitioning of the end-products of food ingestion.
So what does all of this mean in practical terms? Well, it means that it’s your insulin levels that will determine what is to become of the calories you’ve ingested. A high insulin level (resulting from consumption of a high carbohydrate meal) will do two things, primarily (1) it will shunt the excess ingested calories to be stored as fat, and (2) it will shutdown the release of FFAs from the body’s fat deposits. The flip side of this is the maintenance of a low insulin environment via the elimination of simple carbohydrates and the limitation of complex carbohydrates. In other words, and from a purely biological or homeostatic perspective, lean people are not those who have the willpower to exercise more and/or eat less. They are simply people whose bodies are programmed to send the calories they consume to the muscles to be burned rather than to the fat tissue to be stored —the precise reason that Lance Armstrong and his ilk can get away with the massive amounts of carbohydrates they consume with no (outward) noticeable affect. A less active a person would tend to go the other way, shunting off calories to fat tissue, where they continue to accumulate to excess. This shunting of calories toward fat cells to be stored or toward the muscles to be burned is a phenomenon known as fuel partitioning. It is also why I think of the body more as a capacitor, rather than a simple thermodynamic machine; a capacitor whose charge/discharge properties are controlled primarily via insulin, the level of which is primarily controlled by the type and amount of carbohydrate ingestion.
So, is a calorie just a calorie? Well, no more than a bullet is just a bullet, I suppose. Would you rather be shot by the rubber variety, or a “cop killer”? Keep that metaphor in mind before you fork-up that next mouthful of pasta.
SOOOOOO very glad you posted this! Very informative and cut & dry. So simple, folks! : )
Great post, Keith. I had just published my Sunday link list and had to go back and add a late entry. 🙂
Well deserved, and thank Zeus I didn’t have to end that post on morons. BTW, check out the BCGC review I link. It’s awesome, though a bit to annoyingly riddled with typos.
Keith, too much fruit I assume is not good for one who wants to lose fat? And what about nuts? they are fairly low carb
That’s the idea; not that fruit is “bad’ by any stretch of the imagination, though you do want to minimize fruit intake if you’re actively attempting to cut weight (fat), as it does provide for a bit higher insulin kick. Nuts are a “go” — as long as they’re not peanuts (which are actually a legume. And raw or dry roasted is preferred.
As usual, wonderful post.
Aspects of this are discussed heavily in the newly released documentary Fathead. He did count calories, though in his deficit he ate ~50% of his kcal from fat, mostly saturated. He lost more than his deficit would mathematically add up to, but he was still in a caloric deficit…not losing fat at 5500kcal whilst leading a mostly sedentary lifestyle no matter the macro ratio.
I’m sure you already have this though, being a reader of Richard’s blog.
One thing I find myself coming back to is wondering how exactly we determine whether a diet is hypo/hypercaloric, anyway? Although there are all those calculators and ‘established’ BMRs, I still don’t know how anyone knows (without individual metabolic testing, maybe) what their own personal daily caloric need is, since the range seems to skew so widely (again, this seeming to be largely dependent on type of calorie).
It’s still a good point, none the less. Thanks for bringing it up again. I’ve yet to see the documentary, though I’ve heard so much about it, it seems that I have.
You’re exactly right — and it’s yet another reason the “Paleo” way is the only sensible way to eat. No one knows what their energy expenditure is day to day. It’s nearly impossible to measure outside of living in a completely closed, laboratory environment, and a fool’s errand beyond that. Energy intake, of course, can be measured (or at least approximated), for whatever good that would do. Eat Paleo, eat ’til you’re full and go live life. It’s the easiest and most effective “diet” there is.
Another valuable, articulate post on the caloric balance discussion. It would be interesting if the diet study also had Paleo as one of the candidates, but that’s probably considered too ‘fringe’ for the JAMA.
So, I’m pretty well grounded regarding nutrition, and I probably know the answer to this question, but what’s your take on promoting the proper homonal / enzymatic response for exercise?
I often wonder if my intake is higher or lower than it used to be pre-Paleo. For science’s sake, it would be REALLY interesting if I’m eating many MORE calories and STILL able to maintain my weight – that would go far to show a calorie is not a calorie, right?
I certainly never feel deprived. It’s so much easier to maintain my weight this way, not having to worry about counting, measuring, etc, that I thankfully no longer really care about calories 🙂
I want to add that I agree entirely with Sarah’s point. Also, I ask the same questions about the calories in/calories out theory. Once you understand all the processes that go on in the body, how can you really believe it is that simple??
I have buddies that have terrible high-carb diets, do little exercise and are very lean. What’s the deal with that? Is it an age thing (early 20s)?
I’d concur that the Paleo way sure is easy and delectable!
Chalk it up to the fabulous hormonal profile that is the providence of youth. The growth/maturation process itself requires a massive caloric load. The BMR of a sedentary 20-something is (on average) much, much greater than that of a similarly disposed 40-something. Just take a look around any American shopping mall, though, and you can see that even a fan-tab hormonal profile can be overloaded by egregious dietary habits. Kinda like being dealt a king-high straight and still loosing the hand.
I really haven’t the slightest idea of how many calories I take in a day. It would be interesting, though, to map a precise caloric intake vs. use over the course of a week sometime. Not that I’m offering myself up to live as a lab rat for that time period 🙂
I’m not sure I fully understand your question? I can say though, (although I don’t have any studies to back this up – it’s only a gut feeling), that insulin interferes with testosterone production. In that sense, then, it (a high insulin level) would really inhibit peak athletic performance. This would include females as well, though to a lesser degree.
Well, insulin causes fat storage, and fat storage leads to increased production of estrogen in both men and women, and in men that would interfere with T production, especially if the fat’s collecting around the middle. I did happen to see an article someplace about the latter recently, because my little girl’s dad just found out his T is low (he’s got other health problems and had a full blood workup), and I was trying to find info that might help him.
Dr. Atkins wrote about a patient of his whose caloric intake was just huge once he got on the program. He dropped weight anyway. I once calculated myself as getting between 2000 and 2900 calories a day when I was low-carbing and my weight was coming off too.
Part of it is that not everything you eat gets turned into fuel. Your body’s always replacing and repairing stuff and it needs fat and protein for that, so once those are broken down into fatty and amino acids, some of that’s gonna get shunted off into those rebuilding and repairing efforts. The other piece is what you’ve said here about the effects of insulin. A low-carber eating a lot of fat isn’t going to store it because his insulin is not spiking; instead he’s going to take whatever he hasn’t used for hormones or cell walls or whatever, burn some of that for fuel, and pee the rest of it away as ketones.
I ran across something in the paper recently in the food section about “protein calories” being “burned” and my eyes bugged out. They were actually trying to tell people that protein’s a fuel. This is the same newspaper whose food section trumpets preachy articles about “healthy” low-cal, low-fat eating on its front page and is then chock-full of recipes involving sugar and flour on the inside. I’m sure they’re mystified as to why Ohio has such a tremendous population of fat people, myself included.
Like most low carb fanatics who are ignorant of all but the most pop-physiology, you’re incorrect to think that fat balance is all about insulin.
You need to understand that there are a multitude of enzymes that are involved in triacylglycerol synthesis and lipolysis. “Insulin” is not a pathway. It’s one of several hormones that have an effect on the enzymes that comprise the actual pathways. What enzymes am I talking about? For fatty acid uptake, there’s FAT/CD36, FATP-1 to -6, and FABPpm. For fatty acid synthesis, there’s fatty acid synthase. For glucose uptake, there’s Glut1 and Glut4. For esterfication, there’s GPAT, PAP1, and DGAT1 and DGAT2. For lipolysis, there’s HSL, perilipin, and Protein kinase A.
What “regulates all this?” It’s definitely not just “insulin”. That’s an incredibly simplistic, insulinocentric view. You know what else has an effect on these lipogenic/lipolytic enzymes besides insulin? There’s angiotensin II, the adrenergic receptor (catacholamines), FoxC2, PTP1B, and last but not least ASP.
ASP stimulates triacylglycerol synthesis more than any other known adipose tissue factor. It’s also a potent stimulator of glucose transport [PMID: 9130021]. It works independently of insulin, through a different signaling pathway. It effectively synthesizes triacylglycerol even in the absence of glucose and insulin [PMID: 8492712]. Finally, guess what the primary regulator of ASP production is? Dietary fat (packaged as chylomicrons) [PMID: 9694837]. Fat intake and ASP will lead to a positive fat balance just as much as carb intake and insulin will. Which is why it’s all about calories. Unfortunately, low carb nuts never look past insulin. They ignore (or are ignorant of) the fact that fat stores itself with tremendous efficiency without any insulin whatsoever.
Take a look at the broader picture. Fatty acids are taken up into adipocytes via facilitated diffusion, mediated by fatty acid transporters like the ones I mentioned above. You don’t need insulin for this. Dietary FFAs will diffuse into adipocytes down the concentration gradient. There may even be passive diffusion. You then need a triacylglycerol backbone and the acylation (esterfication) steps that lead to the production of a triacylglycerol. ASP can stimulate both. After all, it’s called “acylation-stimulating protein.” This process works just fine with basal levels of insulin or glucose. And as explained before, ASP is produced in response to FAT INTAKE.
Weight loss is all about negative calorie balance, not lowering of insulin. Research clearly shows that when isonitrogenous diets are compared, higher carb diets (with higher insulin levels) do JUST AS WELL as lower carb diets at reducing bodyfat. While low carb diets have lower insulin levels, they have higher ASP levels. And vice versa with a low fat diet. Why? Because carb intake (or type) and insulin levels are absolutely unable to account for fat loss. It’s all about energy balance.
What I explained above is why it’s such nonsense for people like Dana (above) to say things like:
“A low-carber eating a lot of fat isn’t going to store it because his insulin is not spiking; instead he’s going to take whatever he hasn’t used for hormones or cell walls or whatever, burn some of that for fuel, and pee the rest of it away as ketones.”
Absolutely incorrect. Fat doesn’t need insulin to be stored when ASP (produced in response to fat intake) stores it quite effectively.
Like most high-carb/energy balance fanatics who are incapable of juggling two contrasting (though of differing degree) physiological actions, you’re incorrect to think that the action of ASP trumps that of insulin. I’m not being sarcastic when I say that you’ve done a fantastic job, though, of explaining fat synthesis – you’re spot-on. Your problem is in your failure to realize matters of degree, or existing body fat levels. In addition, you fail to tell, as Paul Harvey would have said, the rest of the story. Metaphorically speaking, while you’re pissing an ASP stream into “Fat Lake”, I, on the other end, have kicked the dam in with my low insulin environment.
Of course evolution has equipped the body with a mechanism by which to store ingested fat; that has never been the point of contention. We are made to survive, after all. The flip-side (and the more important, in a dieting sense) of that however, is the fact that a low insulin environment allows for the continual release of FFAs from the body’s fat stores, the net effect of which is a draw-down of body fat levels. The lower end of this phenomena is regulated (again, survival, evolution at work), so that the body will not, even in the complete absence of carbohydrate, deplete body fat levels to too low a point. The big problem now days (as evidenced by the obesity epidemic), is that while the lower-end of the body’s BF level is regulated, there seems to be no corresponding, upper-end regulation. But again, this makes sense in evolutionary terms, as there was never any evolutionary prompt, even while our genome was busily storing away ingested fat via the ASP action you so eloquently explained, for such a mutation.
I’d have to agree with Keith, as in my personal case and counting now dozens of rapid successes among friends, family, and people who’ve commented on my blog or emailed. Many of us eat what would be considered enormous amounts of fats, but in a low-carb environment and we lose fat. We see it over and over.
It’s a Theory to Practice sort of thing, I guess.
So, it’s not that you can’t gain fat in a low-carb environment, it’s that it’s really hard to lose fat on a high-carb diet. Does that about sum it up?
I think this is well exemplified by the fact that, when I’m eating a high-fat, low carb, IF style diet, skipping meals is no problem for me. I can store fat when I eat, and then effectively release it throughout the day to stay extremely energized. When I eat a higher carb diet, however, it seems like any fat I store is stored for good, because a few hours after I eat, I’m tired, hungry, and wondering while all this energy I clearly have stored inside me isn’t causing me to leap out of my seat.
Thanks, Conciliator, for that explanation of fat synthesis! A very nice, concise explanation.
I think that does sum it up, and, I look at it like this.
I might suggest to Keith that a better metaphor than kicking down the [fat lake] dam is that a low insulin environment keeps the floodgates well open most of the time. So, even when there may be brief periods after high-fat meals where more is going into fat lake than is coming out, we spend far more time in 24-hours not eating than we do eating and soon enough, we’re back to negative fat accumulation.
Add to that that we Paleo eaters don’t get physically ill when we haven’t eaten is 3 (or 2, or 1) hours and that in fact, most of us usually develop a certain affinity for the kind of hunger that comes with a high-fat, low carb lifestyle and we often push out mealtimes. I have no such thing as “mealtimes” in my life, anymore. I eat when I’m hungry. It’s 9:30am here, and I’m hungry and enjoying the focus of mild hunger. I’ll probably eat in a hour, maybe two, but it’s no big. I could eat now, I could easily go three hours. I have no idea when I’ll actually decide to eat. This is completely different from the old life.
Now, I know what Conciliator is likely to say: ‘see, it’s calories.’ You’re essentially fasting so over time, you’re taking in less calories, and so on.’ Well, the calories in / out debate has never interested me very much and the reason is that in the end, it’s about hunger. I don’;t care whether you’re eating 1k kcal or 5k kcal per day. If you have unnatural, consuming hunger, it’s only a matter of time until the cake, cookies, pizzas and burger, fries, shakes become part of your life, again.
What I do know is that sometimes I have zero calories in a day, and sometimes well in excess of 6k when I do a fat bomb for breakfast, a big steak for lunch, a hugely fatty sauce with whatever I’m making for dinner, and then 3-4 handfuls of nuts in front of the TV, polished off by a late night omelet.
Now, I rarely do that, anymore, but I did it a lot when my journey was beginning, before I reached no-hunger bliss, but that also corresponds to my period of most rapid fat loss.
theorytopractice, I’m not incorrect at all. What I said is that “ASP stimulates triacylglycerol synthesis more than any other known adipose tissue factor.” I provided a pubmed reference, though I’m not sure you can appreciate controlled research. From that reference, we read “Acylation Stimulating Protein (ASP) is the most potent stimulant of triglyceride synthesis in human adipocytes yet described.”
And from the landmark study in which ASP was discovered [PMCID: PMC288301]: “ASP is much more potent than insulin in stimulating the esterification of fatty acids into intracellular triglyceride in human fibroblasts and adipocytes (3). The increase in triglyceride synthesis induced by ASP is achieved by a dual effect. That is, ASP causes translocation of glucose transporters from intracellular vesicles to the cell surface, thereby increasing specific membrane glucose transport (4). By contrast, membrane transport of fatty acids is not directly affected by ASP. However, net fatty acid uptake does increase secondary to stimulation of the enzyme, diacylglycerol acyltransferase, which controls the rate limiting step in the synthesis of a triglyceride molecule (5, 6).”
Makes ASP sound quite a bit more significant than just a little “stream” into a “fat lake”, doesn’t it? That’s because it is. Your analogy is completely unfounded.
You say I “fail to realize matters of degree, or existing body fat levels.” What is that supposed to mean?
It’s ironic you quip that I’m “incapable of juggling two contrasting physiological actions” when this is the problem from which you suffer. You have your blinders on when it comes to fat synthesis, thinking fat loss is all about lipolysis and not net efflux (the balance between synthesis and lipolysis).
Insulin is highly antilipolytic. No doubt. Even fasting levels of insulin are antilipolytic. The problem is when you equate “a low insulin environment” with “a draw-down of body fat levels.” The one does not entail the other. Yes, “a low insulin environment allows for the continual release of FFAs from the body’s fat stores”, but “a draw-down of body fat levels” occurs ONLY WHEN the release exceeds synthesis, and that doesn’t always happen. In a caloric surplus, there will be more synthesis than lipolysis. And this can happen perfectly well in a low-carb state where ASP is high, though insulin is being stimulated only by amino acids.
For a given protein and calorie intake, high-carb diets work just as well for fat loss. Is insulin higher than in a low-carb diet? Yes. But 1) there are much fewer fatty acids available for diffusion into fat cells and 2) ASP is much lower. The effect is that you have less lipolysis AND less synthesis. At maintenance calories with any diet, fat synthesis and lipolysis are in balance. As you drop below maintenance with a high-carb diet, and eat fewer carbs, insulin levels drop. The fewer you eat, the more it drops. This means reduced inhibition of lipolysis and net efflux, resulting in fat loss. Now with a low-carb diet, reducing calories below maintenance doesn’t do much in terms of insulin, but as you reduce fat intake there is a reduction in synthesis. The result is the same… net efflux.
And this is exactly what research comparing the two finds. Assuming calories and protein intake are equal, low-fat diets do just as well as low-carb diets at reducing body fat. There’s no reason to think they wouldn’t, unless you have a myopic fixation on just insulin or lipolysis.
You say I “fail to realize matters of degree, or existing body fat levels.” What is that supposed to mean?
C’mon, step up your game. If you can’t figure out what I mean by this, I haven’t got the time to quibble with you. You “energy balance” morons remind me of the friggin’ Rainman. I realize you guys play the Rush Limbaugh of the Paleo-bash crowd, and that’s cool and all – seriously, I’m in the pharmaceutical business so it’s in my best interest that you and your kind multiply – but still…
Anyway, you can spout all the findings you like – none of which, by the way, I’ve ever said were wrong – just wrongly interpreted by you and your ilk. If you can’t take these findings and put them in a proper context, they become no more than useless, meaningless blather. I have no problem with someone playing the intelligent devil’s advocate, but at least put some real-world contextual results behind what you’re purporting.
Not that zero carb is for everyone but this is a good post on calories. http://forum.zeroinginonhealth.com/showthread.php?tid=112
Nice posts Conciliator. Very informative.
“And this is exactly what research comparing the two finds. Assuming calories and protein intake are equal, low-fat diets do just as well as low-carb diets at reducing body fat.”
I, and many others — if you care to look around — have utterly _falsified_ that hypothesis. Now, you may think they’re lying, and some certainly exaggerate, but I’ve seen it many, may times in myself and many others.
Several low carb docs out there have also related case studies of their own patients losing fat on upwards of 10,000 calories per day. James Carlson is one of those, and of course Atkins had many similar experiences over many years. Eades will tell you the same thing.
Finally, this reads like a typical lab rat:
“At maintenance calories with any diet, fat synthesis and lipolysis are in balance. As you drop below maintenance…”
Maintenance? What a laugh and it shows how little you really grasp about the Paleo way. There is no such thing as “maintenance.” We eat from zero to double and triple your silly notion of “maintenance” on any given day. I have no “maintenance.” I am a dynamic animal, always changing things up.
You guys need to get out of the lab and conduct some _practice_. failing that, how about some self experimentation? You don’t even need to get fat. Predict what happens, here:
1,000 kcal per day
– 2 weeks of nothing but carbs
– 2 weeks of nothing but protein
– 2 weeks of nothing but fat
(of course, there’s trace amounts of the other macronutrients in each version)
Are you saying the fat loss is going to be equivalent? If you predict that, you’re wrong, and everyone can verify for themselves. On the carbs, you’ll lose a bit to nothing, and some might even gain. On the protein, you’ll lose a lot and on the fat, you’ll lose one giant hell of a lot.
I have done this on myself. You don’t even need 2 weeks each.
Here’s the best review of GCBC, along with a good smashing of the calorie is a calorie fantasy.
BTW, since I took my dog off the grains-based kibble food and replaced with high-fat meat and with a heaping teaspoon of lard added for good measure (he’s only 16 lbs.), he has dropped 20% of his body weight. Now 11-yrs-old, he’s more fit and active than when he was 6.
Fat is where it’s at. Anyone who actually eats that way knows, very well.
The success stories that you and your friends have had are consistent with the research on low-carb diets that highlight the role of calories. While in your mind you’re losing fat because you’re in a “low-carb environment”, the real reason you’re losing fat is because you’re in a “low-calorie” and “high protein” environment. One study that examined low-carb diets found that when people were left to eat ad-libitum (as much low-carb food as they wanted) they spontaneously ate 1000 fewer calories per day. Why? Well besides the fact that there is a reduction in food choices, all calories are coming from fats and protein, which are much more satiating (filling) than carbohydrates. Low-carb diets often suppress hunger. In addition, protein intake usually goes up significantly with a low-carb diet, and it’s well established that higher protein intakes are superior to lower intakes for fat loss.
For the above-mentioned reasons, many people do well on low carb diets. They can eat until they are full, they get more protein, and they end up eating fewer calories, without needing to count them. I think they can work well for a lot of people, though they fail for athletes in being unable to provide sufficient energy for high intensity exercise.
Back to my point, though… you can gain fat just fine in a “low-carb environment” if you eat more calories than you burn. People who are on low-carb diets routinely gain some fat back after great initial fat loss and then a period of maintenance. It’s a mistake to think that low-carb diets work because of some magic caused by low insulin levels. If you made sure the caloric content and protein content were the same, a high carb diet would work just as well for fat loss [PMID: 16331300]. Also, don’t forget that low carb-diets begin with a large decrease in body water, which deceptively adds to the sensation of success.
You are apparently confused about what maintenance means. It does not entail that your intake fixed. Nor does it entail that your expenditure is fixed. It means that whatever they are, they are matched, and energy is in balance. You say it doesn’t exist? How could it not? You’re either in a hypercaloric, maintenance, or hypocaloric state.
Your thought experiment with different macronutrient intake shows how clueless you are. First, realize that you’re not comparing equal protein content, like I stated. Second, unless you’re a very light female, you would definitely lose fat on a 1000 Cal/day diet from carbs. Fat loss on the pure fat diet would be about the same. I hope you realize that fat has a lower TEF (thermic effect) than carbs, not to mention that a zero carb intake will lead to a good amount of gluconeogenesis in the initial stages (meaning more protein loss and less fat loss). The pure protein diet would yield the greatest fat loss without a doubt, as it’s essentially a PSMF (protein sparing modified fast). Protein has a much higher TEF than either carbs or fat. In sum, you’re very confused.
To answer bryce, it’s neither. It’s not that you can’t gain fat in a low-carb environment (you can just fine). Nor is it that it’s really hard to lose fat on a high-carb diet (you can just fine when there’s a caloric deficit). It’s that low-carb diets help people spontaneously eat fewer calories and more protein. It’s a lower caloric intake and a greater net caloric deficit that makes low-carb diets successful.
That’s a good link Bill tossed up. That guy seems to get it. Just like everyone does who, rather than paying attention to dietary “studies” designed to confirm the prevailing view (rather than falsify, as real science does), goes the high-fat route, finds out for themselves, and dismisses the “experts” out of hand. That is, those of us who don’t heap scorn on a daily basis.
It’s a cause & effect reversal, i.e., we don’t get fat because we overeat, we overeat because we get fat. In my own case, it took years, and all I ever did was slow the progression from the point at which weight began creeping up. Finally, it was 2002 when I hit 200 pounds (5’10) and that was the last straw. I had two 3.5 mile courses laid out through nice neighborhoods and I set out. Religiously, every morning, five days per week. Five years and over 5,000 miles later I weighed 230 pounds at 35% BF. That was last May of 2007. Now, almost two years later I’m closing in on my goal of 10% BF, now 180 at 16-17%. There is no doubt whatsoever that I got fat by eating the wrong foods, with emphasis on bread in particular. As I got fatter, the urge to eat more and more was always there. I was eating more because I was fatter.
Begging Keith’s indulgence in another link to my own blog, here’s how I explained Taubes some months back.
You say we don’t get fat because we overeat, we overeat because we get fat. That’s not quite correct. Schoeller, an expert on doubly labeled water, recently addressed this in a review [PMID: 19136994]. He explains that it’s both. We get fat because we overeat AND we overeat because we get fat:
“Because energy can be neither created nor destroyed, obesity must result from a positive energy balance; yet weight gain increases energy expenditure, but this increased expenditure does not generally result in a return to energy balance and a halt to the slow increase in body weight. Thus, it is apparent that the mechanism underlying this annual weight gain for most individuals does not generally lie in a low energy expenditure in the face of an average energy intake, nor a high energy intake in the face of an average energy expenditure, but rather a continued imbalance between energy intake and expenditure. These differences, as discussed, are very small when presented on an average daily basis. Before weight gain, the energy intake and expenditure can be quite average but after the accumulation of excess fat to the point of obesity, both energy intake and expenditure will be higher than ‘normal’.”
That said, I hoped you noticed his mention of energy conservation, since comprehension of the laws of thermodynamics seems to be lacking. To quote the first sentence of Schoeller’s abstract, “Obesity is defined as the excess storage of energy in the form of fat that results from imbalances between energy intake and expenditure.” This is not an hypothesis. This is the laws of thermodynamics. If energy intake exceeds expenditure, there will be a surplus that the body stores.
Further, in the first few lines of the full text, Schoeller states “Energy can be neither created nor destroyed. Thus, the change in metabolically usable body stores is the difference between energy intake and energy expenditure, where energy intake is the metabolizable energy from the diet, and energy expenditure is the totality of all energy released as heat.”
Now if you want to argue that higher carb intakes are inferior because they have a negative effect on either intake or expenditure (for example, causing rebound hunger), then you have an argument consistent with the laws of thermodynamics for why carbs might lead to fat accumulation.
However, when you fixate on insulin, and suppose that a person cannot gain fat with the levels that are produced basally and from protein intake, you’re off in la-la land. Where does the extra energy go when you have a surplus of calories, but insulin levels that are elevated only from protein (i.e. low carb)? Is the body not able to absorb it? I don’t think so. Does the surplus get negated because of an isoenergetic increase in thermogenesis? Again, I don’t think so, especially considering that carbohydrates have an even higher TEF than fat does.
YOU have the burden of explaining how a surplus of fat calories on a low carb diet can fail to result in fat gain. And you must do it in a way that’s consistent with the laws of thermodynamics. There’s no good reason to think you’re right (all you have is uncontrolled anecdote), and plenty of reasons to think you’re wrong (the laws of thermodynamics and a large body of controlled research).
“For the above-mentioned reasons, many people do well on low carb diets…
…though they fail for athletes in being unable to provide sufficient energy for high intensity exercise.”
I’m almost afraid to ask, but what’s your supporting reasoning behind this bit of lunacy?
“While in your mind you’re losing fat because you’re in a “low-carb environment”, the real reason you’re losing fat is because you’re in a “low-calorie” and “high protein” environment.”
Not true in my case. When I first went at this I ate MORE, far more than I did before. Yes, lots more protein, but in terms of calories?
Before, a breakfast was a bagel and cream cheese. Lunch was a tuna or turnkey sandwich, sometimes with chips. Dinner was usually real food, i.e. a sirloin and salad, fish, etc. Once per week was pizza night, and I did always pig out there. And we might get fast food an ave of once per week. I’ve never been a sweets or dessert person, and I had been consuming diet beverages since college (I don’t like sweets that much).
Now, when I began this, breakfast was 6-8 strips of bacon, 4 eggs (with sour cream if in omelet form and always cooked in a 1/4 cube of butter, and sometimes a bit of fruit, tomatoes, or cottage cheese — every day. Lunch was at a local diner that has a great steak special and corned beef special, with a salad (blue cheese dressing). Hold the croutons. By this point, I’m already closing in on 2k kcals. Dinner was usually the same sorts of real food as before, but I became ver adept at various fat-based sauses, using butter, lard, coconut oil, sour cream, heavy cream, etc. Easily another 300-400 calories right there. Then, it was 1/2 to 1/2 pound of cheese and 3-4 handfuls of nuts in front of the TV. I also consumed a number of calories via alcohol (spirits, not beer / wine).
Did this day after day, engaged in high intensity training at the gym twice per week for 30 minutes, and weight began coming off. The more weight that came off, ONLY THEN DID I BEGIN EATING LESS, NATURALLY.
I sincerely thing you have cause & effect reversed, as I posted above.
“I think they can work well for a lot of people, though they fail for athletes in being unable to provide sufficient energy for high intensity exercise.”
How sure are you about that? Now, I’m no world class athlete, but if you go to my blog and check the Intermittent Fasting category, you’ll find that since I incorporated that about a year ago, I now do 90% of my workouts — not only low-carb — but fasted. Anywhere from 18 to as much as 36 hours, kinda like the state an animal would be in hunting prey. This has totally transformed not only my hunger mechanisms and my body composition (photos on website) but just my whole understanding of everything from an evolutionary perspective, which is why my focus is more on paleolithic eating, which will usually be low to moderate carb depending on fruit availability, and not so much low carb.
I think really weird things happen to metabolism for a lot of people when they ingest grains and processed vegetable oils. I am open to persuasion that’s it’s not really carbs at all (so long as consumed at natural levels) but processed foods, frankenoils, and all the derivative crap. However, my point would simply be that it’s those toxins that are causing fat accumulation, which in turn causes overeating.
” In sum, you’re very confused.”
Go do the experiment yourself, as I have.
“That said, I hoped you noticed his mention of energy conservation, since comprehension of the laws of thermodynamics seems to be lacking.”
Oh, my. Well, let me do a little quoting of my own.
“I was somewhat confused to see this. Surely the nutritional scientists did not not really believe this, right? I mean, any idiot undergraduate student knows that the 1st Law is only useful in a closed system, and humans live on the planet Earth, not in an insulated box. Right?
Enter a rebuttal by G. Bray in the journal Obesity Reviews. Bray is a to be a major obesity researcher and one of the 2nd tier villains in the book. Taubes relates a story of Bray excising a section of a British report on obesity, where Bray removed the material pertaining to the relationship between insulin and obesity. He clearly has editorial support to make his case. Bray is one of the second-tier villains in Taubes’ book. Taubes has a footnote (p. 421), which suggests that Bray actively suppressed the carbohydrate-insulin hypothesis.
*** According to Novin, when he wrote up his presentation for the conference proceedings Bray removed the last four pages, all of which were on the link between carbohydrates, insulin, hunger, and weight gain. “I couldn’t believe he would make that kind of arbitrary decision,” Novin said.***
Unfortunately, to a physicist this energy balance hypothesis looks like a silly hand-waving exercise, not a serious argument. Frankly I was flabbergasted when I first read this article. This conservation of energy argument is on the same scientific level as the ridiculous “drink cold water to lose weight” idiocy. A human organism is:
-Not in thermal equilibrium with their environment. Last time I checked I have a body temperature around 38 °C and spend most of my time in 21 °C rooms.
-Capable of significant mass flows (e.g. respiration).
-Capable of sequestering entropy (e.g. protein synthesis).
Is wearing a sweater fattening (by insulating you from your environment)? Here’s a quote from the rebuttal,
***Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result. An energy deficit produces weight loss and tips the balance in the opposite direction from overeating.***
According Bray’s thermodynamics argument, wearing sweaters makes you fat. This illustrates the greatest fallacy of trying to apply the 1st Law to a human: it makes the implication that living organisms consume kilocalories for the purpose of generating heat rather than perform useful work (i.e. breathing, contracting cardio and skeletal muscle, generating nervous action pulses, etc.). In reality heat is the waste product of basal metabolism. The first law does not distinguish between different types of energy. Heat, work are all equal under the First Law of Thermodynamics.
Applying the 1st Law to living organisms is Proof by Tautology. Yes, 1 + 1 = 2, but this tells us absolutely nothing about the underlying mechanics. The 1st Law does not (I repeat N-O-T) tell us whether you store excess energy in the form of fat, or bleed it off into the atmosphere by dilating blood vessels next to the skin, sweating, etc. To do so would require an accounting of entropy.
What would a semi-rigorous description of the thermodynamics of a human organism look like? Look at the title strip on the top of the page. See that equation in the background?
This type of equation would be a bare starting point for energy balance in a complex system like a living organism. Good luck actually accounting for all the terms. Those Σs are sums.”
The above quoted from here:
I believe, as a physics (condensed matter) Ph.D. candidate, that you are applying the 1st law of thermodynamics incorrectly. Now I’m not a world expert on thermodynamics, but I have TAed the 3rd year thermo course for mechanical engineering twice, and I have graduate level courses in the subject on my transcript.
The 1st law, or conservation of energy, is only valid for a closed system, which humans clearly are not. I’m constantly losing body heat to my environment, breathing out CO2, taking bathroom breaks, etc. I’ve not seen a study that attempts to break down each input and output flow through the envelope of our skin, as any reasonable application of thermodynamics would require. In fact, since we are machines and we are both generating and destroying entropy (think protein synthesis) we also have to incorporate the 2nd law, which greatly complicates any such analysis.
Realistically a proper thermodynamic analysis should include all heat flows, all mass flows, changes in entropy, and the amount of work generated. I have not seen this done for a human; if you have, I would be interested in seeing such an analysis and what approximations had to be made.
Claiming that any surplus of energy must go into adipose tissue is clearly not supported by thermodynamics. What prevents it from simply being radiated away as heat or increased motion? Since you cannot answer that question, the thermodynamics argument must be discarded as invalid.
The ASP research you cite doesn’t support your position as strongly as you claim either. Please see Cianflone’s review, “Critical review of acylation-stimulating protein physiology in humans and rodents.” I’d like to direct you to a particular section:
see section 3.4:
Finally, the most intriguing finding was that although the KO mice were leaner, food intake was much greater (up to 18% more caloric intake) with a normal fat absorption , raising the question: Where does all this energy go? How does the lack of ASP result in repartitioning and disposal of excess energy? The balance of body energetics would predict that any calories ingested, and not stored in some form, would have to be expended as energy. The major options are increased activity or enhanced thermogenesis. Preliminary results presented at a recent meeting (late breaking abstract, NAASO 2001) demonstrated increased oxygen consumption in KO mice, but no changes in overall activity, suggesting alternate disposal routes in the absence of efficient adipose tissue storage.
While we ascribe the differences in the KO mice to the absence of ASP rather than C3 (for the reasons outlined above), it would be important to test this further in a mouse that has C3, but not the capacity to generate ASP (such as in a factor B or adipsin KO mouse). One fascinating area to probe will be the control mechanisms between energy storage and energy utilisation, and the mechanisms by which lack of ASP results in a shift to increased oxidation.
Please notice that Cianflone is the senior author on the references you provided. To suggest that we have a complete understanding of human physiology and that ASP is a fatty acid analogue to insulin-glucose would be inaccurate, in my opinion.
I have expanded on my original comments regarding ASP on my own blog:
It does appear that insulin is the primary regulator of ASP expression after all, so Keith was correct. You two are merely arguing proximate versus immediate causation.
Conciliator, I would like to thank you for pointing out the role of ASP in lipid-protein metabolism. I wouldn’t have otherwise thought to look at such a specialized area of metabolism. It may well be the missing link in the metabolic advantage of low-carbohydrate diets. A very interesting result for almost no work on my part.
Why, in your opinion, is this (wrong application of the first law of thermodynamics) so difficult to see for nutrition/obesity researchers? Hell, I’m a hack/laymen, and it still makes perfect sense to me that the first law just cannot be applied to a living organism. Is there so little cross-disciplinary interaction in academia? Vested interests? Pride? Admittedly, this is a semi-rhetorical question, but I’d still like to hear from someone inside the “machine”, so to speak.
I took one semester of Thermodynamics in college (electrical engineering major), in lectures the prof used various machines and systems as examples to demonstrate a point and put it to a tangible level.
The human calorie in/calorie out “machine” was mentioned by a student in trying to grasp a concept and the prof quickly showed the error in this. The professor pointed out human metabolism is far from a closed system and impossible to use to explain any laws of thermodynamics in a simplistic manner (especially an interdisciplinary intro to thermo course).
It could be done, but the the human body grows and breaks down tissues (muscle, bone, nerves, connective tissue, etc), produces heat, wastes energy/conserves energy, respirates, produces waste products, grows, shrinks, adapts, survives, thrives, dies. Very very difficult to control for all those variables that occur simultaneously in any mammal’s metabolism, so it is very naive to claim the first law of thermodynamics says “a calorie is a calorie”.
The prof, an engineer, understood it clearly as not applicable to metabolism, the fellow student (an exercise physiology major) had already been indoctrinated to the “calorie in calorie out” message (we all are fed that daily, I certainly never thought to question it until recently) and saw it all as a simple matter that the human metabolism must obey the laws of thermodynamics.
I’m certain our metabolism does indeed follow all the laws of thermodynamics, it is just the the system is so complicated that different pathways are taken depending on the macronutrients given. X number of calories from fat, will be used differently than X number of calories from carbs, but both pathways no doubt follow the laws of thermo, just how can we nail it down in such a convoluted system?
I’ve seen the change in my own diet (eliminating carbs) has radically changed my metabolic systems to the better.
Exactly! Human metabolism isn’t a closed system. Do these “educated” idiots who spout “a calorie is a calorie and nothing else matters” realize just how stupid they sound?
An interesting review. I should point out that you left out the part about growth hormone.
Imagine growth hormone being the Yin to Insulin’s Yang.
(Growth hormone regulates Fasted metabolism, Insulin regulated fed state metabolism.)
I think you would really enjoy the body of research on growth hormone and fat/glucose metabolism.
“I should point out that you left out the part about growth hormone.”
Good get. Thanks for pointing out that omission.
The silence is deafening around here.
I wish I could understand everything Robert wrote in his blog post. Looks like an opportunity to study so that I’m not so “confused.”
Inside the machine? …haha, no not really
“Now, it’s obvious to the most casual of observers that caloric restriction below the basic metabolic rate (BMR) and total calorie expenditure will result in weight loss”
Now what exactly is it you are looking for from me? Don’t disagree with the quote above and thats all I was getting at in the other discussion, so I’m not sure what you’re getting at.
Restate your question, please. We wasted a lot of time in our last discussion arguing two different points entirely. I’m not concerned with overall weight loss (or weight gain, as the case may be). I’m only interested in discussing fat loss and/or lean tissue gain/maintenance (or a combination of the two).
Tim’s comment sums it up, you can technically evaluate a living organism by the laws of thermodynamics, but it is very complicated and it’s likely you will get errors propagating through the derived system of equations. It hasn’t been done satisfactorily to the best of my knowledge, and I from what I know of physiology, we absolutely do not have all the pieces of the puzzle yet, so some approximations would have to be made. It would probably involve putting a mouse in a sealed box and waiting for it to die under fixed conditions. Analytical physics is very much the method of approximations, and where those approximations break in special cases (e.g. superconductivity).
The problem with
delta(E) = E_in – E_out
is the logic. E_in – E_out -> if delta(E) is positive an organism gains weight isn’t valid, or what we say is the conclusion doesn’t follow the hypothesis. It’s well understood by any lay-person that if one consumes an excess of calories, those excess may result in fat deposition, but it also may result in increased activity or it also may result in thermogenesis (the production of heat for no reason other than to produce heat).
Where the nutrition establishment falls flat is proving that an excess of calories obligates an organism to increase fat deposits. That is absolutely wrong. Similarly, a negative energy balance may result in fat loss, but it could also result in reduced thermogenesis. People on semi-starvation diets typically feel cold, right?
This is why the quotes I dug up on Acylation-Stimulating Protein (ASP) are so interesting: they show that there exists a hormonal way in that thermogenesis or increased activity is used to burn off excess calories instead of fat storage. It’s the “missing link” that shows why on a biochemical level, macronutriets (like carbohydrate intake) and other endocrine factors (like steroids, sex hormones, inflammation) can effect the flux of glucose and fatty acids in and out of fat tissue.
As to why the field of medicine has trouble with math, well, that’s an on-going issue with all the soft science (i.e. everything but physics, chemistry (physics of the outer electron orbital) and biology if I’m feeling charitable). Biology is gradually becoming more physicified (or to use a real word, quantifiable) so the results using gene expression or other parameters are far far stronger than they would have been forty years ago. In medicine you have a large influential group that are essentially body technicians (i.e. surgeons) who have essentially no interest in understanding the underlying physics/physiology (same word, historically speaking). If we eliminate cardiovascular disease there’s no market for heart stents.
If you look at the flow chart for research and development, it goes:
scientists -> engineers -> technologists/technicians -> users
So scientists do the research, then engineers apply that research to do design (development), and finally technicians service and deploy the technology. The medical/nutrition field is trained at a technician level. Some get professor positions and filter up the ladder but they weren’t trained as scientists and don’t have the pre-requisite, fundamental skills.
It’s probably important for me to note that KO mice are those that are genetically unable to manufacture ASP. They are uniformly lean and eat more. Otherwise, it’s mostly a matter of going through the vocabulary item by item and understanding what each mix-mash of letters and numbers is.
I hope this discussion continues, because I’m learning a great deal. I didn’t know much about ASP before, and since I’ve read this, I’ve learned more about the metabolic pathway than I have since my days as a BioMed student at Carnegie. Thank you to every poster here!
Some posters seem keen to point out that consumed fat is primarily turned into body fat through the ASP pathway. Therefore, eating fat can make you fat. I don’t have a problem with the assertion that you can gain fat by eating fat. However, I haven’t seen much from these folks that talks about how much more quickly or slowly, or to what degree, sugar/carbohydrate are turned into body fat when compared with consumed fat being turned into body fat. Are we not considering that part of the equation?
It seems like we are comparing apples to oranges when we say “insulin isn’t primarily responsible for fat loss, because ASP is the main converter of ingested fat to body fat.” I believe that it is true that ASP is the mechanism that turns ingested fat to body fat, but it doesn’t address the conversion of consumed carbohydrate, specifically refined carbohydrate, to body fat. It’s like some are trying to assert that, because the fat to fat pathway doesn’t involve insulin much, that insulin isn’t a key player in body fat. What about the carb to fat pathway? Did we somehow just forget about this? We went through all this trouble to prove that fat is converted to body fat w/o insulin. This doesn’t disprove that insulin turns carbs into body fat. At all. Am I wrong?
We also decided not to discuss the idea that insulin causes our bodies to stop turning over fat stores. Anytime this is mentioned, people get called “insulincentric low-carb crazies” or something like that. Sure, there are other ways to get fat, but what about the fact that insulin does present an obstacle to fat loss? I think it is great that when insulin is accused of being the only fat storage vehicle, an intelligent discussion on ASP developed. Now let’s hear this discussion develop around how insulin interferes w/ body fat store turnover. Or around the propensity of ingested fat to trigger this body fat turnover.
Though I think that Ian and Concilliator are certainly doing a great job of adding to my knowledge of human metabolism, I think the best thing, for me personally, about this discussion is that my confidence in the Paleo diet remain unshaken. The Paleo community touts itself as being a “think for yourself,” “question the system” group, but I’ve occasionally found myself hitting the ‘I believe’ button occasionally just because I trust people like Keith, Richard, Mark Sisson, etc, due to their continued output of quality information.
Now I can say that I’ve officially questioned my beliefs, thanks to Ian and Concilliator, and found them to stand firmly as the dust settles. Nothing that has been discussed here has cast doubt in anyway from the fact that when I eat Paleo, I am leaner, healthier, more energetic, stronger, more durable, and feel more rested, focused, and well than I EVER DID on ANY RESTRICTED CALORIE diet that had a ‘normal’ carb intake.
Is it possible that I eat less? Yes. Occasionally I do eat in the vacinity of 1400-1500kcal a day. Frequently, however, I eat 3000+. I’m 185, 6ft, and maybe 12%bf, down from nearly 22% in 1 year. Is 3000+ my base caloric need? doubtful. I think that a low carb diet causes you to eventually require less food as your metabolism normalizes. This isn’t a ‘hole’ in the low-carb argument, it’s an amazing bonus to it. However, I also think the low-carb diet allows you to occasionally, even frequently, eat in a caloric surplus, and not gain weight, as the added calories lead to increased energy levels, body warmth (I feel less cold when i eat a lot now!), and etc.
I’m sure I’m “an idiot” for missing something, so let me have it.
You’ve brought up a good point about why (in my opinion, at least) the current western diet is such a disaster for the human genome (hell, any genome); a high franken-fat (vegetable oil, etc.), high simple carbohydrate combination is the worst of all possible dietary worlds. Now you’ve got the combination of ASP and insulin calling for fat storage, coupled with insulin’s shutdown of fat storage release. One thing that struck me many years ago, and really got me to questioning the American diet, was returning stateside after military deployment — really, you get numb to the American mall scene, until you’ve been (and I’m sure you’ve noticed this as well, Bryce) removed and desensitized by what large gatherings of “normal” people look like. Fat is (or was, at least) the exception in the larger world. Coming home to the ubiquitous “mall waddle” is quite a shock.
“Nothing that has been discussed here has cast doubt in anyway from the fact that when I eat Paleo, I am leaner, healthier, more energetic, stronger, more durable, and feel more rested, focused, and well than I EVER DID on ANY RESTRICTED CALORIE diet that had a ‘normal’ carb intake.”
Alright, Bryce, just another “uncontrolled anecdote.”
I have a bunch of ’em too, only I call them: the real lives of real people.
I seems fairly evident to me now that ASP is a lower level mechanism to insulin and other endocrine factors. The originating author, Cianflone, did ask the question in her earlier review as to whether ASP is a paracrine (local) hormone or if it has body-wide influence (endocrine). I think, from what I’ve read, that it’s paracrine. That implies that measuring things like blood serum ASP concentration isn’t very helpful since it’s only supposed to act at the tissue scale.
Wow, thats some good “taking research waaay outta context”
Now to be serious
Where the nutrition establishment falls flat is proving that an excess of calories obligates an organism to increase fat deposits. That is absolutely wrong. Similarly, a negative energy balance may result in fat loss, but it could also result in reduced thermogenesis. People on semi-starvation diets typically feel cold, right?
I think you are either taking the nutrition field out of context or have created a strawman so you can bash it down.
Provision of calories to an organism does not immediately result in fat gain, or reduction does not immediately result in fat loss. Through changes in activity, thermogenesis etc. However, these changes are also reflected in the overall energy model of the individual. If eating X food magically increases tehrmogenesis, this is measureable energy loss from the organism. If eating X food decreases thermogenesis, this is also measurable.
This doesn’t disprove that insulin turns carbs into body fat
there is plenty of work available showing that denovo lipogenesis is a pretty trivial pathway.
You say “Claiming that any surplus of energy must go into adipose tissue is clearly not supported by thermodynamics.” No one disputes this and no one has said this. What I did say is that “If energy intake exceeds expenditure, there will be a surplus that the body stores.” This is very straightforward. I also said that to “have an argument consistent with the laws of thermodynamics,” you’d have to explain the inferiority of a high carb diet (or the superiority of a low-carb diet) in terms of an effect on either intake or expenditure. I talked about obvious candidates such as absorption or thermogenesis, which I think fail as explanations. I never said that any surplus of energy must go into adipose tissue, however I do think that most will in most situations. That’s the whole purpose of adipose tissue, to store surplus energy.
You ask, “What prevents it from simply being radiated away as heat or increased motion?” The answer is nothing. Questions of efficiency or spontaneous activity are not problems to the law of thermodynamics as it realtes to animals. In humans, wasted energy (in the form of thermogenesis) is an integral part of energy expenditure. Note that you talk here about a “surplus” being radiated as heat. However, radiated heat would be treated as expenditure, not surplus. For example, say you have a maintenance caloric intake of 2000 Cal for a given diet/activity level. Say you increase your protein intake by 500 Cal while keeping all else constant. If 200 of those calories were lost as heat due to TEF, you wouldn’t treat them as surplus, but an increase in expenditure. In this case, your intake is 2500 Cal and your expenditure is 2200 (2000+200). The surplus is 300 Cal. There’s no conundrum here. Issues of inefficiency are part of energy expenditure. If you take something like DNP that uncouples oxidative phosphorylation and that releases massive amount of energy as heat, what you’ve done is increase expenditure.
You say that “Since you cannot answer that question, the thermodynamics argument must be discarded as invalid.” What on earth are you talking about? The thermodynamics argument is not invalaid at all. As Schoeller explained, “Energy can be neither created nor destroyed. Thus, the change in metabolically usable body stores is the difference between energy intake and energy expenditure, where energy intake is the metabolizable energy from the diet, and energy expenditure is the totality of all energy released as heat.” Everything I’ve said fits within this simple framework. It’s not hard to comprehend.
What I don’t understand is why you think a higher-fat, lower-carb diet is going to increase energy expenditure compared to a low-fat diet. We’re not talking about ASP KO mice here. We’re talking about humans. Research shows that reducing carbohydrates and increasing fat content produces no metabolic advantage (unless you focus on studies with poor controls, differing protein intakes, or no accounting of early water loss).
Take, for example, this long term study [PMID: 17413100]. They compared a moderate-fat diet, high in monounsaturated fatty acids (MUFA) with a low-fat diet (LF). After 6 months of administration, they examined 24-hour energy expenditure (EE) using indirect calorimetry in a respiration chamber. What happened is exactly what I’ve been saying would happen: “The major finding of the present 6-mo controlled dietary intervention was a tendency toward a lower 24-h EE with the MUFA diet than with the LF diet, but this trend did not remain after adjustment for changes in FM and FFM. However, the LF diet produced a significantly greater MIT [thermogenic effect] than did the MUFA diet, both acutely and after the 6-mo chronic exposure. Moreover, there was a slight decline in SPA [spontaneous activity] in both diet groups, with a trend toward a greater decline in the MUFA group than in the LF group, particularly during sleep. BMR was unaffected by the diet.” I’m sure you’ll point out that this was not a low-carb diet, but what difference does it make with where you draw the carb cut-off? There’s data showing that a ketogenic diet provides no more metabolic advantage (which is none) when compared with a non-ketogenic diet.
You quote Cianflone for evidence that “The ASP research you cite doesn’t support your position as strongly as you claim.” Yet nothing in the quote serves to detract from the importance of ASP or the references I’ve provided. In fact, it clearly shows that ASP plays a massive role in fat regulation, crucial for fat storage. Why on earth would you interpret that quote as meaning that ASP is anything less than incredibly significant to fat regulation?
I don’t know where you got the idea that “it appears that insulin is the primary regulator of ASP expression after all.” The research review that you reference in your blog states quite the opposite: “With the many factors that change postprandially or in insulin-resistant states such as diabetes, it is difficult to pinpoint exactly which component might be responsible for the stimulation of C3 and ASP production. Experiments with cultured human adipocytes have demonstrated that insulin (to a moderate degree), but especially chylomicrons, appear to stimulate both C3 and ASP production [44–46]. On the other hand, Koistinen et al.  showed that a euglycemic (4 h) hyperinsulinemic clamp had no effect on C3 mRNA levels.” That’s far from saying that insulin is the primary regulator. She said insulin has a moderate effect, and that it’s especially chylomicrons.
One of Cianflone’s most recent studies (done years after that review) examined the effects of insulin on ASP [PMID: 18702682]. She explained that “Production of ASP by adipose tissue is stimulated by postprandial chylomicrons, which enhances the cleavage of complement C3 to generate ASP. 24,25 In vitro, insulin also increases C3 and ASP production from human adipocytes. 26 However, little is known of the acute or chronic influence of hyperinsulinaemia on ASP regulation in vitro or in vivo.” So she examined the effects of increased insulin (via euglycaemic/hyperinsulinaemic clamp), this time in vivo.
The dicussion states: “Our results highlighted the wide interindividual variations of ASP levels in response to the EHC, even in a selected group of relatively homogeneous obese postmenopausal women. ASP values changed over the course of the EHC from –60% up to 250% relative to fasting levels.” In sum, there was no consistent effect. Of the 76 subjects, 42 had an increase in ASP, 24 had a decrease, and 10 had no change. Compared with those who showed a decrease in ASP, those who showed an increase demonstrated “a more compromised metabolic profile, with increased body weight, BMI and visceral adiposity, as well as increased fasting insulin and HOMA index [insulin resistance].” The group showing a decrease in ASP in response to insulin was the healthiest. Insulin is hardly the “primary regulator.” It’s a known modulator, with differential effects.
You’ve taken the ASP research completely out of context and are now making the unfounded argument in your blog that it supports the idea of a low-carb metabolic advantage. It doesn’t. Your argument is that:
1. Insulin is the primary regulator of ASP
2. Low-carb diets produce low insulin levels
3. Low-carb diets result in low ASP levels (from 1 and 2).
4. In ASP KO mice, the effect of ASP is lost
5. ASP KO mice are lean, despite eating more food
6. ASP KO mice demonstrate a metabolic advantage from the lack of ASP
Conclusion: Low-carb diets reduce ASP, similar to the KO mice, and people on a low-carb diet demonstrate a metabolic advantage, similar to the KO mice.
What’s so insane with this argument is that it’s not insulin, but fat intake (chylomicrons), that stimulates ASP production. If anything, this is an argument for the metabolic advantage of a low fat diet. Your first premise is completely incorrect, as explained above in the quotes from Cianflone’s recent study. And that’s not to mention that it’s a leap of faith to equate low ASP levels with a pathological KO state, but I guess that’s not so surprising when you consider low-carb proponents are always trying to equate a low carb diet with other pathological models like type 1 diabetes.
A good litmus test is this: If you’re on a diet in which you have to count calories, you’re on the wrong diet. And, you’re also unlikely to succeed because fighting hunger is a losing battle.
It seems you have questions about the “carb to fat pathway” or “how much more quickly or slowly, or to what degree, sugar/carbohydrate are turned into body fat when compared with consumed fat being turned into body fat.”
The answer is that sugar/carbohydrate is rarely converted to bodyfat. This pathway is called de novo lipogenesis (DNL) and it’s rare. Even massive carb copnsumption will result in only a few grams of fat being produced. For example, one study found that after administering 500g (2000 Calories) of dextrin maltose, there was synthesis of only 4-5 g of fat [PMID: 3799507]. Another study overfed subjects by 50% for 96 hours with either sucrose or glucose. They estimated that during that time only 2-10 g of VLDL was synthesized. Carbs are rarely converted to fat. Rather, they get oxidized for energy or stored as glycogen. However, they can obviously still make you gain fat by decreasing fat oxidation [PMID: 6755166]. Basically, when you eat carbs, the carbs are preferentially used for energy. This displaces fat that otherwise would have been burned, which is then stored. It only time you’ll get appreciable DNL is when glycogen levels start maxing out, after days of carbohydrate overfeeding.
Also, no one is saying that “insulin isn’t primarily responsible for fat loss, because ASP is the main converter of ingested fat to body fat.” Both play a very large role. It’s interesting that research has shown that ASP levels after a meal have a direct positive correlation with fat synthesis, whereas insulin does not [PMID: 9555951].
So Conciliator, etal —
Put your theory to practice in the real world. You’ve just been hired by Oprah, and she wants fat–loss results — lasting results (because, hey, she doesn’t need to relive the embarrassment of past failures). She’ll be 100% compliant; whatever you say, goes. What will you have her do?
I’ll entertain the red herring:
Like I said, I think low-carb diets work well for a lot of people. Generally, protein intake increases and caloric intake spontaneously decreases. People tend to lose weight on them. They’re not bad diets, especially for people who don’t do well watching calories. I just don’t think they’re magic. It’s not impossible to gain fat on them, though that’s probably unlikely initially.
No red herrings, no verbal traps — just trying to see how you’d apply your interpretations of these studies to a real-world situation/client. We read the same studies, but interpret them differently, and, being the curious sort, I’d just like to find out why. For instance, I don’t think that it’s impossible to gain fat, over- eating (whatever macro nutrient) in a Paleo way. As I mentioned in another discussion (w/Ian, maybe?), it’s my belief (no studies to back this, only gut feeling) that there is some mechanism by which the action of the ASP pathway is enhanced in people as body fat levels approach a certain point (men, 7-ish% — women 12-ish%, for example). This makes sense in evolutionary, survival terms. If this were not the case, of course, the Paleo dieter, (even in the complete absence of carbohydrates) would just continue to melt away body fat on into the low single digits (and on into death). The flip-side of this, of course, is that there seems to be no corresponding, upper-level regulation/feedback mechanism; but there was never an evolutionary pressure to produce one. In my mind, then, one must apply the correct diet manipulations to the applicable situation, and the first question that must be addressed is, what is the current body fat level? I would love to see a study done on very low BF individuals to measure the relative hormonal/enzymatic response to various macro nutrient stimulus. Again, just my gut feeling, but there seems to me to be classical/quantum physics-like transition in relative hormonal/enzymatic action at very low body fat percentages. To your average Joe, though, who just wants to lose some flab and feel healthy and well, this is of no matter, as he’s well within the “classic physics” zone. Bodybuilders, wrestlers and the like? Different story, and different dietary tweeks must be employed, one of which is calorie restriction. Now personally, I’d still employ a Paleo diet under calorie-restricted conditions and maintain carb intake nil (most of the time), but that’s another discussion entirely. Anyway, this is why I think that we have to first define the starting point of the “dieter/client” before we discuss the importance of (1) overall calorie intake and (2) relative hormonal/enzymatic response.
Thanks Conciliator. Once again, I learned something new.
I notice that we didn’t really get into trying to disprove the claim that insulin precipitates a shut-off of FFA release from atipose, stopping the ‘turnover’ of fat. This is a claim the Paleo crowd makes, and one that from my own personal experience w/ perceived energy levels, I’m highly inclined to agree with. Do you think this effect is overestimated, or false?
Also, you mention appreciable adipose gain, directly from ingested carbohydrate, can only happen from carbohydrate consumption, through the DNL pathway, when glycogen stores ‘start maxing out, after days of carb overfeeding.’ Do you not think most American’s are currently in such a state?
Few people really deplete their glycogen stores with rigorous, frequent aerobic and anaerobic activity. Even in the service, I’d say it’s a minority of people who exercise with the intensity to do this. I can’t believe the people reading People Magazine while plodding along on the elyptical at a glacial pace are doing so. On top of that, Americans eat pancakes covered in syrup, big bowls of sugar cereal, huge muffins, coffee filled with sugary creamers, and juice, and that’s just breakfast. Doesn’t this qualify as carbohydrate overfeeding? Even if they’re eating ‘healthy,’ they’re eating weight watchers bagel and orange juice, sandwiches with light potatoe chips, wheat pasta, and etc. Still an amazing carbohydrate load.
The studies you mention seem to adress single instances of over consumption of carbohydrate, and their effect. What about the effect of chronic over consumption of carbohydrate (a state that most people I personally know are in, as described above). Are there studies addressing the resulting DNL in subjects who are in this overfed state, and are eating this way every day? By your own admission, once glycogen stores are full, DNL can start contributing to body fat. How can their levels be anything but completely full.
Maybe my understanding of glycogen turnover in the musculature is lacking.
Keith & friends,
I can’t debate with the scientists in the group and I am not an expert on much of anything dietary, but I know what works for me. My eating plan (notice I didn’t say “diet”) mirrors Keith’s with the exception that I include raw milk products…because I can.
One observation that I would like to make/share is that low carb and paleo are not the same thing and should not be used interchangeably. I use Paleo protocols to help achieve low-carb intake in a healthy way. Similarly I include IF and seasonal eating into my plan. They all work together.
Low-carb in and of itself, achieved in unhealthy ways, will eventually have unhealthy outcomes and is not a panacea. One migbht lose weight, which might not mean anything other than a lighter coffin in an early grave.
I have absolutely nothing to back this up scietifically…but I know that commercially produced and packaged pork rinds and low-carb candy are not healthy the same way I know that playing in traffic or jumping off of a bridge aren’t healthy. I don’t need a journal citation to back me on this.
And this is really all that matters. The rest is mere commentary. BTW, I’m leaning toward a trial run with raw, unpasteurized milk. I can get a partial “cow share” through my local co-op, so I think I might give it a go. I’d still like to get some feedback from Dr. Connelly first, though.
There are two things being argued here:
2. Body Composition
There has been a lot of talking past one another (save for a few posts) in this thread. Assuming protein is high enough, one could get lean with the remaining calories being skittles, as long as there is a deficit and in spite of the insulin. I wouldn’t want to do it this way, but I have no doubt that it would achieve the desired effect.
My health, on the other hand, might not like it.
Yup, no doubt about that Skyler. Cut intake low enough and the weight will come off. Unfortunately, much of it lean tissue. For some people, though, the scale is the only thing that matters.
You say it’s your belief that “there is some mechanism by which the action of the ASP pathway is enhanced in people as body fat levels approach a certain point.” You say “If this were not the case, of course, the Paleo dieter, (even in the complete absence of carbohydrates) would just continue to melt away body fat on into the low single digits (and on into death).”
It seems to me that you think a paleo diet will necessarily result in fat loss because insulin levels are low. Yet that’s clearly not the case, as we’ve hashed out. Further, you seem to think that there must be something countering the low insulin as body fat levels drop (such as a rise in ASP). This shows a disregard of caloric intake (which is primary) and instead, a short-signed focus on insulin and the regulation of storage/lipolysis.
Instead of thinking this is a matter of ASP (storage pathways) based on a gut feeling, you should be looking at calores and hunger. Leptin offers a much more convincing explanation. Leptin is produced by bodyfat and leptin levels increase as fat mass increases (scaling incredibly closely to fat mass). Leptin regulates bodyweight by reducing hunger. As people get leaner, leptin levels get lower and hunger increases. With increased hunger, food intake increases, which leads to weight gain. All this regulation can occur with no change in fat storage hormones like ASP.
If you’re eating a paleo diet (or any diet), you’re not going to lose fat unless you’re eating fewer calories than you’re burning (assuming proper protein intake). You ask, what stops you from “melting away body fat on into the low single digits”? Assuming you’re in a caloric deficit and losing weight, there are two clear answers based on caloric intake. One, as you lose weight your metabolism will drop more and more, since you have less body mass to maintain. There’s also possibly an adaptive component dropping it even more. So even if you keep eating the same amount of food, your expenditure will drop as you lose weight until it matches your intake. At that point, you’re not going to be losing any weight.
However, intake probably won’t remain the same. It usually increase as you get leaner, since hunger tends to increase. All in all, set point/settling point is largely a matter of calories, regulated by hunger. If you’re thinking low insulin = fat loss, such that something opposing low insulin (like ASP) must be acting to prevent fat loss from occurring indefinitely, you’re ignoring the things that matter, like hunger and caloric intake/expenditure.
“It seems to me that you think a paleo diet will necessarily result in fat loss because insulin levels are low. Yet that’s clearly not the case, as we’ve hashed out.”
Our differences arise from your insistence upon looking at the available relevant studies through the prism of employing the 1st Law of Thermodynamics in studies of the human organism, whereas I reject the notion of applying the 1st Law to the human organism. On this we won’t agree and, therefore, our assessment of each hormone/enzyme’s influence upon fat storage and/or dissipation will forever be at odds. This is fine by me, as I’m not in the business of changing minds. I simply report what I do as it relates to diet and fitness, and why I do it. I’ve taken my interpretation of the available science and applied it in the lab of the real world (which is all that ultimately matters to me); my blog is about chronicling those results. All I’m asking you to do now – now that you’ve fully clarified your theory — is to demonstrate the application of your theories in the lab of the real world. Take your interpretation and apply it to the “Oprahs” of the world; tell us how you would have her eat and train. Then tell me what you would do different with a wrestler (already less than, say 8% BF) trying to shed a few pounds of fat while maintaining muscle mass, strength and adequate energy levels. This is the “mission statement” if you will, of my blog – to take from science that which can be practically applied to diet and fitness pursuits.
All “theory” and no “practice”, Conciliator?
Most of this sails right over my head, but here’s my contribution from:
“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law. Homeostatic mechanisms are able to insure that, a good deal of the time, weight does not fluctuate much with changes in diet – this might be said to be the true “miraculous metabolic effect” – but it is subject to many exceptions. The idea that this is theoretically required in all cases is mistakenly based on equilibrium, reversible conditions that do not hold for living organisms and an insufficient appreciation of the second law. The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.”
‘Nuff said. Thanks for the link, nonegiven.
I don’t know half of what your discussion was about. When in college – I majored in graduation.
Anyway, I started following a paleo way of eating 4 months ago. I haven’t exercised a single minute. I lost 40 pounds – while eating more calories. When I ate the foods that are supposed to be “good for weight loss” I gained weight – while eating less calories.
So, by my personal example I don’t believe that a calorie is a calorie. The type of calorie makes the difference and no scientific study is going to convince me otherwise. If this is ignorance in the face of overwhelming evidence, then ignorance is definitely bliss.
And real-world results are ultimately what matters. What can be realistically practiced, and what can be realistically sustained in the course of everyday living? The rest, as I’ve said, is mere commentary. Interesting for folks like me, but still, mere commentary.
This is very up-to-date info. I think I’ll share it on Facebook.
I just have to say, this is a fantastic explanation. Thanks.
To give another point of view on the matter:
“We did not confirm previous findings that low-carbohydrate or high-protein diets caused increased weight loss at 6 months and that the advantage of these diets usually eroded by 12 months, with weight loss that was nearly or fully equivalent to that with low-fat diets or other diets. Other studies showed increased weight loss at 1 to 2 years with diets that were high in unsaturated fat or with low-fat, high-carbohydrate vegetarian diets. These divergent results suggest that any type of diet, when taught for the purpose of weight loss with enthusiasm and persistence, can be effective.”
This was from one of the very few long-term studies on the subject: