Applebee's Quesadilla Burger

One of my readers sent me a link to a segment on ABC News with Charlie Gibson showing just how disgustingly slanted and inaccurate mainstream media reports can be.

Gibson leads into the segment about two reporters who underwent self experimentation on the adverse effects of unhealthy eating.  The reporters, ABC’s Yuji de Nies and Jon Garcia, set out to see what would happen if they consumed a giant meal containing over 6,000 calories.  Here is the result as they reported it.

Pretty brutal, eh?  But let’s shine the piercing light of good sense on what is going on here.  As you might expect, the reality is vastly different from that portrayed by ABC.

First off, let’s look at the actual nutritional content of the food eaten.  As reported in the piece, the total energy content of the meal was 6,190 calories, which included 187 grams of saturated fat.  These were the only parameters reported.  I took the time to go through the links in the article accompanying the video to find exactly where these foods came from.  Here’s what I found.

The burger is an Applebee’s Quesadilla Burger (served with fries, of course); the snack is The Cheesecake Factory Fried Macaroni And Cheese; and the dessert is Uno Chicago Grill Mega-sized Deep Dish Sundae (listed as cookie below).  How do I know these are the exact ones?  These were the ones referenced in the CSPI’s List of Most Unhealthy High-Calorie, Fat and Salty Restaurant Foods That May Clog Your Arteries.  After seeing the photos and comparing to what I saw on the video, these selections are the ones the reporters ate.

I then tracked down the Nutritional Facts for the foods involved (here, here, here and here) and put them into an Excel spreadsheet.  Take a look.

The first thing you might notice is that the total calorie count is 5,708, which is considerable, but is actually 482 calories fewer than the 6,190 reported.  Second, and this is a biggie, the saturated fat content of this meal is only 88 grams, not the 187 grams reported.

The reporters stretched the truth a little in that they reported as if the Mega-sized Deep Dish Sundae were a single treat to be consumed by one person at a sitting.  I’m sure it could be so eaten, but it’s actually designed for four people to share.  The Nutritional Facts list the calories per serving as 690 and the saturated fat as 17 grams.  I’ve used the amounts in all four servings, i.e., one entire four-person dessert, in my spreadsheet.

As you may have noticed, the total carb content of the meal is 745 grams, which converts during digestion to a little over three cups (3.1 cups to be exact) of sugar.  The ABC report, of course, failed to mention the carb content of the meal and ignored any immediate effect this huge intake of carb might cause.  One of the reporters, Jon, claimed that he was ’sluggish’ and ‘tired’; the implication being that this sluggishness resulted from his huge saturated fat intake.  No mention, naturally, of the enormous amount of carbohydrate and the large increase in insulin release it might cause.  From what I can see from the video, Jon looks to be sporting a little abdominal obesity, which would imply a degree of insulin resistance and hyperinsulinemia.  People with this disorder tend to over secrete insulin in response to carb intake causing an overshoot and reactive hypoglycemia (low blood sugar), which will indeed result in sluggishness.

It’s pretty impressive when the lab tech holds up the tube of blood taken after the meal and compares it to the one taken before the meal.  There is a lot of fat swimming in the serum, that’s for sure.  What the producers of this piece (and, sadly, the doctors commenting although they should know better) want you to take away from all this by the way they set it up is that all that saturated fat went directly into the blood.  And how can you argue with them?  It’s there for all to see.

Problem is, that’s what blood samples look like after almost any meal, especially one that contains carbohydrates.  The fat you see isn’t the fat the two reporters ate; it is the fat the liver has made from the carbohydrate.  It’s the same picture a tube of blood would show after either of the two doctors had eaten a high-carb, low-fat lunch.

The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route.  The process that breaks down dietary fat into its component fatty acids is a lengthy process as compared to the breakdown of carbs.  Once the fat has broken down, it has to combine with bile salts to make it into a form that is water soluble and can be taken up by the intestinal cells.  Once taken up, unlike carbs, which are sent directly to the bloodstream, fats go into the lymphatic system, a much smaller and more static transport system than the vasculature.  Once in the lymphatics, fats make their way to the thoracic duct, which empties into a large vein in the upper chest.  The lymphatics are small vessels and take a long time to move their contents along since there is no heartbeat pushing them as there is with blood.  As I say, the fat in the blood you see on the video didn’t come from the saturated fat in the diet, although that was definitely the implication.

But what about the ultrasound showing the blood vessels had changed?  Wasn’t that because of the fat?

I’m afraid not.  The fat from the diet wasn’t in the blood vessels yet, so it couldn’t be the dietary fat causing the change.  So what was it?

How about a little normal physiology.  Let me explain.  The body gets blood where it needs to get it by opening certain blood vessels while closing others.  Let me give you an example.  Have you ever jumped into cold water to go swimming and noticed that not long after jumping in you have to urinate?  What happened?

Your arms and legs have a radiator effect.  Since these appendages have little padding the blood circulating there is exposed to the cold water, and if nothing is done, the cold water cools the blood creating a big problem.  Your body compensates by shutting down the circulation to the skin and areas close to the surface in your arms and legs and shunts that blood to your core.  Your core already has plenty of blood when this happens, so it has to get rid of some.  It does so by sending it through the kidneys where the liquid portion is filtered out and becomes urine.  Suddenly your bladder is full and you have to go.

The body has the ability to direct blood wherever it needs by its manipulation of blood vessel size.  Where do you think blood is needed after an almost 6,000 calorie meal?  That’s right.  The digestive tract.  It takes a lot of work to deal with 6,000 calories, and a lot of work requires a lot of oxygen, which comes from the blood.  So after a heavy meal, the body shunts extra blood to the guts where the works is being done.  It does this by opening or dilating the arteries carrying blood to the intestines and by narrowing the blood vessels in other parts of the body.

Now, think back to the video of the woman whose blood vessel (in her arm) is being examined by ultrasound.  When it’s compared to the previous ultrasound, the one before she ate, notice how much faster the heart is beating.  (The little swishing sounds you hear, each of which represents a heart beat, are spaced much closer together.)  The heart is beating faster because the body is working to digest an enormous amount of food, and this work stresses the heart in the same way that running down the street would stress the heart.  Work is work.

The digestive tract needs extra oxygen to do its work, this extra oxygen can get there only via the blood, so the intestines require more blood than normal.  This extra blood gets shunted there by opening the arteries that feed the gut and narrowing those that go other places where a lot of blood isn’t needed at the moment.  Such places as, say, a relaxed arm.

Anyone with a smattering of knowledge of normal physiology (and apparently an open mind) could predict that the artery in a relaxed arm would narrow after a heavy meal and that that artery would be back to normal six hours later (which it was so reported in this video).

What you’re seeing in this video is normal physiology at work interpreted as being abnormal by a couple of lipophobic doctors who should (and probably do) know better.  It makes for dramatic theater, but their interpretation is nothing but prevarication or ignorance or both.

But had they reported the truth, there would have been no story.  Kind of sad, isn’t it.

Instructor teaches Friedewald equation and bad cholesterol

This week sees the publication of yet another study showing the superiority of the low-carbohydrate diet as compared to the low-fat diet.  This study, published in the prestigious American Journal of Clinical Nutrition, demonstrates that subjects following the low-carb diet experience a decrease in triglyceride levels and an increase in HDL-cholesterol (HDL) levels; and that these changes are accompanied by a minor increase in LDL-cholesterol (LDL), which prompts the authors to issue a caveat.

Yes, although just about all the parameters that lipophobes worry about improved with the low-carb diet, the small increase in LDL has caused great concern and has prompted the authors to gravely announce that this small increase is troublesome and should be monitored closely in anyone who may be at risk for heart disease.  Since most people who go on low-carb diets do so to deal with obesity issues, and since obesity is a risk factor for heart disease, it would appear that this small increase in LDL often seen in those following a low-carb diet could put these dieters at risk.  Does it?  We’ll see.

Let’s take a look at the study. But before we do, let’s digress for just a bit and look at low-carb diet studies in general.

As we’ve discussed in these pages before, there are a couple of ways to do dietary studies in which on diet is compared to another.  You can compare a low-carb diet to a low-fat diet in a way that reflects what happens in real life.  For example, you could randomize your study subjects into two groups, then give those in one group a low-carb diet book (Protein Power, maybe) and those in the other a low-fat diet book (an Ornish or McDougal book, perhaps).  You would instruct both groups to follow their respective diets and come back periodically for evaluation.  When these kinds of studies are done, the low-carb diet invariably brings about more weight loss and greater changes for the better in just about all parameters.  But the folks who are proponents of low-fat diet cry foul.  Why?  Because in virtually all of these studies the subjects on the low-carb diet consume fewer calories than those on the low-fat diets.  Lower-carb, higher-fat diets are satisfying, and it has been shown over and over that those following such diets actually consume fewer calories while still feeling full than do those following ad libitum (eat all you want) low-fat diets.

So, the low-fatters attribute all the improvement in those on the low-carb diets as simply a result of their lower caloric intake.

If you want to eliminate this caloric-deficit difference from your study, then you design a protocol in which calories are the same in both the low-carb and the low-fat arms of the study.  This strays from the real-life way of looking at what is likely to happen when people buy diet books and follow them, but it does offer the advantage of getting rid of the calorie issue.

In these kinds of studies you randomize your subjects into either a low-carb or a low-fat diet group and put both groups on the same number of calories.  At the end of your study, you can see the differences between the two diets – if any – that are brought about without calories being an issue.

The study under our consideration today is of the latter type; it’s one in which both groups were kept on an equal number of calories, a so-called isocaloric diet.

Here’s the setup for the study titled Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo.

The researchers recruited 118 subjects who had abdominal obesity and at least one other metabolic syndrome risk factor and randomized them to either a low-carb or a low-fat diet for one year.

The diets were designed to be isocaloric with moderate energy restriction (≈6000 kJ/d [1433 kcal] for women, ≈7000 kJ/d [1672 kcal] for men). The planned macronutrient profile of the LC diet was 4% of total energy as carbohydrate, 35% as protein, 61% as total fat (20% saturated fat) with the objective to restrict carbohydrate intake to <20 g/d for the first 8 wk and to <40g/d (with the inclusion of an approved 20-g carbohydrate exchange) for the remainder of the study. The target profile for the LF diet was 46% of total energy as carbohydrate, 24% as protein, and 30% as total fat with the objective to restrict saturated fat intake to <10 g/d and <8% of total energy, with the inclusion of an approved food exchange (equivalent to the energy content of 20g of carbohydrate;) between weeks 9 and 52, so that the diets remained isocaloric.

Sixty nine subjects completed the study, and, fortunately, all the results reported in the paper were for the 69 completers, so we don’t have to worry about data contamination we would have gotten had the researchers done an intention-to-treat analysis.  We know how the people fared who actually hung in there for the entire study period, which is what we want to know.

And how did they fare?

Those on the low-carb diet lost 26 percent more weight than those on the low-fat diet (14.5 kg vs 11.5 kg), but the difference wasn’t statistically significant.  As you can see from the graph below of the weight loss between the two groups over time, the difference was widening, and we can extrapolate that the difference would have become statistically significant had the study gone on longer, but we can’t say for sure.

As for the other parameters, blood pressure, glucose, insulin, insulin resistance and C-reactive protein were the same for both groups.  There was a difference in lipid outcomes, however.

The LC [low-carbohydrate] diet also provided greater improvements in triglycerides and HDL cholesterol than did the LF [low-fat] diet, which occurred independently of differences in energy intake and weight loss. This finding is consistent with those of long-term ad libitum studies. High triglyceride and low HDL-cholesterol concentrations are 2 of the MS risk factors, a syndrome that is associated with an increased risk of type 2 diabetes and CVD. Elevated triglyceride concentrations have also been identified as an independent CVD risk factor, and the triglyceride:HDL cholesterol ratio is considered a strong predictor of future cardiac events and is a surrogate measure of insulin resistance. Our data show that the triglyceride:HDL cholesterol ratio was halved after the LC diet and was approximately double the improvement observed with the LF diet. A recent review suggests that biological markers typically associated with the MS are those improved by carbohydrate restriction, which suggests that LC diets may offer the greatest clinical benefits for overweight populations who are insulin resistant and have several metabolic risk factors.

So far, so good.  But now the other shoe is ready to drop.

Whereas the LC diet improved a range of cardiometabolic risk factors, greater increases in total and LDL cholesterol also occurred. Other studies that compared LC and LF diets reported similar findings, although the overall magnitude of the differences was smaller: 0.60 and 0.20 mmol/L in favor of the LF diet.

Let’s see how much the total cholesterol and LDL changed.

Those in the low-fat group started with an average total cholesterol of 212 mg/dl (5.5 mmol/L) and ended up a year later at same number.  These same subjects also started out with average LDL levels of 131 mg/dl (3.4 mmol/L) and ended up the same at the end of the study.  The low-carb dieters began the study with average total cholesterol levels of 209 mg/dl (5.4 mmol/L) and ended the study a year later with average total cholesterol levels of 232 mg/dl (6.0 mmol/L).  Their average LDL levels started at 124 mg/dl (3.2 mmol/L) and ended up at 147 mg/dl (3.8 mmol/L).

The authors of this study bestow great significance on this fairly minor increase in LDL levels in those subjects on the low-carb diet.  In their summary of the results of this study, they list the many benefits of the low-carb diet, then end on an ominous note:

However, these potential benefits may be counteracted by the detrimental effects of an increase in LDL cholesterol, which should be monitored…

The abstract of the study echoes this warning.

However, the increase in LDL cholesterol with the LC diet suggests that this measure should be monitored.

It was my impression that the tone of the authors was one of a little foreboding.  Kind of a ‘this looks too good to be true, and, hey, look at those LDL levels; it is too good to be true’ aura about it.  But is it too good to be true?  Is the rise in LDL seen in most low-carb diets the hidden stinger?  Is what all the lipophobes say true?  You know, the old ‘Well you may lose weight on those diets, but you’ll clog your arteries at the same time.’

It’s all hogwash, of course, but before we get to the heart of the explanation as to why, let me remind you that numerous studies have shown that whenever subjects go on low-carb diets, they end up increasing the size of their LDL particles.  Large, fluffy LDL particles are not only harmless, but may be protective.  If they are protective, what’s wrong with having a bit more of them?

At the same time, numerous studies have shown that low-fat diets usually decrease LDL levels, but do so while reducing the particle size.  Followers of such diets end up with lower levels of LDL made of smaller, denser, more atherogenic particles, which, in my mind, isn’t a good trade off.

The authors of our paper acknowledge this fact and cite some of this research, but they are still fixated – as are most lipophobes – on LDL levels.  They just can’t get their heads around the notion that there is more to cardiovascular risk and health than LDL-cholesterol.

Since these researchers placed so much emphasis on LDL levels in their interpretation of all the data from their study, I got to wondering how they measured LDL levels.  I looked in the Methods section of their paper and found the following:

Plasma glucose, C-reactive protein, serum lipids, and apolipoprotein B (apo B) were also measured by using standard methods (11).

The #11, of course, means that the description was in another paper that I had to go to the trouble of looking up.  I always find it annoying when authors do this when they could just as easily stick a short paragraph in their paper and save people who really want to read it critically a lot of trouble.

Tracking down the other paper in the Journal of the American College of Cardiology, I found the following:

The LDL-C was calculated according to the method described by Friedewald et al.

What this means is that the researchers did not measure LDL levels directly in their study subjects, but calculated them using the Friedewald equation.

For reasons we don’t need to go into here, LDL is fairly difficult (as compared to total cholesterol and HDL) to measure.  It can be done, but it’s expensive.  So instead of measuring it directly, most labs calculate it based on an equation derived by William Friedewald and others in 1972.

Friedewald realized that it was pretty simple to measure total cholesterol, HDL-cholesterol and triglycerides.  He knew that total cholesterol was the sum of all the various subfractions of cholesterol, which can be presented by the following equation:

Total cholesterol = HDL-cholesterol + LDL-cholesterol + VLDL-cholesterol

Rearranging this equation to solve for LDL gives us this one.

LDL = Total cholesterol – HLD – VLDL

Friedewald knew that it was easy to measure total cholesterol and HDL but difficult to measure the others.  His insight was that the triglyceride level if divided by five could give a close approximation of VLDL.  In running his experiments he also realized that this relationship held only if triglyceride levels were 400 mg/dl or under.  If they were over this, all bets were off.

So, Friedewald substituted triglycerides (TGL) divided by 5 for VLDL in the above equations, giving us the so-called Friedewald equation for calculating LDL.

LDL = Total cholesterol – HDL – TGL/5

And this is how it is still done in labs all over the world 27 years after Friedewald’s paper.   If you’ve had a lab report showing an LDL figure, I can guarantee it was calculated by the Freidewald equation and not measured directly.

What’s wrong with this if it works?  Nothing.  If it works.  Problem is, it doesn’t always work.  Friedewald himself found that in subjects with triglyceride levels greater than 400 mg/dl the equation didn’t hold.  Anyone reading this who has had a lipid test showing triglycerides greater than 400 will have note on their lab report saying that LDL couldn’t be calculated because triglycerides were too high.

I’ve always thought the same held true for triglycerides under 100 mg/dl, which would apply to almost everyone who sticks to a low-carb diet for any length of time.  Triglyceride levels of 40-90 mg/dl are not uncommon, and are, in fact, typical.  When Friedewald did his work, the triglyceride levels were mainly up in the 150 – 250 mg/dl range, and in this range his equations match pretty well to directly measured LDL levels, but all bets are off with triglycerides above 400 mg/dl and, I suspect, triglyceride levels below 100 mg/dl. MD and I did find this ourselves in a few patients that we did direct LDL measurements on in our practice.

A paper published a few years ago in a pathology journal corroborating what we found. (Full text here.)

This paper is basically a case presentation of a 63-year-old man with a total cholesterol level of 263 (all results in mg/dl), an HDL of 85, a triglyceride level of 42, and an LDL level of 170.  The LDL level was, of course, calculated using the Friedewald equation.

For some unexplained reason the authors of this paper decided to repeat the lab results and got the same readings.  They then wondered if his very low triglyceride readings might be having an effect, so they measured his LDL levels directly and found that instead of the 170 predicted by the Freidewald equation, his actual LDL levels were only 126.

More recently a paper appeared in – of all places – the Archives of Iranian Medicine showing the same phenomenon.  These authors tested 115 subjects with low triglyceride levels.  You can get the full text of the paper, but a line in the abstract says it all:

Statistical analysis showed that when triglyceride is <100 mg/dl, calculated low-density lipoprotein cholesterol [LDL] is significantly overestimated (average :12.17 mg/dL or 0.31 mmol/L), whereas when triglyceride is between 150 and 300 mg/dL no significant difference between calculated and measured low-density lipoprotein cholesterol is observed.

The authors of this paper derived their own equation to be used in lieu of the Friedewald equation when the triglyceride levels are below 100 mg/dl.  I suspect that if we were to apply this equation to the labs of the 33 subjects who finished the low-carb arm of the study we started out discussing in this post, whose average triglyceride levels were under 100, the LDL levels would have averaged much lower than the 147 mg/dl they were calculated to be by the Friedewald equation.  If you subtract the 12.17 mg/dl that the Iranian paper estimates as the difference from the average triglycleride levels (an admittedly extremely unscientific and non-statistically valid way to do it), you find that the average drops to 135 mg/dl, which I doubt is significantly different than the 131 average of the low-fat dieters. If you did it the right way – subject by subject and then average – I suspect it would be greater yet.

The moral of this story is that if you have been following a low-carb diet and your triglycerides are low (or if your triglycerides are just low) and your LDL reading comes out a little high – or even a lot high, don’t let anyone mule you into going on a statin or undergoing any therapy for an elevated LDL.  Demand to have a direct measurement of your LDL done.  Or if you get an insurance physical and your triglycerides are low and your LDL up a little, fight to get a direct measurement so they don’t stick you with higher premiums because they think you’ve got an increased risk for heart disease.

What we do know based on the work of many is that low-carb diets change LDL particles to the large, fluffy, harmless variety.  Thanks to these other papers we also know that the LDL levels so many people end up with on their lab reports after being on low-carb diets for a while are artificially high.

Now when you hear people say that low-carb diets may help you lose weight but run your LDL levels up and increase your risk for heart disease, you’ll know this is just so much gibberish.  Sadly, your doctor will probably spout the same thing, and it will be up to you – who after reading this post will know more about this point than 99.9 percent of doctors practicing today – to educate your trained professional.

And if you are a researcher studying the effect of the low-carb diet on LDL, for crying out loud, hit your grant up for the extra few bucks it takes to get LDL cholesterol measured directly in your subjects so you won’t be in the embarassing position of having your data become worthless.

Dr. George Bray's model of obesity

In July 2008 I posted on Dr. George Bray’s critique of Gary Taubes’ book Good Calories, Bad Calories that appeared in Obesity Reviews.  Included in my post was a copy of Gary’s response.  Now Dr. Bray is back with a rebuttal to Gary’s response to his (Bray’s) original critique.  In conversation, Gary told me he has elected to drop the issue because the discussion is going nowhere.  Gary makes substantive points; Bray obfuscates the issues and will continue to do so.  I, however, am not going to drop the case.  Maybe I’ll have the last word here.

I want to go over Dr. Bray’s response to Gary’s letter in some detail because it is emblematic of all that is wrong with obesity research today and clearly demonstrates why we will never get anywhere until the people of Bray’s generation fade away. I don’t know that I’ve ever seen so many instances of one writer missing the point as often as Dr. Bray does in this short reply.  The entirety of his response is an example of either shoddy thinking or intellectual dishonesty.  Or maybe both. It brings to mind Mary McCarthy’s famous quote about Lillian Hellman: “Every word she writes is a lie, including ‘and’ and ‘the’.

(You can read Dr. Bray’s original critique of Good Calories, Bad Calories along with Gary’s response in my July 2008 post.  The full-text of Dr. Bray’s letter of reply we’ll be discussing in today’s post can be found here.  You should pull it down in pdf and print it so you can follow along.)

Right off the bat, in the very first line, Bray leads off with his first porkie.

In his nearly 5000-word response to my book review, Mr. Taubes has raised a number of issues.

Gary’s response was slightly under 2000 words.  You might think this just simply a typo, and normally I would too, but the entire piece is filled with so many inaccuracies seemingly designed to denigrate Gary’s response that I don’t think so.  Why even put the number of words?  Why not simply say: In his response to my book review…?  By quantifying the number of words the way he does, Bray casts a pejorative shadow on Gary’s response from the get go.

If you read Gary’s letter, you will see that he methodically refutes Dr. Bray’s criticisms of GCBC and identifies those issues in which he feels Bray misses the point.  In his response, Bray says Gary’s critique of his (Bray’s) review of GCBC

opened the door for [him] to contrast [Taubes’] hypothesis for obesity with [his own].

It’s a kind of disingenuous way for Bray to get his own hypothesis of obesity into play in what amounts to a review of Gary’s book, but let’s take a look at what he has to say.  First, he completely simplifies and basically mischaracterizes Gary’s hypothesis of obesity.  Here is Gary’s hypothesis of obesity and his proposed treatment as interpreted by Dr. Bray:

As you can see, it appears pretty simplistic, which, I’m sure, was the intent.  Not shown are all the feedback loops and intricacies Gary has described at length in GCBC .

In referring to this diagram, Dr. Bray admits that it is based on “two sentences from the letter,” which doesn’t seem like a lot out of a 5,000-word letter (or even the 2,000-word letter that it was).  Then he goes on to use three sentences to establish the basis for the diagram.  (See what Mary McCarthy meant about even ‘and’ and ‘the’?)

After giving short shrift to Gary’s hypothesis of obesity, Dr. Bray then goes on to lay out in great detail his own theory of obesity as represented by the Rube Goldbergesque diagram at the top of this post.  Bray’s entire hypothesis, for which he recruits leptin, insulin, the brain, glucocorticoids, and God knows what else to help make his point, is based on a faulty premise.  But it’s a faulty premise he has accepted uncritically.

His hypothetical model of obesity, he authoritatively states

starts with the First Law of Thermodynamics, which states that the change of energy in a closed system is the difference between the heat added to the system and the work done by the system.

Dr. Bray then restates this hypothesis (and the First Law) in the form of this equation:

Δ E = Heat (q) – Work (w)

Readers of this blog know this as the energy balance equation, which looks like this in its more familiar form:

Δ Weight (the Δ means change) = Energy in (food) – Energy out (exercise plus metabolism)

The fatal flaw in Dr. Bray’s hypothesis (which is a flaw we’ve discussed often in these pages) is that he doesn’t understand that the components on the right side of the equal sign are not independent variables.  They are dependent variables.  If one eats less, the rate of metabolism falls to compensate.  If one exercises more, the appetite increases, and one eats more to compensate.

Were these components truly independent variables, life would be easier (but we may not have survived).  According to Dr. Bray, Anthony Colpo, and countless others, however, these components are independent variables.  Eat less, say they, and you’ll lose weight.  Which is true, to a point.  But once the energy-out component of the equation kicks in, weight loss stalls, even if you are eating less, a fact everyone who has ever dieted knows.  Exercise more, they pontificate, and you’ll lose weight.  Which, again, works (maybe) in the very short term.  But once appetite kicks in, you unconsciously eat enough more to compensate for your increase in exercise, as anyone knows who has tried to lose weight by walking or other exercise alone without consciously restraining eating.

Now don’t get me wrong, it is possible to lose weight by decreasing food intake and increasing exercise.  It worked well in the concentration camps in WWII and in Ancel Keys’ starvation studies in the 1940s.  But in those cases, people were under lock and key.  It doesn’t work for the long term for the majority of people unless they are coerced.

This fairly obvious observation that the energy in/energy out components are not independent variables seems to elude most (if not all) obesity researchers, including George Bray.  These people persist on basing the foundation of any obesity treatment on the admonition to eat less and exercise more, which is a total folly.  Yet Bray and his ilk continue to clothe this folly in the garments of academic respectability and work to pass it off as the latest fashion in scientific thinking.

Dr. Bray believes that the reason so many people are fat is twofold. First, he thinks  humans have a ‘hedonic’ drive that inexorably pushes them to increase their food intake.  And, second, he reckons that this ‘hedonic’ drive also overrides the “appropriate negative feedback signals to stop eating.”  What stimulates this ‘hedonic’ drive?  According to Dr. Bray

It is caused by the pleasurable effects of high-fat, high-sugar foods.

Well, at least he’s half right on that one.  No one binges on pure fat.  It’s impossible because of feedback inhibition to eat a lot of pure fat at a sitting.  Try sometime to sit down and eat some butter all by itself.  See how much you can choke down.  I can guarantee you it won’t be much.  Then add a little sugar to the mix and see what happens.  Suddenly the butter is converted to frosting, and you can put away a lot of it.  What’s the difference?  It’s the sugar.  Sugar – and carbohydrates in general – override the stop-eating center in the brain.  That’s why all binge eaters binge on a combination of fat and carbohydrate.  That’s also why you can go out to dinner, eat ‘til your stuffed, not be able to eat another bite of any kind of meat or other real food, yet perk up when the dessert tray comes around.  As the old saying goes: there’s always room for dessert.  Why? Because your brain knows the stop-eating center will be overridden by the sugar and carb in the dessert.

Dr. Bray would have been more accurate had he said that the stimulus for the ‘hedonic’ drive is carbohydrate.

But he doesn’t.  He is trapped in the fat-is-bad paradigm.

In experimental animals, highly palatable food or a high-fat diet is one of the easiest ways to disturb this homeostatic system [as defined by Dr. Bray], and this may apply to human beings as well.

Dr. Bray seems to believe that we live in a toxic world in food terms.  We are unable to help ourselves, and are therefore destined to be fat because of our ‘hedonic’ drive.  We are helpless.  There is no cure save eating less and exercising more, which even he more or less admits doesn’t work despite his entire model being based on the idea.  As I have discussed in another post, Dr. Bray is a major proponent of drug therapy to treat obesity.

In a way, I agree with him about the idea that we live in a toxic world, one with all kinds of the wrong kinds of food available to tempt us 24/7.  Problem is that Bray and his ilk are a major part of the reason we live in such a world.  But that’s a topic I’ll leave for a future post.

Dr. Bray makes a bizarre case for why he thinks the majority of dietary studies show better results in those subjects following low-carb diets than in those consuming low-fat regimens.  I’m going to use his own words, so you won’t think I’m making this up.

the principal studies that directly support this model [Taubes’ theory on low-carb dieting] included the word ‘Atkins’ in their clinical trial. When similar low-carbohydrate diets were tested without using this ‘name’, the low-carbohydrate diets had no more effect than those to which they were compared.

There you have it.  All you have to do to make a diet work is include the name ‘Atkins’ in the title.  I wish MD and I had known that when we wrote Protein Power.

What is truly ironic about this nonsense is that in this very same issue of Obesity Reviews containing Bray’s rebuttal is a long review article titled Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities.  This article takes an in depth look at studies comparing low-carb diets to low-fat diets.  Here is the conclusion as written in the abstract:

There was a higher attrition rate in the low-fat compared with the low-carbohydrate groups suggesting a patient preference for a low-carbohydrate/high-protein approach as opposed to the Public Health preference of a low-fat/high-carbohydrate diet. Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year.

Dr. Bray lists five other issues about Gary’s letter to which he wishes to respond, but before he gets to the list, he makes one last flippant point.

I thus conclude that if any diet ‘cured’ obesity as their proponents often claim, there would be no obesity and thus no need for the next diet. Yet the past 150 years, since the publication of Banting’s first popular diet, have seen a continuing stream of new diet books.

The reason, of course, is that we dieting fish all swim in waters that have been polluted by Bray and his brethren, more about which in a later post.

Now to the list.

1.    Near the end of the letter, Mr Taubes suggests that my review of his book may be a ‘conflict of interest’. He says ‘I [Bray] may be defending what my scientific research has led me to believe’. If this is a conflict of interest, then all scientists have a conflict of interest.

This first short point of only three sentences tells you everything you need to know about Dr. Bray’s scientific credibility.  I have no problem with the first sentence.  The second sentence is purportedly a quote from Gary Taubes letter.  It isn’t.  It is a paraphrase…sort of, but put in quotation marks.  This is a real no no.  It was done so for a particularly egregious reason, which was for a set up for Bray’s final sentence.  But that sentence even further diminishes his credibility.  Scientists are supposed to constantly challenge their own hypotheses, not accept them as fact simply because they’ve spent their careers enraptured with them.   All true scientists don’t have this conflict of interest.

2.    The first paragraph of his letter dealt with lipoproteins that I said he had not covered. The issue was not the lipoproteins but their receptors, from which we have learned so much in the past 30 years.

This one is a real copout.  In Bray’s original critique he wrote:

As I read through Good Calories, Bad Calories, I found a number of errors of omission or commission that are important when relating diet to heart disease.  There is no mention in the Diet-Heart section of low-density lipoprotein-cholesterol (‘bad cholesterol’) or of high-density lipoprotein-cholesterol (‘good cholesterol’).

The issue may have been the receptors and not the lipoproteins, but as you can see from his direct quote above, that’s not how Bray characterized it.  Gary set him straight with a list of about two dozen pages and groups of pages where LDL and HDL were mentioned, yet Bray weasels instead of admitting his mistake.  When I read his first letter, it made me wonder if he had even read the book.

3.    In his letter he mentions doubly labelled water only to conclude that we knew this already from the 19th and early 20th century and he did not need to discuss it in his book. I would submit that we did not know that people under-report their intake by as much as they do and that overweight people under-report more than normal-weight people do.

Okay.  There’s a total non sequitur.  What does the second sentence have to do with the first?  Weird.  Was Bray on dope when he wrote this?

4.    Mr. Taubes say ‘the goal of science is to determine causality…’

(What Gary actually wrote was ‘The goal of science is to correctly determine causality,’ but who’s counting?)

Then Bray wades into this strange discourse about the theories of Karl Popper, whom he misnames as Hans Popper.  (Does this guy ever bother to look anything up?)

This is significantly different from the views of Hans Popper, the philosopher of science, whose search is for ‘reality’ rather than ‘causality’. Popper says ‘there is a reality behind the world as it appears to us, possibly a many-layered reality, of which the appearances are the outermost layers. What the great scientist does is boldly to guess, daringly to conjecture, what these inner realities are like. Popper also espouses the concept of ‘falsification’, which is at the heart of rationalist thought. To quote him again –’a false theory may be as great an achievement as a true one. And many false theories have been more helpful in our search for truth than some less interesting theories which are still accepted’.

If you can make sense of this gibberish, you’re a better man than I am.  All I know is that Bray misses Popper’s point about falsification in a major way.  (We discussed Popper and his theory of falsification in an earlier post.  And it ain’t anything like Bray makes it out to be. I seriously doubt he has even read Popper’s work.)

The last sentence of the above paragraph I find particularly interesting.  Writes Bray, apropos of nothing really:

And many theories have been more helpful in our search for truth than some less interesting theories which are still accepted.

I don’t know about the search for truth, but I can tell you that the inability of Bray and the rest of the academic obesity ‘experts’ to shake loose from their own ‘less interesting theories’ have led us into the obesity epidemic we’re in the throes of now.

Dr. Bray’s fifth comment, which I’m not going to reproduce in full, is a world-class case of totally missing the point.  After commending Gary for proposing an experiment to validate his hypothesis, he goes on to quote Gary’s rebuttal letter:

He says ‘the positive energy balance hypothesis of obesity asserts that the only way to lose excess fat is to eat less and/or exercise more – that without consciously inducing a negative energy balance we will not lose weight’. His hypothesis is ‘the carbohydrate/insulin hypothesis asserts that if we restrict carbohydrates in the diet/and or improve the quality of the carbohydrates consumed then insulin levels will be lowered, reducing the accumulation of fat in the fat tissue independent of the nutrition state of the subject’. I would take exception to his use of the word ‘consciously’ in his statement of the energy balance hypothesis. For example, the current level of oil prices may increase human energy expenditure through more walking as it decreases automobile use. This is not a ‘conscious’ choice in the sense used above but would have the same effect.

Say what?!?!?!

Let me get this straight.  Dr. Bray thinks if we walk more because we decrease automobile use as a consequence of the high price of gasoline that we’ll lose weight because we are unconsciously exercising instead of volitionally exercising?  As I say, he misses the point, which is that the two components on the right side of the energy balance equation are not independent variables, but are dependent variables.  It doesn’t matter if one walks as a part of exercise or because one can’t afford the gas, the body compensates by increasing food intake.

Dr. Bray ends his response by resorting to the old conservation of energy principle, which all the eat-less, exercise-more folks hew to.  They seem to believe that no one who advocates low-carb diets can understand the laws of thermodynamics when it is they themselves who don’t understand them as applied to diet.  There is nothing inconsistent with Gary’s theories of the cause and treatment of fat accumulation and the laws of thermodynamics.  It’s Bray and friends’ lack of understanding of these laws and/or their refusal to accept the dependent nature of the energy in/energy out components of the energy balance equation that are the heart of the problem.

This entire rebuttal of Dr. Bray’s reminds me of my own favorite lines from Good Calories, Bad Calories.  They are my favorite because I’ve seen first hand what they describe.

The institutionalized vigilance, “this unending exchange of critical judgment,” is nowhere to be found in the study of nutrition, chronic disease, and obesity, and it hasn’t been for decades.  For this reason, it is difficult to use the term “scientist” to describe those individuals who work in these disciplines, and, indeed, I have actively avoided doing so in this book.  It’s simply debatable, at best, whether what these individuals have practiced for the past fifty years, and whether the culture they have created, as a result, can reasonably be described as science, as most working scientist or philosophers of science would typically characterize it.  Individuals in these disciplines think of themselves as scientists; they use the terminology of science in their work, and they certainly borrow the authority of science to communicate their beliefs to the general public, but “the results of their enterprise,” as Thomas Kuhn, author of The Structure of Scientific Revolutions, might have put it, “do not add up to science as we know it.”

The result is an enormous enterprise dedicated in theory to determining the relationship between diet, obesity, and disease, while dedicated in practice to convincing everyone involved, and the lay public, most of all, that the answers are already known and always have been—an enterprise, in other words, that purports to be a science and yet functions like a religion.

Is it any wonder that Dr. Bray didn’t enjoy the book?

There is an old joke that goes something like this:

Question: What is Mozart doing in his grave right now?
Answer: De-composing.

The same question could be asked of the living right now who are working hard on their diets and seeming to go nowhere body weight-wise.

Question: What’s happening right now? Why am I not losing weight?
Answer: You’re Re-composing.

As you can see from the picture above, body composition matters a lot.  It’s not the particularly the weight you carry as much as how it is distributed that counts.  As I’m forever asking my female patients, What difference does it make if you weigh 200 pounds if you’re wearing a size 4?  Although that situation is unlikely, they get the point.

A soon-to-be-published study by Donald Layman and his team at the University of Illinois demonstrates this phenomenon nicely.  And shows that by increasing protein intake – even while keeping carb intake much higher than I would recommend – increases fat loss while increasing muscle and lean tissue mass.

Here is how the study was set up.

One-hundred thirty overweight men (58) and women (72) between the ages of 40 and 56 were recruited into the study.  None of the subjects smoked, took cholesterol-lowering drugs or had any medical condition that might affect the outcome of the study.  In other words, the study subjects were relatively healthy overweight middle aged people.

These subjects were randomized into two groups.  One group was started on a diet (PRO) containing 1.6 gm protein per kg body weight per day and under 170 g carbohydrate per day.  The other group went on a diet (CHO) composed of 0.8 g protein per kg per day (the minimum Recommended Daily Allowance (RDA) for protein) and over 220 g carbohydrate per day.

The diets for both groups were formulated to be equal in energy with  1900 kcal/day provided for males and 1700 kcal/day for females.  Total fat content was the same in both the PRO and CHO diets.

Diet differences between groups were designed to reflect direct substitution of foods in the protein groups (meat, dairy, eggs, and nuts) for foods with high-carbohydrate content (breads, rice, cereals, pasta, and potatoes).  The education guidelines for the CHO group followed the USDA Food Guide Pyramid and emphasized restricting dietary fat and cholesterol with use of whole-grain breads, rice, cereals, and pasta.  For the PRO group, the education guidelines emphasized use of high-quality, low-fat proteins including lean meats, reduced-fat dairly, and eggs or egg substitutes.  Both diets included 5 vegetable servings/d and 2-3 fruit servings/d.

This study is unusual in that it provided a comprehensive nutritional education program along with an intense degree of nutritional monitoring throughout the 12 months of the study.  Most nutritional studies give the subjects a lead in lecture or series of lectures, then pretty much leave them alone.  To help ensure compliance, these researchers met with the subjects weekly throughout the study.

Subjects were evaluated at the start, after a 4 month period of active weight loss and finally after an 8 month maintenance period.  The entire length of the study was 12 months.

At the end of the 4 month weight-loss period, subjects on the PRO diet fared substantially better than those on the CHO diet.  Fewer people in the PRO group had dropped out of the study, and those who remained experienced an increase in HDL-cholesterol and a substantial reduction in triglycerides as compared to those on the CHO diet.  Those subjects on the CHO diet had greater reduction in LDL-cholesterol than did those following the PRO diet, but those changes didn’t old over the full 12 months.

Most interesting was the finding that although both groups lost equivalent amounts of weight over the first 4 months (actually, the PRO group lost a little more, but not a statistically significant amount), those in the PRO group lost 22 percent more fat than the subjects in the CHO group.  Since weight was essentially the same in both groups, those in the PRO group maintained or lost less lean mass while losing fat.  Which means that, despite the weight being the same, those in the PRO group ended up smaller than those in the CHO group.

As I’m sure everyone knows, fat is lighter than muscle.  If you trade a pound of muscle for a pound of fat, the scales don’t change.  But size does change because a given weight of fat occupies much more volume than the same weight of muscle.  You can see from the photo to the right how much less space 5 pounds of muscle take up than does 5 pounds of fat.  Plus, muscle is more metabolically active in that it burns more calories, and it actually does something for you.  Muscle makes you stronger; fat just weighs you down.

I know that many female readers will not want to gain extra muscle.  They shouldn’t worry, however, because in the absence of exogenous anabolic steroids women won’t become ‘muscle bound’ or non-feminine appearing.  What generally happens is that the muscle replaces fat within the muscle.  We’ve all seen marbling in beef, which is fat within the muscle tissue.  With the extra protein, new muscle replaces this fat, and the muscle may even become a little smaller in females while at the same time becoming more dense and stronger.

Let’s take a look at a couple of graphs that demonstrate nicely the difference in fat loss with greater protein intake, even in the face of what I consider way too many carbs.

The graph on the top shows the difference in fat loss between those PRO and CHO subjects who completed the entire 12 months of the study irrespective of how much weight they lost.

The bottom graph shows the difference in fat loss in those who were able to maintain a weight loss of at least 10 percent of their starting weights.

As you can see, the fat loss in those in the PRO group were substantially greater than those in the CHO group even though both groups were on an equivalent number of calories.

The series of graphs to the right show what happened to lipid values in the subjects in both groups.  HDL-cholesterol went up more and stayed up in the PRO subjects.  Triglycerides went down more and stayed down in the PRO subjects.  Subjects following the CHO protocol tended to have a reduction in LDL-cholesterol as compared to those in the PRO group, but as the study continued, the LDL-cholesterol began to return to pre-study levels.  This finding has been replicated in many other studies.  A high-carb, low-fat diet reduces LDL in the short term, but the changes don’t last.

The authors of this study made some interesting points in the discussion part of the paper.

Across all 3 analyses [the data was analyzed in three different ways], the PRO group averaged ~21% greater weight loss and 27% greater fat loss than the CHO group.  Further, irrespective of the amount of weight lost, participants in the PRO group obtained greater improvements in body composition as reflected by greater FM [fat mass] loss and attenuated relative lean mass loss.

In addition to the beneficial effects of the PRO diet for changes in body composition, more participants in the PRO group completed the study (64%) than in the CHO group (45%) and attained ≥ 10% weight loss (31 vs 21%, respectively).  These findings demonstrate greater compliance with a moderate PRO diet designed within the DRI [Daily Recommended Intake] guidelines for macronutrients for long-term weight management than the CHO diets often advocated for weight loss.

This is information you can use with friends and family who are, for whatever reason, adverse to going on a real low-carb diet.  The beauty of this particular study is that all the protein, carb and fat recommendations are within the government-approved RDAs.  The PRO group had a protein intake that was at the upper end of the RDA for protein and carb at an amount that was far from the lower end of the RDA for carbs.  (Of course those of us in the know realize that there is no lower end requirement for carbs  – many people get by with zero or close to zero carbs.  But we’re talking the government here. So, nuff said.)  What this means is that you can encourage friends and family to go ahead and eat a government-approved diet yet still get some of the benefits of a semi-sort-of low-carb diet.  A real win win.

Multiple mechanisms have been reported to explain increased loss of body weight and body fat with higher protein diets.  Higher protein diets appear to increase satiety, increase energy expenditure, and/or maintain lean tissue with higher metabolic activity.

Improvements in body composition, including reducing body fat and maintenance of lean tissue, are critical for prevention of weight regain and long-term health status.  Evidence is accumulating that the RDA for protein is inadequate to maintain muscle mass in adults during aging, with a physically inactive lifestyle, or during energy restriction for weight loss.  The current RDA for protein represents the minimum protein needs for healthy young adults with adequate energy intakes.  During weight loss, energy restriction increases the protein needed to maintain muscle mass and protein needs expressed as percentage of the reduced energy intake nearly double.

Just to give you an idea of the amount of protein we’re talking about here, let’s take the so-called average person who weighs 70 kg (154 lbs) and calculate daily protein requirements based on the protocol of this study.  70 kg  X 1.6 g/kg/day = 112 gm protein per day.

If you want to use pounds instead of kilograms, use 0.73 gm protein per pound per day.  If you weigh 200 lbs, then the calculation would be 200 lbs X 0.73 gm/lb/day = 146 gm protein per day.  Since meat contains about 7 gm protein per ounce, this 146 gm could be gotten in about 21 ounces of meat per day.  So we’re not talking about a small amount.

I’ll leave you with the conclusions of the authors of this study, with which I mostly concur.

The findings of the current study demonstrate that although energy deficit is the major factor for body weight loss, the macronutrient composition affects body composition, blood lipids, and long term compliance.  Specifically, a PRO diet with protein at the upper end and carbohydrates at the lower end of the AMDR [Acceptable Macronutrient Intake Range] is more effective for reducing % Fat and improving dyslipidemia.

I can only add that were the protein kept high (along with the fat) and the carbs slashed to around 30-50 gm per day, the results would have been even more impressive.

When I put out the call for what people wanted to read about on this blog in 2009, numerous folks commented that they would like to know why it seems so much more difficult to successfully follow a low-carb diet the second or third time around.  Over the years I’ve noticed this phenomenon in myself and in many others whom I have treated or advised, so it’s truly a subject worthy of exploration.

I’m going to list the reasons experience has taught me below, starting with situations over which we have no control and ending with those over which we have total control.

Aging

We all get older every day.  Sadly, with aging, all systems deteriorate.  Some slower, some faster, but all get a little older and a little less functional every day.  If you achieve success on a low-carb diet and find yourself 70 pounds lighter, you’ll also find your self five or six months older.  If you regain that lost weight, then decide to start another low-carb diet to re-lose it, you will probably be a couple of years older than you were when you tried your first low-carb diet.  Just as it’s a little more difficult to pick up tennis at age 46 than it is at age 44, it’s a little more difficult to get everything moving with a low-carb diet when you’re a couple of years older.

Built-in survival mechanisms

Although most dietary recommendations are fairly simplistic, our bodies are unimaginably complex.  Not only do we have a complicated metabolism centered around and directed by the liver, we have multiple neurological and endocrinological feedback pathways between the liver-directed metabolic system and the central nervous system.  And we have gut hormones that get into the act sending signals of fullness or lack thereof.  It is an intricate system designed to allow us to survive on all kinds of food and to keep us alive as long as possible in the face of famine.  I like to think of this entire interconnected system as having its own memory.  It will allow you to fool it once or maybe twice, but then it gets wise.

Almost everyone who starts any kind of diet for the first time sees pretty rapid results.  Pounds seem to fall off quickly and effortlessly.  At a point down the way in the diet, it starts becoming progressively more difficult to lose more weight because the body starts catching on to what’s happening and starts fighting back.  This phenomenon seems to occur less with a low-carb diet because if it is a good quality low-carb diet, the body is getting all the nutrition it needs, so it doesn’t rebel quite the same as it does with some other nutritionally inadequate diets.  But it does rebel a little, nevertheless.  And worse, it remembers.

If you lose weight then regain it and restart a low-carb (or any other) diet, the body is not quite so willing to shed the first pounds as quickly as it did the first time.  It remembers.  If you, like many people I’ve met do, give low-carb a serious, diligent go for about a week, then fall off because of a party, wedding, etc. that you attend, then try again for another week before falling off, you program your body to hang in there for at least a week before letting loose its fat.  The body says, ‘Well, here we go again with another week of this nonsense.  Let’s hold steady on and we’ll be back to our regular high-everything diet within a week.  Let’s not go into starvation mode yet and starting getting rid of our fat.’  What you will find after a few turns of this cycle is that although the first time through with low-carb you may have lost six pounds the first week, the forth time through you will lose almost nothing the first week.  Then the doubt creeps in.  And you begin to wonder if the low-carb diet will really work for you.  It will, but you’ve got to get past the body’s diet memory for it to.

Increased insulin and leptin resistance

All the studies aren’t in yet on this issue for sure.  But, those that are (both animal and human studies) indicate that we become progressively more insulin and leptin resistant as we age.  This is especially true for people who have become overweight or obese and have maintained that state.  Sadly, it is also true for those who became overweight or obese and lost the excess weight, which is most of us.  The more insulin and leptin resistance we are, the more difficult it is to lose weight.  So, the increase in this phenomenon just from the years passing between the first go round and the second on a low-carb diet makes it a little more difficult the next time.

Hormonal dysfunction

Women who are wildly successful on a low-carb diet when they are in their 30s or 40s and premenopausal then try again when they are in their menopausal years often find it almost impossible to lose.  It requires fiddling with hormone levels by replacing with natural hormones and getting the system back into balance before a lot of weight can be lost.  It takes a while to do this.  Even if the hormones do get back to where they need to be quickly, it takes some time for the body to respond.  Often just getting the hormones balanced results in weight loss spontaneously without dieting.  But dieting helps the process along more quickly.

Now we get to the issues that we do have control over.  I don’t want anyone to be offended by this list or think I’m pointing any fingers because I’m not.  But I would guess that I’ve (MD and I as a team) taken care of more overweight people on low-carb diets than anyone alive today.  We’ve had thousands and thousands of patients in our clinics and we’ve dealt with many others second hand through books, lectures, etc.  And we’ve had many friends, relatives, friends of friends, associates, etc. whose care we have monitored.  In shepherding all these people (not to mention ourselves) on low-carb diets, we have learned a few things.   What follows is a summary of what we’ve learned.  Not about the biochemistry and physiology of low-carb dieting, but about the psychology of low-carb dieting.

Lack of commitment

It has been my experience that people just don’t seem to commit as strongly the second, third, etc. time around.  The first time, people make a major commitment.  They lose weight.  They feel better than they have in years.  They are excited.  Then they either stay continue on their low-carb diet and maintain or they don’t.  If they don’t, the weight comes back.  Then a couple of years later when it’s time to start again, they just don’t have the commitment they did the first time around.  And, due to the above reasons, it’s a little more difficult the second time around.  They never really get into the swing of it like they did the first time, and then the notion that maybe it won’t work starts to gnaw.  And then they start doing a ‘half-fast’ (if you get my drift) low-carb diet, which works okay for maintenance, but not for weight loss.  Discouragement sets in, and they bolt from the diet.  I’ve seen this cycle in action countless times.  Don’t fall into it.

People learn how to cheat in their first low-carb go round and remember how when they start again

The first time around on a low-carb diet is exciting.  You’re actually getting to eat all these forbidden foods – steak, eggs, real butter – that you’ve been taught make you fat and are losing weight like crazy.  It’s unbelievable.  But sooner or later, you get a little weary of steak, eggs and real butter, and you start looking to expand your food choices.  If you stay on your carb restriction, you start to figure ways that you can keep carbs low, but eat facsimiles of the high-carb foods you enjoyed before you started your low-carb diet.  You make the major discovery that low-carb brownies exist (or at least they call them low-carb brownies) so you give them a try.  Then you find out about low-carb waffles, pancakes, bagels, etc.  You discover that there is a whole low-carb world of what you’ve always thought of as high-carb foods.  You are in heaven.  You can have your cake and eat it, too, so to speak.  But around about this time, the weight loss starts to really taper off and maybe even comes to a halt.

A few years later, you’ve regained your lost weight plus some, remember how effortlessly you lost it on a low-carb diet, and decide to do it again.  But this time, instead of starting with the steak, eggs and real butter all alone, you stock your low-carb larder with low-carb brownies, bagels, chips, and other junk as well.  Strangely, the low-carb diet just doesn’t seem to work as well this next time around.

If you want to be successful the next time around on a low-carb diet, you’ve got to follow a low-carb diet.  And it takes commitment.  You’ve got to realize it’s going to be a little more difficult than it was the first time, and you’ve got to go on an honest-to-God low-carb diet filled with quality low-carb real foods.  And you’ve got to stick to it.  You want to hang in there until you get to what was called in the old medical literature the dynamic weight stage.  The dynamic weight stage is when weight is changing rapidly in either an upward or downward direction.  Anyone who has gained or lost a lot of weight has experienced this. You can gain rapidly once you get into this phase, but ultimately you stabilize and hit the static weight phase.  It works the same going the other way.  Once you get your weight loss momentum built up, you seem to lose effortlessly while in this dynamic phase.  This is where you want to be.  But you have to commit for a few solid weeks to get there.  You can’t just diddle with it, go on a few days and off, fill up on calorie-dense, low-or-no-carb junk, say you’re doing a low-carb diet, and wonder why you aren’t losing.  You’ve got to get up into the low-carb saddle and ride.

In the next post in this series of two, I’ll present some tips that have helped me enormously and have helped others achieve the level of commitment needed to see us through years of low-carb dieting.

In the above list of reasons I think the low-carb diet (or any diet) is more difficult the nth time around, I’ve probably forgotten something.  Which is why I rely on you and your comments to fill in the missing info.  If you have reasons I’ve not mentioned, send them in.  Don’t be shy.  Or if you disagree.  Let me know.  I’ll be eager to hear from you.

I’ve gone through and compiled a list of the most common questions and presented them to Gary.  Here are the questions followed by his responses.

The most commonly asked question was how do Asians and others living a seemingly high-carb existence manage to escape the consequences?

The Asian question first. I do address this in the book and I address it again in the afterward of the paperback. There are several variables we have to consider with any diet/health interaction. Not just the fat content and carb content, but the refinement of the carbs, the fructose content (in HFCS and sucrose primarily) and how long they’ve had to adapt to the refined carbs and sugars in the diet. In the case of Japan, for instance, the bulk of the population consumed brown rice rather than white until only recently, say the last 50 years. White rice is labor intensive and if you’re poor, you’re eating the unrefined rice, at least until machine refining became widely available. The more important issue, though, is the fructose. China, Japan, Korea, until very recently consumed exceedingly little sugar (sucrose). In the 1960s, when Keys was doing the Seven Countries Study and blaming the absence of heart disease in the Japanese on low-fat diets, their sugar consumption, on average, was around 40 pounds a year, or what the Americans and British were eating a century earlier. In the China Study, which is often evoked as refutation of the carb/insulin hypothesis, the Chinese ate virtually no sugar. In fact, sugar consumption wasn’t even measured in the study because it was so low. The full report of the study runs to 800 pages and there are only a couple of mentions of sugar. If I remember correctly (I don’t have my files with me at the moment) it was a few pounds per year. The point is that when researchers look at traditional populations eating their traditional diets — whether in rural China, Japan, the Kitava study in the South Pacific, Africa, etc — and find relatively low levels of heart disease, obesity and diabetes compared to urban/westernized societies, they’re inevitably looking at populations that eat relatively little or no refined carbs and sugar compared to populations that eat a lot. Some of these traditional populations ate high-fat diets (the Inuit, plains Indians, pastoralists like the Masai, the Tokelauans); some ate relatively low-fat diets (agriculturalists like the Hunza, the Japanese, etc.), but the common denominator was the relative absence of sugar and/or refined carbs. So the simplest possible hypothesis to explain the health of these populations is that they don’t eat these particularly poor quality carbohydrates, not that they did or did not eat high fat diets. Now the fact that some of these populations do have relatively high carb diets suggests that it’s the sugar that is the fundamental problem. Ultimately we can only guess at causes using this kind of observational evidence. To know anything with certainty we’d need the kind of randomized controlled trials I yearn for in the epilogue of GCBC.

What is your opinion on leptin in the grand scheme of obesity and fat storage?

I mostly ignore leptin in the book because I think leptin is primarily a signaling molecule and so a downstream effect. In other words, leptin is secreted from the fat cells; it doesn’t regulate directly the amount of fat that accumulates. Moreover, if the primary regulator of fat storage is insulin, which it is, and leptin is secreted in proportion to the amount of fat stored, which it is, then insulin has to regulate leptin.

Where leptin may play a primary role is in the liver. A few years ago Jeff Friedman of Rockefeller University published an article in Science showing that leptin down-regulates SCD-1 in the liver (the only place they looked), which worked in turn to increase oxidation of fatty acids. This makes sense homeostatically: if leptin is released in proportion to the fat accumulated then it is a signal of how much fat we have in reserve. So long as the mitochondria in our lean tissue and organs know that we have fat in reserve, they can continue to burn it without fear of systems failure should they run out of fuel completely. Leptin resistance would then work, like insulin resistance, to make us burn less fat and store more, while the rest of the body would have to rely on carbohydrates (blood sugar) for fuel.

In general, though, I’m interested in the cause of obesity and I don’t think discussing leptin adds much. Here’s what I say about this issue in afterward of the paperback edition of GCBC:

“Another variation on the can’t-possibly-be-so-simple argument that I have heard frequently since Good Calories, Bad Calories was published is the molecular biology theme. The last fifteen years, since the discovery of the hormone leptin in 1994, has seen obesity research become a sub-discipline of molecular biology. As a result, a search of the keyword “obesity” in the National Library of Medicine database will now identify over 100,000 relevant articles in the professional journals (nearly 20,000 review articles alone), a large proportion of which focus on the fruits of molecular biology research and the science of genomics.: It’s a burgeoning field with a cast of thousands, including the role of obesity-related gene variations known technically as polymorphisms, of signaling molecules with names like adiponectin, leptin and grhelin, of the receptors for those signaling molecules and the inhibitors for those molecules and inhibitors of the inhibitors, and so on. The obvious question is how can this research be so extraordinarily fruitful, and yet mostly irrelevant to the cause of obesity? It’s hard to imagine it’s not, and so, as I’ve frequently been told, any discussion of the cause of obesity that doesn’t discuss these molecules, receptors, inhibitors, etc. must be considered amateurish and woefully inadequate. The truth must be complicated.

“Again the counter-argument seems itself simple and straightforward: if you’re hit over the head with a hammer, it will cause both pain and inflammation. The mechanisms of pain and inflammation have also yielded up a wealth of knowledge to the tools efforts of the molecular biologists. These physiological phenomena are understood to be mediated via signaling pathways and molecules (in this case, prostaglandins, tumor-necrosis factors, etc.) that emerge in response to the damage done. The more researchers learn about these responses and the molecules involved, the more complex the pathway from hammer to pain and inflammation to healing will appear. But the relevant fact to all those immediately involved is that both the pain and ensuing inflammation were caused by the hammer and perhaps the person who swung it. Everything else is downstream and may be relevant only to the question of which drugs will best deal with the pain and perhaps accelerate the healing process. “

A number of questioners asked why you think it is more difficult to lose weight the second or third time around on a low-carb diet?  And why it seems more difficult to lose on low-carb with increasing age?

I’m curious whether this is in fact true. Another possibility is that it’s more difficult to lose weight on low-carb as we get older; that the carbs effectively do chronic damage to our tissue and so the longer we’ve been overweight or obese, the harder it is to lose weight. I can imagine a scenario in which the fat tissue becomes hypersensitive to the insulin we secrete, or the pancreas becomes hypersensitive to the carbs and secretes even more insulin, or the insulin resistance in the lean tissue becomes less tractable, and so the longer we remain fat, the more our fat tissue compensates when we restrict carbs. It’s also possible that repeated low carb dieting somehow exacerbates this process, but I’d want to see definitive studies (and on all this speculation) before I believed it.

Several people asked for a comment on any important studies that you may have left out of GCBC.

The issue isn’t leaving out studies so much as not wanting to get into the he-said, she-said game of quoting particular studies that support my preconceptions. In this business, you can always find studies that support a particular hypothesis, or at least seem to if you selectively interpret the data. So when I had to make a point about the efficacy of a particular treatment — exercise, for instance, or semi-starvation diets — used meta-analyses or Cochrane Collaboration systematic reviews, which are designed to minimize author bias, to make the general points. When I discussed the saturated fat/cholesterol/heart disease hypothesis in the first few chapters, I did indeed mention virtually every study and certainly every meaningful clinical trial, because I knew if I left anything out I would be accused of cherry picking the data (which, of course, I was anyway). I did omit much of the observational epidemiology on the nature of a healthy diet because I find it meaningless and impossible to interpret correctly, in part for the reasons I discussed above about the Asian diet issue.

When I cut the book down from the initial 400,000 word unfinished draft, a lot of what was removed were indeed the counter- and counter-counter arguments. For instance, obesity researchers will argue that obesity causes hyperinsulinemia, not the other way around. That way they can still say that obesity is caused by over-eating and once we get fat, that causes insulin resistance and jacks up insulin levels. I spent, literally, months writing a lengthy section explaining how this view came about and what the evidence actually did and did not demonstrate. Then when I realized the book had to shrink dramatically, and with the benefit of sage advice from my editor, I decided that it was unnecessary to explain why the mainstream researchers would disagree with my take and then spend yet more space explaining why they were wrong to disagree. One thing I did cut from the book that I regret was a section linking gout to fructose and uric acid, and discussing the history of gout and how it’s frequency in populations and socioeconomic groups paralleled the spread of sugar. Nobody had ever made that point before and I wanted to make it, considering that people have been speculating on what aspect of diet or lifestyle causes gout back to Hippocrates. Still, my friends rightly argued that when your book is a few hundred thousand words long, you can’t afford to keep a section about gout, even if a lot of people get gout these days and, of course, they’re more likely to get it if they’re overweight or obese. Along these lines Dan Harrington asked why his gout goes away on the Atkins diet and that’s my answer: no sugar, primarily, means no fructose and so no fructose-induced hyperuricemia. In other words, fructose raises uric acid levels and gout is caused by the elevated uric acid in the blood stream.

It is true that you can find studies in the literature that seem to contradict the hypotheses in GCBC but are not mentioned in the book, When Gina Kolata reviewed my book in the NY Times, she evoked a study by Jules Hirsch and Rudy Leibel, then both at Rockefeller, suggesting that nutrient composition of the diet has no effect on weight. As I explained in a letter to the Times, the study failed to refute the carbohydrate/insulin hypothesis of weight regulation for a variety of reasons — the subjects, for instance, could have gained as much as 15 pounds a year on one particular diet composition but not another, and the study would not have detected it. And the subjects, almost exclusively, were lean middle-aged individuals. What we’re interested in here, though, is why why people predisposed to obesity get fat, and that may not be something you can study in people who have remained lean into their 40s and 50s. Would Leibel and Hirsch have obtained a different result if they had used, say, obese subjects who had first been slimmed down by some kind of diet (Atkins or a starvation diet)? These types of subjects are considered pre-obese, since they’re so highly likely to go back to being obese. And if Leibel and Hirsch had used them, they might have found that they stay relatively lean on a low carb diet and put on weight easily on a high carb diet. Anyway, rather than get into this kind of too-and-fro in the book, I made the decision not to mention these types of ambiguous studies. I would like to think that had there been a single compelling study refuting the hypothesis — or better yet, two, since you’d like to see things replicated in science — I wouldn’t have written a different book.

What you think of a Slow Burn type of exercise and low-carb dieting?  Do you still stand by your notion that exercise doesn’t help people lose weight?

I haven’t looked into the science behind slow burn exercise (although I know Mike has) but I now do it regularly (with Fred Hahn in Manhattan at Mike’s recommendation) and it seems to be helping my lower back pain immensely. I can let you know next spring whether it helps my softball game, where my ability to hit with power has been deteriorating sadly with the advancing years. What fascinates me about it is the weird confluence of the desire for self-improvement with what seems to be deep-set sadomasochistic tendencies. It’s torture when you do it, and then you look forward to going back.

As for exercise, I do not believe that it causes long-term fat loss. I think it might be helpful in a weight loss program only because it gives you a kind of positive feedback that dieting per se does not. You can feel good after a work-out, while it’s hard to feel too good after a meal that didn’t include either the calories or the carbohydrates you preferred. On the other hand, since it does make you hungry — work up an appetite — I worry whether for some or even most people the psychological benefits could be counterbalanced by the drive to consume even more calories than you might have expended during the work-out.

Are you familiar with the work of Dr. Jan Kwasniewski, and, if so, what do you think of it?

I am not.

What kind of response have you gotten from the medical/scientific community about GCBC?

In general, I think it’s safe to say that I’ve been ignored. If obesity researchers have read the book, they haven’t bothered to tell me. When GCBC was published we sent out 150 copies to obesity researchers, authors of obesity task force reports, foundations that fund obesity research, everyone at NIH who funds obesity research, etc. etc. I heard back from 3 or 4 thanking me for sending them the book. Two followed up to tell me they had read it. Some later told me outright that they didn’t have the time to read a 500 page book, and particularly so when they already know what I think because of the 2002 NYT Magazine article and don’t particularly agree. That said, I may be making some progress in getting people to pay attention.

Whenever I do hear from someone who is sympathetic, I ask them to try to set up a lecture at their institution. Often I ask them to contact other researchers they might know and get me lecturers at those institutions. Through this kind of networking, I’ve been invited to lecture at some of the more influential obesity research centers and at least some of those people have taken my arguments seriously. A few months ago, I heard from some contacts at the NIH, that I might be invited down to lecture to the nutrition coordinating committee at NIH, which would be a big step forward, but the fact that I haven’t heard anything since then (August) makes me pessimistic.

When I do give these lectures a common response that I get from nutritionists and obesity researchers, and one that I find profoundly disturbing, is that they find what I say interesting but don’t see it as anything they should think about further. In other words, they have their schtick (as my wife, an almost-academic calls it); whatever research they get their funding to pursue, and even though in theory we’re all in this to cure and prevent obesity and chronic diseases, their schtick may have nothing to do with my schtick. If they’re studying, say, genetic strains of obese rats or questionnaires to improve the accuracy of diet assessment in epidemiologic studies, what does that have to do with my argument that obesity is caused by carbohydrates? So they listen politely, ask a few intelligent questions (in an ideal world) and then go back to their research, because that’s how they make a living. They don’t say to themselves, I’m going to read Taubes’s book and, if I find it compelling, switch my research over to studying the efficacy of carbohydrate restriction. And even if they did, they wouldn’t get funding to do so because they’d have no track record in that field.

So, bottom line, at the moment is that I know of a handful, maybe as many as a dozen researchers, who find the arguments in the book compelling and are doing what they can, in their limited spare time, to help get the message out and maybe get us to the place where the hypotheses are taken seriously and are rigorously tested. The rest either don’t care or don’t know GCBC even exists or just think what I say is wrong and so not worth further discussion, either because they read the book or some of it and think its crap or because they think its crap based solely on what they know about me or heard about the book and so don’t have to read it.

What’s next?  Another book?

What am I doing next? As suggested by many readers, I am going to write a short, easy-to-read version of the weight section of GCBC. It won’t be a diet book — no recipes — but it will be far more of a self-help book than GCBC. I might also do a weightier (no pun intended) serious investigation into the sugar and corn syrup industries; their history, political influence, lobbying, etc — that would be interwoven with a more intensive look at the potential health effects of sugar and HFCS and fructose particularly. The first book will definitely be done; the second depends on getting the funding to do so. I’d also like to get back to straight science writing for a while, since I do enjoy writing about good science, which is how I started my career, and it would be a pleasant change from the mainstream nutrition and health nonsense.

How about a blog?

As for a blog, I just haven’t got the time at the moment, although I always hope that that will change in the future.

Many wrote that GCBC had changed their lives.  Can you think of a book that has changed your life?

Did any books change my life? Yes, All the President’s Men, by Woodward and Bernstein. I read it in my last year of college or my first year of graduate school and it made me decide that I wanted to be an investigative reporter rather than go to business or law school, which was the direction I seemed to be headed.

What do you know about Dr. Simeon’s HCG protocol?

Mostly nothing.

What led you to the idea that saturated fat doesn’t cause heart disease?

It was a progression of steps. Back in the late 90s, I was reporting a story for Science on the salt-hypertension controversy and one of the worst scientists I ever interviewed (and having written a book about cold fusion, Bad Science, I had interviewed quite a few terrible scientists) took credit not just for getting Americans to eat less salt, but getting them to eat less eggs, meat and butter, too. I literally got off the phone with this guy and called my editor at Science and said, “when I’m done writing about salt, I’m going to do a story on dietary fat. I don’t know what the story is, but if this guy was involved in any substantive way, I know there’s a story to be done.” So that’s what I did. I finished the salt story and then spent a year working on the fat story, which was published in Science.

The story made the point that there was virtually no evidence that a low-fat diet prevented heart disease, but let open a window for saturated fat having some deleterious effect. Then a couple of years later, I was reporting the New York Times Magazine story that would become “What If It’s All A Big Fat Lie?”, when I heard about these five clinical trials comparing low-fat, calorie-restricted diets to Atkins diets. Since the Atkins diet is a high-fat, high saturated fat diet and it improved cholesterol profiles in all these trials, that pretty much clinched it. I’ve been arguing since that these diet trials have to be perceived as tests of the hypothesis that saturated fat is a “bad” fat, although the medical establishment still prefers to ignore that fact.

Is there anything new or updated in the paperback version of GCBC or is it the same as the hardback?

It’s the same as the hardback, but there is a 3000 word (or thereabouts) afterward that’s worth reading.

I tried to come up with a selection of questions that represented the majority of questions asked.  I know that some went unanswered, but when Gary agreed to do this I promised him that he wouldn’t have to answer an exhaustive list that would require days of time.  So, I’m sorry if any specific question went unanswered, and I hope you understand.  Thanks to everyone for the terrific response.

The Food Policy Institute at the Consumer Federation of America just published a report showing the amount of carbohydrate and the number of calories in the 26 best selling alcoholic beverages.

The report is in chart form in pdf format. You can download it here.

Put it on your refrigerator or keep it some place handy, so that you’ll at least know how many carbs and cals you throw back when you quaff one or five or your favorite drinks during the hot dog days of summer.

And remember as you’re trying to lose weight the oh-so-true quote (from I don’t know whom – I’ve seen it attributed to several, including Mark Twain):

Will power lasts about two weeks and is soluble in alcohol.

Truer words were never spoken. My will power last night became soluble in the alcohol found in two margaritas. It became way soluble in the Johnny Walker Blue generously provided by my brother in South Carolina at his daughter’s wedding a couple of days ago. Had I had this nifty chart with me, I could have calculated the damages in real time.

Since I started the previous post on this subject with a letter, I’ll do the same for part 2. God knows we have enough like these to fill a book. In fact, this one was in a book. We published the portion below in The Protein Power LifePlan.

A lady from New England wrote to us complaining that she had diligently followed our low-carb diet to the letter yet,  had lost only four pounds over the first few weeks of the program. She included her food diary to show that she was indeed doing a low-carb diet. Here it is:

BREAKFAST: a four-egg omelet with cream cheese, five or six pieces of bacon or sausage, and coffee.

MID-MORNING SNACK: 4 ounces of nuts and 2 to 4 ounces of cheese.

LUNCH: a large bowl of tune or ham or chicken salad make with real mayonnaise, a bag of pork rinds, and a diet drink.

MID-AFTERNOON SNACK: nuts and cheese again.

DINNER: a 16 ounce piece of prime rib, a green vegetable, and a small salad.

DESSERT: sugar-free gelatin and whipped cream and coffee.

When we received this letter MD and I wanted to shake this woman and say: Does it not surprise you that you’re not gaining weight on your diet? I’m sure the only reason she lost the 4 pounds was that she dumped a bunch of excess fluid as a result of her insulin falling. If you run the calculations you will find that this woman was eating somewhere around 5,000 calories per day. She was definitely not creating a deficit. And she wasn’t losing…but she wasn’t gaining either.

The difficult part of any diet – including a low-carb diet – is the bucking up and staying with it during the weight loss phase. It’s pretty easy for most people right at the start because the weight comes off quickly at first, and most people feel so much better just getting off the carbs. As the early days turn into weeks and (in some cases) months, the diet becomes monotonous for many. Weight loss slows down, the great feelings of renewed health and more energy are still there, but have become the norm instead of something new and exciting, and the urge to expand the palate becomes intense.

First, it’s a little nibbling here and there of the forbidden foods, leading a carb creep. And, as I pointed out in the earlier post, many start snacking on calorically dense, low-carb foods, with cheese and nuts being the greatest offenders. Ultimately the weight loss goes from a crawl to stopping altogether. Frustration sets in, and many people bolt from the program saying: Hey, if this isn’t working for me, why am I torturing myself with it? From this mindset it’s a short hop to being face down in the donuts.

I can tell you from both personal experience and the experiences of thousands of patients that this middle time of low-carb dieting (the time between the heady early days and maintenance) can be a drag. And can be fraught with weight-gain peril if you get sloppy with your carb and/or calorie counting. But if you hang in there, you will be rewarded with great dividends.

Once you’ve reached maintenance you can pretty much eat all you want without gaining as long as you watch your carb intake. Like the lady who wrote the letter above, you can feast on all kinds of cheese, nuts, meats, etc. while remaining at your new lowered weight. The calories that come from these sources will sabotage your weight loss if you eat too many of them, but won’t make you gain weight as long as you keep your insulin low.

As you may recall from the earlier post, a lowered insulin levels opens the door to the fat cells, allowing fat to come out to be burned. If your dietary intake meets all your body’s energy needs, however, your body will simply use these dietary calories and leave the calories in your fat cells alone. And you won’t lose. But lowered insulin levels pretty much prevents fat from going into the fat cells, so even if your caloric intake goes up – as long as your insulin stays low – you won’t store more fat in the fat cells. And your weight will stay the same.

How can this be?

The phenomenon is pretty vividly demonstrated in people with type I diabetes, the type of diabetes in which no (or very little) insulin is produced. Most of the time these people get their diagnosis of diabetes when they come to the doctor because they are losing weight like crazy while eating everything in sight. It’s not all that unusual for a person with new onset type I diabetes (who isn’t aware of having the disorder) to lose 40 pounds in a month. These people have no insulin and a lot of glucagon. Without the insulin they can’t store fat, so they dump fat from their fat cells. Much of this fat is converted to ketones since there is no insulin to shut off the process. The glucagon makes them convert muscle protein to sugar even though their blood sugar levels are already sky high. The end result is that these people have elevated levels of sugar in their blood and elevated levels of ketones. They dump both sugar and ketones in their urine, but not enough to account for the amount of weight they lose. The combination of calories lost to ketones and urine can add up to a few pounds per month, but not 40. Other factors are at work. The body has the ability to waste calories, but doesn’t usually do so unless it has to. In the case of type I diabetes it has to. And people with uncontrolled type I diabetes eat and eat and eat and lose and lose and lose.

The same phenomenon holds true in low-carb dieting. Insulin is low and glucagon is high, making it difficult to gain weight. That’s not to say it can’t be done, but it is difficult. Which means that once you lose your weight and get to maintenance, if you keeps your carbs (and thus your insulin) low you can pretty much go back to snacking on cheese, nuts and other high-fat, high-caloric density foods without the fear of gaining. You won’t lose, but you don’t want to lose on maintenance. You simply want to maintain.

You will ditch these extra calories by a number of means. Your caloric-wasting systems will be going full blast. You will be futile cycling, increasing the mitochondrial proton leak, increasing the number of uncoupling proteins, and spending extra energy converting protein to glucose. You will also increase your NEAT. What’s NEAT? It’s Non-Exercise Activity Thermogenesis. Your total energy expenditure is composed of four things: resting metabolic rate, the thermogenic effect from food (the energy required to metabolize what you eat), thermogenesis from exercise and activity, and NEAT. NEAT is from all the little things you do without conscious effort – fidgeting, moving more, moving more briskly, stretching, standing more, etc. These are activities that you don’t really think about but that you perform to dissipate extra energy. It’s why you feel more like exercising after you get going on a low-carb diet; it’s why you perceive your energy levels to be higher. And it’s why you’re less hungry.  Your body has access to its stored fat and is using it and even wasting it. As Key’s showed in his semi-starvation studies, subjects on low-fat, reduced-calorie diets pretty much got rid of most of their NEAT in an effort to conserve energy. The opposite happens on a higher-calorie low-carb diet.

Blowing off this excess energy is what allows you (and the woman who wrote the letter at the start of this post) to eat a lot yet still maintain. But it comes at a price. There is a caveat.

If you crank up your intake of fat calories and at the same time increase your carb intake you are going to gain like crazy. Why? Because you will increase your insulin levels and drive this fat into the fat cells. And it will happen quickly.

Most people reading this will probably say, that would never happen to me. But it can and does. Especially when people start guestimating how many carbs they’re eating. A couple of years ago I posted about a survey done at the peak of the low-carb diet mania showing that people who thought they were on low-carb diets really weren’t. They were cutting the carbs, but not enough to bring about insulin lowering to the point required to enjoy the benefits of low-carb dieting. Men who claimed to be on low-carb diets were consuming on average about 145 grams (3/4 cup sugar equivalent) of carbs per day while women were eating on average 109 grams of carb per day. For most people this is way too much.

So, if you keep carbs low and keep calories in check you will lose weight. If you keep carbs low and don’t worry about the calories you will maintain. A commenter on the earlier post put it brilliantly and succinctly:

Eat low carb = you CAN’T GAIN fat.

Eat low carb ≠ you WILL LOSE fat. [unless, of course, you create a caloric deficit]

I noticed that in a number of comments about this post people had come to the same conclusion empirically. They wrote that whenever they jacked up their consumption of cheese, nuts and other calorically-dense low-carb foods their weight loss stalled. But as long as they kept the carbs low, they didn’t gain. As always, I welcome comments on this issue. I’m keen to hear the experiences of all.

Today I came upon a couple of treats that could easily torpedo a low-carb diet. Many people following a low-carb diet would grab these and throw them down without even thinking about it. I know it’s true because I’ve done it myself.

The photo at the top of this post is of a small sack of dried fruit and mixed nuts sold at Starbucks stores everywhere. I can’t tell you how many times I’ve popped in to a Starbucks to grab an Americano and walked out with one of these. You can see from the size of the sack relative to my hand that these aren’t very big.

If you take a look at the Nutrition Facts on the back, however, you can see that this little sack holds 2.5 servings and that each serving provides 160 calories. Since no one eats a single serving as defined (everyone eats the entire sack), this little treat adds 400 calories to the day’s total. I know that each serving contains 17 g of carb as per the label, making the entire bag sport 42.5 g of carb. But I also know that most people (myself included) won’t look at that number and will simply throw one of these back thinking, hey, these are just nuts with a little dried fruit. How bad can it be? Then wonder why the weight isn’t coming off. I’m using this example to show just how easy it is to run afoul of the carbs and calories in seemingly ‘healthful’ little snacks like this one.

Above you see a photo of an actual small bag of mixed nuts I pulled from our own pantry. I love nuts, and I snack on them all the time. But they are full of calories and have to be treated with care if you’re trying to lose weight.

As you can see from the nutritional label to the left, each serving of these nuts provides 190 calories, which doesn’t sound all that bad. At least not until you look a little more closely and realize that there are seven servings in this little bag. It’s easy, easy, easy (and I speak from personal experience) to eat an entire bag – that’s seven servings – at a sitting. I can go through one of these puppies while watching a movie without thinking twice about it. And eating a bag of these nuts means that you’ve downed 1330 calories. If you’re on a low-carb diet and are creating a caloric deficit of a couple of hundred calories per day, eating even a serving of these nuts will do your weight loss in. But who can eat just one serving? Each serving contains 4 g of effective carbohydrate (6 total minus 2 of fiber), so the entire bag contains only about 28 g carb. I know purists who read every label and stick religiously to a low-carb diet would avoid eating this entire bag because it would provide too many carbs. But far too many of us simply figure that nuts are a low-carb snack food and go for it. And take in 1330 calories in the process.

The purpose of this post isn’t to hector everyone about noshing, but is to let you know how easy it is to succumb to the lure of these kinds of snacks without really giving it much thought. And then wonder why the weight isn’t coming off. Now you know.

It takes a fair amount of diligence and care to lose all the weight you want to lose on a low-carb diet, and it can seem like a real pain. But it’s a whole lot less of a pain than losing on any other kind of diet. When I hear people complain about the difficulty of following a low-carb diet, I think of Winston Churchill’s great quote about the democratic form of government:

Many forms of Government have been tried and will be tried in this world of sin and woe. No one pretends that democracy is perfect or all-wise. Indeed, it has been said that democracy is the worst form of government except all those other forms that have been tried from time to time.

It’s the same with a low-carb diet: it’s the worst diet available except all those other diets that have been tried from time to time.

In the next post I will bring you some good news to offset the bad news of these last couple of posts. I’ll show you how you can reach the point in low-carb dieting that allows you to snack on cheese, nuts and other low-carb, high-caloric-density treats without paying the price. Stay tuned.

In the meantime, if any of you have your own favorite snacks that are caloric torpedoes you would like to share with the group, please post them as a comment.