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But he still eats O6 oils and wheat and other grains. Just not flour (ground grain of any kind) and sugar. He still is a compulsive overeater (I've witnessed some binges) and is still somewhat fat. He was a gourmet before and still is now, so it's not like he made a dramatic drop in junk food. He mainly ate a lot of pasta before he adopted the diet change. His metabolic syndrome is gone and so is his now-thin wife's. They are members of a group called Food Addicts in Recovery Anonymous.
Very interesting. How can he still eat wheat but not flour?
He can eat wheat berries or rolled wheat/rye/barley. I don't think he eats much of it. He does like multi-grain hot cereal. He can eat corn, not tortillas or chips. He can eat rice, preferably brown, but not rice noodles.
It's probably the acellular carbs and the higher fiber. He gets no carbs without the fiber it came with. He is a binge eater, not thin, but he's pretty active (he was before, too, I met him on the Pacific Crest Trail) so he can keep from total obesity. Looks like a powerlifter. His wife is skinny. You'd never know she lost 130lbs. They are both in their 60s.
Female, 5'3", 50, Max squat: 202.5lbs. Max deadlift: 225 x 3.
The main problem with the notion of metabolic advantage is that it is incoherent, expressed in a confusing manner, and lacking any workable definition, as far as I know. The first mention of the term within the context of dietary approaches that I could find comes from Dr. Atkins' Diet Revolution which contains an entire chapter entitled "Is There a Metabolic Advantage? You be the Judge." While Atkins talks about the "metabolic advantage", he doesn't go so far as to define what that means. The best I could do was this, from Wikipedia :
Originally posted by Wikipedia
Metabolic advantage is a term used in nutrition to describe the ability of a diet to achieve greater weight loss (or less weight gain) than another diet of equivalent calories.
This definition sounds very much like the thermic effect of food, diet induced thermogenesis, specific dynamic action of food, or whatever name you favour from the scientific literature. But if you look at this collection of synonyms, it is quickly apparent that metabolic advantage is different from the others, because it alone contains a value judgement: whatever it is that "metabolic advantage" refers to, that is a good thing, a thing you should want, because it is beneficial.
As a rule, however, scientists don't speak like this. Is diet induced thermogenesis a good or bad thing? That's a qualitative question that cannot be answered because it lacks context. The most a scientist would be willing to do is to offer you a quantitative answer, that is, for a given meal, what percentage of the caloric content would on average be metabolically available. So who does speak in emotionally charged language? Well, politicians, marketing and salespeople, preachers, and in general, people with an agenda who are trying to convince you of something, but who lack the concrete data to do so.
Even if we are to concede that scientists would utilize such a label, the definition itself is problematic and counter-intuitive because it implies that it is somehow advantageous to have a diet that consists of poorly assimilated "nutrients." This being the case, we should all switch to eating copious quantities of soluble fiber, because we cannot digest it and must rely on the microbiota of the large intestine to ferment it to short chain fatty acids that we can absorb. Or, we should all take to eating our food raw, because cooking improves bioavailability of nutrients, and increased bioavailability of nutrients runs counter to the principle of "metabolic advantage." Another technique we could adopt would be to not chew our raw food, because the decreased surface area would result in more difficult digestion, which would thereby increase the "metabolic advantage" of making assimilation of nutrients less efficient. Taking this to its logical conclusion, the ultimate "metabolic advantage" would be attained by eating things that we cannot digest at all, like wood. This, of course, is absurd.
While nobody is advocating eating wood, we have seen carbohydrates being touted here as being more beneficial relative to fats due to their presumed higher thermic effect. Where does this notion come from, and if indeed there is some difference between consuming carbohydrates and fats, what exactly is the magnitude of this effect?
In "The Effects of High Protein Diets on Thermogenesis, Satiety and Weight Loss: A Critical Review (2004)", researchers Thomas Halton and Frank Hu performed a meta-analysis of 15 studies pertaining to the thermogenic effects of protein ( bear with me, we will get to carbs and fats in short order ). Here's what they had to say:
Originally posted by Halton and Hu
In general, the typical thermic effect of protein is 20%35% of energy consumed and for carbohydrate, this number usually falls between 5% and 15%. The thermic effect of fat is a subject of debate. Some have found that fat has a lower thermic effect compared to carbohydrate, while others have found no difference between the two.
Immediately, we see that the fat vs. carbohydrate thermic effect is a contentious issue. The research is inconclusive, and studies exist that both support and refute the notion that there is a "metabolic advantage" to carbohydrates with respect to fats.
It should also strike you that there are some ridiculously broad ranges that are being claimed. The higher end of the estimate for the thermic effect of carbohydrates ( 15% ) is triple that of the low end ( 5% ). If you took your car in to the mechanic to get an estimate for the cost of performing some repairs and he told you anywhere from $500 to $1500 dollars, you would probably come away thinking that your mechanic really didn't know what was wrong with the car, and he was just making up some numbers.
Nevertheless, what is consistently found in studies is that protein has a significantly ( and in this case I'm using the word both as statisticians would, and as normal people would ) higher thermic effect than the other macronutrients. But so what? How would this "metabolic advantage" translate in the real world?
Originally posted by Halton and Hu
In a recent review of high protein diets, Eisenstein and Roberts estimated that for a 8,374 kj diet with 30% protein compared to 15% protein, there would be an increase of 96 kilojoules a day due to thermic effect.
This study measured dietary energy in kj, not calories, but the conversion factor is 4.2 kj per kcal, so the diet above consisted of 2000 kcal, and the "metabolic advantage" of doubling the dietary amount of the most thermogenic macronutrient was ... 23 kcal per day. Or, in other words, about 1%. Which means that on a 4000 kcal diet, this would amount to an underwhelming 40 kcals. To put it bluntly, if you are relying on a daily caloric deficit of 23 kcal to make an impact on your body composition, you are setting yourself up for failure.
Of course, carbohydrates have a much lower thermic effect than protein, so if you are hoping to achieve any results with respect to body composition by exploiting the TEF of carbs, this is nothing more than wishful thinking, and you are probably better off scanning the nightly skies for falling stars to achieve your goals.
In 2004, the journal of Nutrition and Metabolism published another review article on diet induced thermogenesis by Klaas Westerterp which entailed a meta analysis of the results of 22 studies. Even though each of these studies made use of mixed meals, the data Westerterp collected allows us to calculate an implied value for the thermic effect of carbohydrates. If we assume that the TEF of protein is 15%, fat 3%, then this implies a TEF for carbohydrates of 6%.
Armed with these numbers, we can then answer some other interesting questions, such as: if you were to be consuming a diet consisting of 2000 kcal in the form of 30% protein, 70% fat, and no carbohydrates, what would be the "metabolic advantage" ( i.e. increased TEF ) achieved by swapping the fat for carbs? That is, by eating a diet comprised of 30% protein and 70% carbohydrates? I hope that you're sitting down, because your "metabolic advantage" is a whopping 40 calories.
But wait, recall that we assumed that the TEF of protein was 15%, which is actually below the range of 20% - 35% cited by Halton and Hu. What if we used 20% as the TEF for protein? What does that do to the metabolic advantage of swapping our 70% fat calories for carbohydrates? In that case, the implied TEF of carbohydrates becomes 4%, and the "metabolic advantage" of the swap is a paltry 14 calories!
The takeaway from all of this is twofold:
"metabolic advantage" is nothing but a counter-intuitive marketing term, and
if you are attempting to achieve any meaningful results, you won't do so by fiddling with the TEF of carbs relative to fats, you need to manipulate your protein, but even this represents a premature optimization, there are probably other low hanging dietary fruit that you should be going after.
(P.S. If anyone is interested in the calculations for the implied TEF of carbs, just message me)
I am personally alluding to hepatic insulin resistance, which is induced by the excess accumulation of FFAs. Within the hepatocyte, metabolites of the FFA re-esterification accumulate. These excess FFAs cause relocation of several protein kinase isoforms, from the cytosol to the membrane compartment. The membrane isoforms phosphorylate the intracellular portion of the insulin receptor which results in impairment of insulin receptor interaction with downstream insulin signaling proteins. These are all cut of the same thing, usually anyway. Obesity is just hypoxia of the cell leading to the activation of cellular stress response pathways causing autonomous inflammation and the release of pro-inflammatory cytokines, much the same as the interference from FFAs.
I still feel the way it was stated as "fat causes insulin resistance" is very misleading. Basically you have expounded on a mechanism of cell signaling. That does not prove in any sense that the ingestion of any type of fat is the culprit in the development of insulin resistance. I think we have all read studies that have induced IR through a variety of macro and lifestyle changes.... including non-dietary contributors like sleep deprivation, sepsis, and statin drugs just to name a few.
When it comes to Derpamix, I'm of two minds. Either he has a good grasp of metabolism and biochemistry and is purposefully misrepresenting things for some inscrutable reason, or, he has no clue and is like one of the blind men in the elephant parable, handling the tail, and telling us that an elephant is like a rope. My initial leaning was to think that he was one of the blind men, and the data points are increasingly mounting to confirm this view.
The latest datapoint comes from the above quote that Neckhammer pulled out. First of all, I will have to agree with Derpamix. FFAs do induce hepatic insulin resistance, with the effect being particularly pronounced with palmitic acid. Before anyone gets too excited by this concession, the problem is that we are diametrically opposed on the interpretation of this fact, with Derpamix arguing that it is pathological, whereas I maintain, and will maintain, that it is physiologically essential for survival.
From the standpoint of a hepatocyte, one day, you find yourself awash in palmitic acid. Being a curious but dutiful hepatocyte, you wonder what the source of this FFA bonanza is, and being well versed in metabolism, you understand that it is from one of two sources: it is either truly an unesterified fatty acid that has been circulating in plasma, or it is the result of the action of lipoprotein lipase on chylomicrons, the end product of intestinal absorption of a fatty meal.
Unfortunately, from your perspective you cannot directly ascertain the provenance of this palmitic acid, so you apply some heuristics to help you along. First of all, you know that palmitic acid is the predominant form of fatty acid stored in adipose tissue. Moreover, being a hepatocyte and intimately familiar with the process of de novo lipogenesis, you also understand that palmitic acid is the end result of endogenous lipid production. This leads you to suspect that the source of this FFA was endogenous, probably your adipose tissue, and not exogenously sourced from a meal.
You are also exceedingly well versed on the geopolitics of the body, and you understand that based upon your unique position in the circulatory system and your dominance of the portal vein, you get first crack at any insulin that is secreted by the pancreas, as well as any glucose absorbed from the small intestine. When you couple this understanding with the known actions of insulin on lipoprotein lipase, in your hepatocyte mind it becomes increasingly probable that this FFA is endogenously sourced. Your rationale is as follows: insulin suppresses lipoprotein lipase in all tissues save for adipocytes, where it is stimulatory. This being the case, in general, a hepatocyte would not expect to see FFAs under conditions of elevated insulin. But this does not jibe with what you are observing, elevated FFAs as well as elevated insulin. What are you to make of this?
Well, there is a reasonable answer to that question, and that is, you are entering a post-prandial period after a fasting state. During the fasting state, blood sugar and insulin levels drop, adipocytes take over and start liberating FFAs, and everything works like clockwork. Then you eat, and all of a sudden insulin starts to elevate, as well as plasma glucose concentrations.
As Sherlock Hepatocyte you also understand one final aspect of triglyceride dynamics. Specifically, due to the fact that triglycerides are absorbed not into the circulatory system, but rather into the lymphatic system, as well as due to the need to package triglycerides into plasma soluble lipoproteins ( the chylomicrons ) this delays the appearance of dietary fats by hours, as compared to the relative immediate appearance of glucose and the attendant insulin response.
Therefore, the case for the FFAs being endogenous looks to you to be solid. The implications of this is that if you are just entering the post-prandial state after a fast, because of your privileged access to both insulin and glucose, if you were to respond to insulin signalling at this point, you could easily induce hypoglycemia.
So, just to be on the safe side, you perform a risk analysis. You ask yourself about the potential impact of making the wrong assessment. That is, what is the downside of assuming that these FFAs are endogenous, when in fact they are not? You will then compare this to the downside of assuming that they are exogenous, when in fact they are not.
In the first case, if you assume that these are endogenous FFAs, when they are not, then you will not respond to insulin signalling. As a result, the body will experience a slightly longer period of elevated post-prandial blood glucose than it would have if you were responding to insulin signalling and drawing down blood glucose to synthesise glycogen. Meanwhile, adipose cells will respond to insulin signalling and cease FFA release, which will correct your confusing context, leaving you only with elevated insulin, at which point, you can follow the rules and start responding to insulin. All things considered, this scenario isn't of too much concern.
The second scenario, where we assume that the elevated FFAs are exogenously sourced, when in fact they are not, could lead us into hypoglycemia as outlined above, and this runs the risk of coma and brain death. Definitely not a desired outcome.
Accordingly, due to the asymmetry of the risk profiles of these scenarios, you, the ever cautious hepatocyte, play it safe, and do not initially respond to insulin signalling in the presence of elevated FFAs. Derpamix, say hello to physiological insulin resistance, the stuff that keeps you alive.
Metabolism, if you understand it, is a wonderful thing.
I stopped really reading(just glanced) after the first paragraph. Honestly, if you can't even begin your post without attempting to belittle someone, none of the rest is worth reading. I'm sure it's more of the usual cherrypicking(as well as a very long unsupported hypothesis) as you did earlier in this thread with polyunsaturated fats(which you never replied to), and ignoring the long downstream path and several isoforms and substrate interference that excessive FFAs cause.
Edit: I'll debate with you again when you can do it properly.
pklopp's posts are always so well-written and interesting.
I've also been frustrated with the confusion I witness regarding the difference between pathological states and those that are healthy but I'm not nearly as eloquent and learned to express myself properly.
Female, 5'3", 50, Max squat: 202.5lbs. Max deadlift: 225 x 3.