Jun 2012 29
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Chris writes:


Eades is tweeting a new study he says proves metabolic advantage:


I've not read the thing yet but his followers were claiming this refutes you. It is not clear how the participants were controlled, but I'd be interested in your views.

Anthony replies:

It's always an interesting exercise to sit back and watch the die-hard adherents of certain diets loudly and victoriously trumpet a new study as confirmation of their beliefs, when a quick examination of the study in question reveals a completely different story.

And so it is with the recently-published JAMA study that has the ever-hopeful residents of Low-Carbia wetting themselves in delight. If they'd actually bother to read the study instead of twitting/tweeting/twatting about it (or whatever sending messages on that poncey "Twitter" website is called), they'd soon learn their enthusiasm is highly misplaced.

Before I explain why, let's take a quick look at the long-held but repeatedly disproved myth that isocaloric low-carbohydrate diets cause greater weight loss.

The Metabollocks Advantage: A Quick Primer

Low-carb Metabolic Advantage Dogma (MAD) claims that at a given daily caloric intake, low-carb diets cause more weight loss than higher carb diets because of some magical mysterious freakazoid metabolic process that even the MAD believers themselves have never been able to coherently explain let alone provide actual evidence for.

MAD is, quite frankly, complete nonsense. As I explain in great detail in The Fat Loss Bible, metabolic ward studies dating as far back as 1935 have repeatedly shown that when caloric intake is truly kept equal, there is absolutely no difference in fat-derived weight loss between low-carb and high-carb diets.

I say "fat-derived", because some studies show low-carb diets often cause excretion of greater amounts of fluid (and criticial minerals such as sodium, potassium and magnesium along with it). There was also a study (discussed in FLB) that showed one male did indeed lose more weight on a low-carb diet, but that weight didn't come from his waist - he blew it right out of his keester. Yep, the poor guy got diarrhea while following the wonderfully healthy low-carb diet he was assigned to and experienced weight loss in a somewhat more explosive fashion than he did when on the higher carb diet.

The bottom line is that when people are taken out of their free-living environments (where researchers have absolutely no control over what they really eat) and placed in a ward environment where they are watched and all food is supplied to them, there is absolutely no difference in fat-derived weight loss between high- and low-carb diets.

Because low-carbers have shown themselves to be a little challenged in the comprehension department, I will repeat this once more:


And that's a fact, Jack. One rather cocksure low-carb "guru" tried his darndest to dispute me on this, and needless to say, it didn't go too well for him:

The Great Eades Smackdown, 2010! Part 1

The Great Eades Smackdown, 2010! Part 2

Defective Metabolism versus Defective Logic

I will also point out that this failure of low-carb diets to exert a metabolic weight loss advantage has been noted in normal weight, overweight and diabetic volunteers. I mention this because, when presented with overwhelming proof their cherished beliefs are garbage, rather than admit they were wrong most people will quickly scramble for some kind of rationalization or excuse. In the case of low-carbers, the oft-repeated cop-out clause is that the ward studies didn't involve people with "metabolic defects".

Well, that's a most interesting avenue of denial, considering that "metabolic defects" only became important to the low-carbers after it was pointed out to them that their diet repeatedly failed to show any weight loss advantage in tightly controlled ward studies. Nowhere in their hyperbolic books, promotional material or abundant online discussions on the subject did these people ever issue the disclaimer that a low-carb diet will only work for people with "metabolic disorders". Instead, we were told that the metabolic advantage was a universal phenomenon, and that we can all eat all the high-fat, low-carb foods we want and still lose weight.

Low-carb authors enthusiastically assured all and sundry that by cutting their carbs they would lose more weight at a given caloric intake, despite decades of research showing this claim to be utter hogwash. If the low-carbers truly believe the 'metabolic disorders' tale, where's the caveat in their writings that 'normal' folks can expect no such advantage? It's just a convenient excuse to try and slide out of a tight spot and salvage some credibility for their pet belief.

This readily-transparent escape clause is more than just disingenuous - it's scientifically disproved nonsense. Those who trumpet the "metabolic disorders" rationalization often cite a study by Cornier et al (Obesity Research, 2005; 13: 703-709) in support of their case.

Cornier and his team compared diets of lower- and higher-carb content and found those with insulin resistance lost more weight on the lower carb diet. The Cornier et al study was not a ward study, and so the short term results again could be (and in all likelihood were) explained by differences in caloric intake. The way to eliminate this possibility would be to ensure the two groups really did consume isocaloric diets by placing them in a metabolic ward.

Before I discuss how metabolic ward research blows the metabolic disorders argument to smithereens, I should point out the Cornier findings were hardly universal even in free-living scenarios. As I state in The Fat Loss Bible, differences in insulin resistance and blood sugar control are in no way a reliable predictor of weight loss in response to calorie restricted diets in obese women:

McLaughlin T, et al. Differences in insulin resistance do not predict weight loss in response to hypocaloric diets in healthy obese women. Journal of Clinical Endocrinology & Metabolism, 1999; 84 (2): 578-581.

de Luis DA, et al. Differences in glycaemic status do not predict weight loss in response to hypocaloric diets in obese patients. Clinical Nutrition, Feb 2006; 25 (1): 117-122.

Due et al placed overweight and obese subjects on a calorie-restricted diet and randomly assigned them to take the insulin-lowering drug diazoxide or a placebo for eight weeks. While diazoxide did indeed lower insulin levels, no differences in weight loss, fat loss, resting energy expenditure or appetite were observed between the two groups.

Due A, et al. No effect of inhibition of insulin secretion by diazoxide on weight loss in hyperinsulinaemic obese subjects during an 8-week weight-loss diet. Diabetes, Obesity and Metabolism, Jul 2007; 9 (4): 566-574.

So if the metabolic defect of insulin resistance is such a game-changer when it comes to weight loss, why did these studies find it was inconsequential?

The knockout punch was delivered by Miyashita et al, who administered low- and high-carb diets to diabetics under ward conditions and found no difference in overall weight loss or fat loss in type 2 diabetics. I think it's pretty safe to say that diabetics, with their seriously screwed-up blood sugar metabolism, readily qualify as having a metabolic disorder (some would argue that the regular overweight subjects used in ward studies, who often exhibit several metabolic irregularities, also qualify as metabolically defective subjects, but we'll leave that discussion for another day...).

For the one or two of you out there who actually bother to obtain and read the Miyashita study (I know I'm being optimistic) and read it in full with an impartial mind, you'll note there was less visceral fat in the low-carb group at the end of the study. Don't let low-carb shysters convince you that this constitutes a metabolic advantage - again, overall fat and weight loss did not differ between the 2 groups.

There is a phenomenon known as repartitioning, where slightly more fat is lost and slightly more lean mass preserved or gained while overall weight loss remains the same (increased protein intake has been observed to exert this effect in a number of trials). In this study overall fat loss did not differ but a repartitioning effect appeared to be taking place with more fat lost from the visceral region. I'm betting a similar phenomenon would have been observed in the Miyashita study had an intelligently-prescribed low-GI diet also been employed.

Anyway, keeping this near-80 year history of repeated MAD failure in mind, let's take a closer look at the JAMA study that seems to have everybody's panties in a twist.

JAMA Reports the Metabolic Advantage that Never Was

The study involved 21 overweight and obese young adults (mean age 30) and was conducted at Children’s Hospital Boston and Brigham and Women’s Hospital, Boston, Massachusetts, between June 2006 and June 2010.

Each participant went through the study in a number of phases. The first was a 4-week weight stabilization period, which was followed by a 12-week period in which all subjects consumed a run-of-the-mill RDA-type diet in which calories were restricted to achieve a 12.5% bodyweight loss. After the weight loss period, the subjects underwent another 4-week weight stabilization period.

Then came the bit that matters: In alternate and randomly assigned 4-week weight maintenance phases, each subject followed a low-fat (mean carb intake of 310g/day), low–glycemic index (205g carbs/day), and very low-carbohydrate diet (50g carb/day). The three diets were isocaloric, designed to provide 100% of caloric needs in order to continue weight maintenance.

All subjects received a daily multivitamin and mineral supplement, and all subjects received a Metamucil supplement during the low-carb phase in order to counter the well-known turd-retention effects of ketogenic diets.

Oh, and contrary to claims being made by people who evidently believe it's cool to comment on studies they clearly haven't read, this was not a metabolic ward study. Except for the final 3 days of each 4-week test diet period, the entire study was conducted under free-living conditions.

So What Happened?

OK, before I report the results, I must reiterate that this study - published only 2 days ago - is already being loudly paraded all over the Internet as proof of the metabolic weight loss advantage for low-carb diets.

Which is most interesting when one considers absolutely no such advantage was observed during the study. In the researchers' own words:

"Body weight did not differ significantly among the 3 diets (mean [95% CI], 91.5 [87.4-95.6] kg for low fat; 91.1 [87.0-95.2] kg for low glycemic index; and 91.2 [87.1-95.3] kg for very low carbohydrate".

Bodyweight was virtually identical during all three isocaloric diet phases which to me, as a rational indvidual whose head has never been embedded in his culo, quickly refutes the famous low-carb claim that greater weight loss will occur on a low-carb diet at a given caloric intake. At the caloric level calculated by the researchers to maintain weight, the low-carb diet did exactly what the other diets did - it maintained weight. It did not magically produce further weight loss while the other diets simply maintained the status quo.

I could by all rights end the discussion there, but the interesting thing about this study is that the lack of difference in weight status during the 3 diets is being roundly ignored by the very same low-carb advocates who are parading this study as proof of a metabolic weight loss advantage.

Instead, they are wanking on and on about an allegedly greater increase in resting energy expenditure and total energy expenditure experienced by the participants during the low-carb phase. This increase in REE and TEE, they are claiming, is proof that low-carb diets produce greater weight loss - even though the low-carb diet didn't produce any weight loss at all.

Got that?

Let's take a look at what the researchers wrote, and then let's take a look at the actual tabulated data. According to the researchers:

"Energy expenditure during weightloss maintenance differed significantly among the 3 diets...The decrease in REE from pre–weight-loss levels, measured by indirect calorimetry in the fasting state, was greatest for the low-fat diet [–205 kcal/d], intermediate with the low–glycemic index diet [–166 kcal/d], and least for the very low-carbohydrate diet [−138 kcal/d].

The decrease in TEE, assessed using the doubly labeled water method, also differed significantly by diet [−423] kcal/d for low fat; [−297 kcal/d] for low glycemic index; and [−97 kcal/d] for very low carbohydrate".

Neither total physical activity nor time spent inmoderate- to vigorous-intensity physical activity differed among the diets."

Wow, so the low-carb claim that low-carb diets speed up your metabolism really is true, yeah?


It Takes 3 To Make a Thing Go Wrong

Take a look at Figure 3 from the study:


As you can see, it contains 2 graphs; the LHS one shows the changes in REE on each diet, while the RHS graph shows the changes in TEE.

You'll notice that there are 21 black dots lined up above the title of each diet - these represent each participant of the study (the REE graph only shows 20 people for the low-carb diet, as the data for one of the subjects during this phase was considered to fall into extreme outlier territory and was duly ommitted).

Anyway, in between each diet (dot) you'll notice a straight line drawn. This line represents the increase or decrease in REE and TEE that occurred in each subject from one diet to another. As an example, cast your eyes on the 1st vertical row of dots in the TEE graph. Look at the dot second from the bottom; it shows a drop on TEE on the low-fat diet of around 1000 calories per day, but the line rises to the low-GI dot, which shows a drop of only 400 cals a day. The line then plunges back to almost 1000 calories a day again as it arrives at the low-carb dot.

Yes, that's right - in this subject, the low-carb diet caused a similar greater drop in TEE as the low-fat diet when compared to the low-GI diet. I guess his low-carb "metabolic advantage" went AWOL or something...as it evidently did for numerous other participants. If you track the line from the low-GI diet to the low-carb diet on the REE graph, you'll see that five participants experienced greater drops in REE and one experienced little change on the low-carb diet when compared to the low-GI diet.  Compared to the low-fat diet, these subjects experienced similar or greater declines in REE. In other words, they experienced the exact opposite of what the low-carb cheerleaders are proclaiming about this study.

On the TEE graph, 8 of 21 subjects experienced greater declines in TEE on the low-carb diet when compared to the low-GI diet, and four of these folks experienced similar or greater declines in TEE than they did on the low-fat diet.

So you can see that the true story is a little more complicated and somewhat different to the one low-carb shills are trying to portray. Rather than a clear-cut case of reduced drops in REE and TEE during a low-carb diet, the indvidual results are in fact much more haphazard, with some subjects in fact showing markedly greater drops in REE and TEE during the low-carb diet.

Meaning that if you adopt a low-carb diet expecting an increase in metabolism, based on the results of this study, there's a very strong possibility you'll be sorely disappointed. Heck, you may just suffer the same fate as other well known purveyors of this belief and be forced to don a belly-restraining girdle to hide the contradictory evidence hanging from your waist.

Things got a little crazy backstage at the 2012 Low-Carb Fashion Awards.

The marked individual variation notwithstanding, when these somewhat random results are pooled together, it does produce a lower aggregate drop in REE and TEE during the low-carb diet.

Now why would that be?

Well, it certainly wasn't because the subjects' thyroids went into overdrive on the low-carb diet; as previous research has repeatedly shown, the low-carb diet resulted in the lowest T3 levels. T3 levels were similar on the low-fat and low-GI diets.

Leptin levels were highest on the low-fat diet, intermediate on the low-GI diet, and lowest on the low-carb diet. Given that leptin levels decline along with REE during dieting and that researchers have prevented this drop in REE by injecting leptin into obese subjects undergoing weight loss, the differences in serum leptin would be expected to have favoured lower EE declines during the low-fat and low-GI diets.

The researchers also measured HDL and total cholesterol and triglycerides, but these have been shown to have pretty much sweet FA influence on EE and weight loss.

Insulin sensitivity was also measured, but as I explained above, clinical research has repeatedly shot down the cherished low-carb "insulin makes you fat" fairy tale.

Which leaves us with cortisol and CRP.

CRP (C-reactive protein) tends to be elevated during inflammatory states such as illness and infection. While CRP was lower on all three diets compared to the pre-weight loss baseline, it remained highest on the low-carb diet (CRP levels were almost identical during the low-fat and low-GI diets).

For the three diets, cortisol excretion measured via 24-hour urine collection was 50 μg/d for low fat, 60 μg/d for low glycemic index; and 71 μg/d for very low carbohydrate. This adds to the numerous other studies showing carbohydrate restriction to increase cortisol levels (I've written about this here).

So what we appear to have here, folks, is a metabolic milieu during the low-carb diet that indicated a more catabolic and inflammatory state.

In other words, in the subjects that did experience lower declines in REE and TEE during the low-carb phase, the culprit may have been increased catabolism. If so, the lower drop in EE was not necessarily a good thing - it may have in fact been reflective of harmful rather than beneficial processes occurring in the body.

We do know that in humans, induction of hypercortisolism via hydrocortisone administration increases EE, and that this increase in EE accompanies an increase in protein breakdown and synthesis.

Obviously, there's a difference between the degree of cortisol elevation you'll experience when receiving regular injections of hydrocortisone designed to induce hypercortisolism and when following a low-carb diet. Nonetheless, low-carb diets have been shown in clinical trials to raise cortisol levels and to increase catabolism - and to simultaneously increase protein synthesis and breakdown. It's not a huge stretch to suspect that a lower-grade but chronic state of catabolism and inflammation produced the increases in EE and TEE seen in some of the subjects during the low-carb diet. The subjects who experienced these increases may have been more sensitive and susceptible to the catabolic, inflammatory effect of the low-carb diet.

So much for a metabolic advantage. If heightened catabolism and inflammation constitute an 'advantage', then I'll give it a miss, thank you. I'll stick to my highly disadvantageous regimen of intelligent nutrition and regular exercise that sees me maintain with minimal fuss the kind of single-digit bodyfat levels most low-carb devotees will only ever be able to dream about.

What's especially pathetic about this whole situation is that the JAMA study is being cited in the media as proof the "calorie is a calorie" theory is now dead in the water, and that low-carb diets may offer an advantage for weight maintenance in the long-term.

Reality check:
A diet that elevates your cortisol levels, depletes you of critical minerals, and has been shown repeatedly to induce euthyroid sick syndrome, is likely to be about as advantageous to long term weight loss as surgically implanting an anvil in your gut.

Take Away Points From This Article:

1. The Low-Carb "Metabolic Advantage" theory remains as big a wank as ever.

2. Learn to think for yourself. You know, outlaw motorcycle gang members refer to themselves as 1%ers, but here's a news flash for ya: If you develop an independent, impartial, analytical mindset and learn to truly think for yourself, you'll be a .01%er. Yep, 99.9% of human beings can't think for themselves to save their banal lives. Interestingly, governments are far more threatened by .01%ers than 1%ers, which is why traditionally they have gone to much greater lengths to oppress and eradicate the former.

3. Read studies for yourself. Anyone can write any old bullshit and then cite a bunch of studies that appear to back it up (hi Pee Pee!). The only way you'll know whether or not they're yanking your chain is if you read those studies for yourself. Yeah, I know this means doing shit like reading and thinking, which will cause your brain to experience the strain of effort, but you'll get over it. Like other muscles, the brain gets stronger with regular use.

4. Trust a low-carb shill no further than you can throw him (or her). These people are dietary sectarians, and like most devoted sectarians they will pretty much say and do anything to support their beliefs. The funny thing about prominent low-carbers is that the vast majority are overweight; one rather well-known proponent of these diets is downright obese. Umm, tell me again how your low-carb diet gives you a fat loss "metabolic advantage"?

5. Develop a high degree of skepticism towards diet, health and nutrition 'information' in the popular media. Your average journalist wouldn't know a scientifically valid nutrition fact if it climbed up his/her ass and started a bonfire. Journalists typically receive press releases sent to them by researchers, drug companies, government agencies, PR firms, etc, and assume these jokers are all valid sources of information. Which means that if the story in the press release is deemed newsworthy, it makes it into print or onto your screen with virtually no critical analysis beforehand. Very unawesome.

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

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