February 22, 2012

Biochemistry

Why Weight Watchers is actually a low carb diet

Read Time 12 minutes

Invariably I get asked the question, “If carbohydrates are so bad, why did [so-and-so] lose weight on the [such-and-such] diet?”, where “such-and-such” diet is not a “low-carb” diet. Obviously, this is an important question and a pretty complex one.

There are several layers to this and, frankly, there are some things we can’t fully explain – I’ll always acknowledge this. That said, many of the successes (at least weight-wise, though hopefully by now you realize there is much more to health than just body composition) of popular diets can be explained by a few simple observations. Above is a list of this year’s most “popular” diets, according to Consumer Reports. Popularity, of course, was determined by a number of factors, including compliance with current government recommendations (sorry Atkins), number of people who have tried the diet, and reported success on the diets. So it’s actually quite misleading when the report says it’s reporting on the “most effective diets.”

Keep in mind the average American (i.e., at baseline) consumes about 2,500 to 2,700 calories per day (different sources, from NHANES to USDA will give slightly different numbers for this, but this range is about correct), of which about 450 grams (about 1,750 calories worth or about 65% of total caloric intake) comes from carbohydrates. You can argue that those who are overweight probably consume an even greater amount of carbohydrates. But for the purpose of simplicity, let’s assume even the folks who go on these diets are consuming the national average of approximately 450 grams of carbohydrate per day (in compliance with governmental recommendations, as a percent of overall intake).

Take a look again at the figure below, which shows you how many calories folks are consuming on each diet and, more importantly, where those calories come from. [It’s not actually clear to me how Consumer Reports was able to figure out exactly how much folks eat, beyond self-reporting or diet-book recommendation, mind you. In other words, these numbers could actually be wrong, but it’s what we’ve got for now.]

 

Why diets work

[Note: in a more recent (2017, consumerreports.org) analysis, the following categories were included: initial weight loss, maintenance, calorie awareness, food variety, fruits and vegetables, and exercise.]

You’ll note that people on these diets, including the strictest low-fat high-carb diets, significantly reduce their total amount of carbohydrates (therefore reducing the amount of insulin they secrete). Even the Ornish diet, which is the most restrictive diet with respect to fat and most liberal with respect to carbohydrates, still reduces carbohydrate intake by about 40% from what people were likely eating pre-diet.

The reason, I believe, most of these diets have some efficacy – at least in the short-term – is that they all reduce sugar and highly refined carbohydrate intake, either explicitly or implicitly. No one on the Ornish Diet or Jenny Craig Diet is eating candy bars and potato chips, at least not if they are adhering to it. Hence, these diet plans do “clean up” the eating habits of most folks.

Someone made a great point in response to my post on why fruits and vegetables are not actually necessary for good health. The point was, essentially, that telling people to eat 5-6 servings per day of fruits and vegetables can hopefully drive a beneficial substitution effect. If you tell someone who eats Twinkies, potato chips, and candy bars all day to eat more fruit (and they do), you’ve almost guaranteed an improvement in their health if they eat bananas and apples instead of the aforementioned junk food. That doesn’t mean bananas and apples are “good for you” – it just means they are less “bad for you.” Here’s the kicker, though. We’re led to believe that the reason such folks get leaner and more healthy is because they are eating more fruits or more vegetables or more grains or more [fill-in-the-blank], rather than because they eliminated the most egregious offenders from their diet.

I can’t really overstate this point. I have no intention of engaging in a battle with proponents of plant-based eating or no-saturated-fat diets. I’m reasonably confident that the proponents of these diets are good people who really want to help others and have nothing but the best intentions. But that doesn’t mean we can or should overlook the errors being made in drawing their conclusions. Many people do very well on plant-based (e.g., vegan) diets, for sure. But why are they doing well? That is the single most important question we should be asking ourselves. Why did the people in the China Study who ate more plants do better than those who ate more animals (assuming they did)? Parenthetically, if you actually want the answer to this question, beyond my peripheral address, below, please read Denise Minger’s categorically brilliant analysis of the study.

I know a lot of people who eat this way and, I’ve got to say, these folks do not eat a lot of sugar or a lot of highly refined carbohydrates. In fact, many are so conscientious of their health that they actually have far better carb-habits than most (e.g., which breads they choose, which fruits and vegetables they eat).

While I do plan to write an entire post on this topic of what one can and cannot conclude from an experiment, I do want to at least make the point here: The biggest single problem with nutrition “science” is that cause and effect are rarely linked correctly. Stated another way, it’s one thing to observe an outcome, but it’s quite another to conclude the actual cause of that outcome.

Let me digress for a moment to provide an important example of this phenomenon. One of the most prominent figures in the diet/nutrition space is Dr. Dean Ornish. I don’t know Dr. Ornish personally, and I can only assume that he is a profoundly caring physician who has dedicated his life to helping people live better lives. He is nationally, and internationally, regarded for his efforts.

One of the reasons for his prominence, I believe, is the work he did in the early 1990’s on lifestyle modification and the impact it can have on reversing coronary artery (i.e., heart) disease. In particular, Dr. Ornish was the principle investigator on a trial published in the journal The Lancet in 1990. An abstract of the paper can be found here. But as always, I STRONGLY encourage folks with access (or folks who are willing to purchase it) to read the paper in its entirety. For people who don’t want to read the study completely, or who may not have much experience reading clinical papers, I want to devote some time to digging into this paper. Why? Well, for starters, reading abstracts, hearing CNN headlines, or reading about studies in the NY Times doesn’t actually give you enough information to really understand if the results are applicable to you. Beyond this reason, and let me be uncharacteristically blunt, just because a study is published in a medical journal it does not imply that is worth the paper it is printed on. My mentor at the NIH, Dr. Steve Rosenberg, once told me that a great number of published studies are never again cited (I forget the exact number, but it was staggering, over 50%). Translation: whatever they published was of such little value that no one ever made reference to it again.

I am, to be clear, not implying this is the case for this trial, but I want you to understand why it’s important to read papers fully.

This trial, The Lifestyle Heart Trial, prospectively randomized a group of not-so-healthy patients into two treatment groups: the control group and the experimental group (or what we’d call the “treatment” or “intervention” group).

The experimental group (22 patients) was asked to adhere to the following changes for one year:

  1. Change their diet to a low-fat vegetarian diet (10% fat, though obviously no animal fat; 15-20% protein; 70-75% complex carbohydrates) with several other restrictions (e.g., no sugar, flour, or refined carbohydrates; limited alcohol; no caffeine; limited salt; limited cholesterol intake; no egg yolks)
  2. Smoking cessation
  3. Exercise regimen (minimum of 3 hours per week, at minimum of 30 minutes per session)
  4. Stress management (e.g., meditation, progressive relaxation, breathing modification)
  5. Join social support groups for help with adherence (twice weekly)

The control group (19 patients), obviously, remained under “usual-care” (i.e., no change in lifestyle).

One aspect of this trial that made the results particularly interesting was the use of angiography to actually measure and document the coronary artery lesions (i.e., blockages in the coronary arteries) in the patients before and after the lifestyle interventions. The study was not powered to measure “hard” outcomes (e.g., heart attacks, strokes, cancer, death), so the use of blood markers, physical parameters, and angiography were the best proxies for a reduction in disease risk. In other words, there were not enough subjects in the study to determine a difference in these “hard” outcomes, so we can’t make a conclusion about such events, only the changes in “soft” outcomes. I’m not discounting soft outcomes, only pointing out the distinction for folks not familiar with them.

So what happened after a year of intervention versus no intervention?

First off, and perhaps most importantly from the standpoint of drawing conclusions, compliance was reported to be excellent and the differences between the groups were statistically significant on every metric, except total average caloric intake. In other words, for every intended difference between the groups a difference existed, except that on average they ate the same number of calories (though obviously from very different sources), which was not intended to be different as both groups were permitted to eat ad libitum – meaning as much as they wanted.

Who was “healthier” at the end of a year? The table below shows the changes in both groups. If you want a quick primer on p-values, this is as good a time as any to get one. These tables (i.e., results tables) are a bit cumbersome if you’re not used to looking at them, so let me walk you through one row in detail. Let’s look at HDL cholesterol concentration. In the experimental group, HDL-C fell slightly from 1.00 +/- 0.26 mM (39 +/- 10 mg/dl for Yankees like me) to 0.97 +/- 0.40 mM (38 +/- 15 mg/dl), while it slightly fell from 1.35 +/- 0.52 mM (52 +/- 20 mg/dl) to 1.31 +/- 0.38 mM (51 +/- 15 mg/dl) for the control (i.e., no-intervention) group. It’s hard to tell if this change was statistically significant by inspection, so you glance at the p-value which tells you it was not. (To be exact, the p-value of 0.8316 tells you there is an 83% chance that this difference was random – as a general rule we don’t consider a difference to be statistically significant — meaning we’re going to assume it wasn’t just a chance fluctuation, the roll of the dice — until the p-value is below 0.05, and ideally below 0.01).

Take a moment to look over the rest of the table (or just skip reading it since I’m going to keep talking about it anyway).

 

Ornish Lancet paper

What else was not significantly changed?

  • Triglyceride level
  • Apoprotein A-1 (not surprising, I guess, since HDL particles carry the bulk of apo A1)
  • Blood pressure, both systolic (“top number”) and diastolic (“bottom number”)

What was significantly changed?

  • Total cholesterol concentration (down in both groups, but significantly more in the experimental group
  • LDL cholesterol concentration (same as above)
  • Apoprotein B (again, to be expected given that LDL particles carry apo B)
  • Body weight (this was, as you can see from both visual inspection and the p-value, the most significant change between the two groups)
  • Though not shown in this table, the experimental group also reported less chest pain severity (though chest pain frequency and duration were not statistically different).

What about the angiographic differences? That is, how did the actual measured lesions in the subjects’ coronary arteries change? 

Seven patients were excluded from this analysis: 1 patient in the control group (patient underwent an emergency angiogram in another hospital, but lesion sizes were not measured); and 6 patients in the experimental group (1 died while exercising in an “unsupervised gym,” 1 could not be tested at follow-up due to a large unpaid hospital bill, 1 patient dropped out, 1 patient’s pre-intervention angiogram was lost, and 2 patients did not have adequate overlay of pre- and post-images).   To justify the findings of this trial we need to believe that the exclusion of these seven patients did not alter the conclusions, but we’ll never know.  This disproportionate exclusion of 6 patients from the treatment group and only 1 patient in the control group, for (perhaps) the most interesting outcome, is (perhaps) the most significant methodological flaw of this trial.

Excluding these seven patients, the experimental group experienced an overall reduction in coronary artery stenosis (blockage) from a mean of 40% to 37.8%, while the control group experienced a progression in coronary artery stenosis from a mean of 42.7% to 46.1%, which was statistically significant.  This trend also held for larger lesions (i.e., those starting out over 50%).  Most importantly, in my mind, within the experimental group there was a strong correlation between adherence score and lesion regression.  Translation: The more rigorously a patient was compliant with the lifestyle changes, the greater was the regression of their coronary artery lesions.  This correlation is quite suggestive that the lifestyle change was responsible for the regression of coronary lesions.

I know what you’re thinking…Is there a point embedded somewhere in here?  Yes.

Here is my point: This was a well-done trial from the standpoint of testing what it set out to test.  It set out to test if a comprehensive lifestyle change could reduce markers of coronary artery (heart) disease, which it did. But that’s it.  It did not tell us if a comprehensive lifestyle change reduced actual heart attacks, which it very well might have if there were hundreds of patients in the study.  It is equally important to understand what we cannot conclude from this study.  We cannot conclude which element of the lifestyle intervention led to the reduction in markers of heart disease.  We know that in aggregate the lifestyle changes made a positive difference, but which ones actually caused the change and which were bystanders remains unknown.

Let’s take a leap of faith and hypothesize that the dietary intervention (rather than, say, the social support) had the greatest impact on the measured parameters in the subjects.  It’s certainly the most likely factor in my mind.  But what, exactly, can I conclude? Can I conclude that a low-fat vegetarian diet is the “best” diet for reducing the risk of heart disease?  Nope.  I can only conclude that a low-fat vegetarian diet is better than the average American diet consumed by the control group (if you are willing to stipulate that the dietary intervention was the most significant driver of outcome).  Why?  Because that’s what was tested.  Unfortunately, this study (and hundreds like it) can shed no light on which specific aspect of the diet in the experimental group provided the advantage.  Was it the reduction in fat intake?  The reduction in animal protein?  The reduction in sugar?  The reduction in simple, highly refined carbohydrates? Unfortunately, we do not know.

SLIGHT DIGRESSION: Tragically, all of U.S. nutritional guidance and follow-from-it policies, recommendations, and food-based infrastructure were derived from this type of science. Maybe their conclusions are correct.  Is fat bad for us?  Are complex carbs the best thing we can eat?  Though theoretically possible, there is no scientific evidence telling us this.  In fact, there is ample evidence actually suggesting the opposite is true.  Hence, this is why – exactly why – we are founding the Nutrition Science Initiative (NuSI) with a group of scientists who all agree that we need to actually test these hypotheses in the most rigorous manner possible, and only then make dietary recommendations.

How bad is it that nutritional recommendations are based on weak science?

Consider the following hyperbolic example: Imagine a clinical trial of patients with colon cancer.  One group gets randomized to no treatment (we’ll call them the “control group”). The other group gets randomized to a cocktail of 14 different chemotherapy drugs, plus radiation, plus surgery, plus hypnosis treatments, plus daily massages, plus daily ice cream sandwiches, plus daily visits from kittens (we’ll call them the “treatment group”).  A year later the treatment group has outlived the control group.  Great news, to be sure.  The treatment worked!  Here’s the problem…we “conclude” it was the 7th and 9th drugs in the group of 14 drugs, plus the kittens that caused the treatment effect and we enact recommendations based on that.  Are we right?  Sure, it’s possible, but actually it’s quite unlikely.  The only way to know for certain if a treatment works is to isolate it from all other variables and test it (in a randomized prospective fashion, of course).   Do the kind of science we were taught to do in 8th grade.

So what do I think happened in Dr. Ornish’s study?  I think the reduction in sugar and simple carbohydrates played the largest single role in the improvements experienced by the experimental group, but I can’t prove it from this study any more than one can prove a low-fat vegetarian diet is the “best” diet.  We can only conclude that it’s better than eating Twinkies and potato chips which, admittedly, is a good thing to know.

Ok, back to the Consumer Reports “best diet” list I started this discussion around.  Another point you’ll note in this table (up at the very top) is the overall amount of caloric restriction in each diet – an average of about 1,500 calories per day.  The caveat here is that these numbers are self-reported, so everything needs to be taken with more than the proverbial grain of salt.  I know what you’re thinking, “Hey, but you said calories don’t matter – why should it matter how many calories these folks are eating?”  Remember, you can always “force” weight loss by creating energy imbalance.  What I mean by that is you can force an energy imbalance if folks are willing to suffer (e.g., work really hard and/or starve).  The reality TV show, The Biggest Loser, is a great example of this.  Participants on the show are basically starved (under 1,000 calories per day) relative to their expenditure (6 hours per day of exercise at a cost of possibly as much as 4,000 calories per day).  The question is, or at least should be, does this form of “dieting” result in long-term, sustainable weight loss?  The overwhelming evidence is that calorie restriction (i.e., reducing calories significantly below active or deliberate caloric expenditure) results in transient weight loss, not sustained weight loss.  Why?  There are a few reasons, but I think the biggest two are:

  1. People don’t like to be hungry, and if they are reducing their caloric intake by reducing fat intake, they seldom find themselves satiated.
  2. Semi-starvation reduces basal metabolic rate, so your body actually adjusts to the “new” norm and slows down its rate of mobilizing internal fat stores.

Furthermore, most people can’t do six hours of heavy exercise a day (not to mention the world is full of people who do six hours of physical labor a day and are obese; I was fat doing 4 hours of exercise per day).  The real tragedy of this is that when folks restrict calories and then resume, when they can’t tolerate the discomfort of relative starvation anymore, they usually end up gaining back all, if not more, of the weight they lost in the first place.

Not to beat a dead horse, but I’d be remiss if I didn’t make this point one more time: When someone reduces caloric intake to 1,500 calories per day – even on a “balanced” diet – they are considerably reducing carbohydrate intake in aggregate and almost always disproportionately with respect to the worst offending carbs (e.g., sugars, simple refined carbs).

Ultimately, the question we’re driving at is, why do these diets work? I argue that each of these diets does some good, especially with respect to eliminating the worst offending agents along the insulin-fat-metabolic derangement axes.   The problem, unfortunately, is that the scientific community is completely confused as to why they work.  Most people think the primary reason these diets work is that they reduce fat intake and total calories.

I argue that reduction of fat intake has nothing to do with it and that the reduction of total calories has a transient effect. And, the majority of the benefit folks receive comes from the reduction of sugars and highly refined carbohydrates. But now I’m repeating myself, aren’t I?

 

Photo by Markus Spiske on Unsplash

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155 Comments

  1. I’m glad you wrote this because this is something I’m having to accept is that all research I look at needs to be viewed with a much more critical eye than I previously used. Otherwise I’m just deferring to someone because of their standing. One thing that has bothered me about a lot of dietary studies of the “American diet” is they appear to be controlling for something way too broad. They never factor in that the chicken was breaded or that when someone ate steak or fish they had a large amount of bread of potatoes along with it. Plus maybe the person was drinking a big glass of Coke or Sweet tea with every meal. The end conclusion is the whole thing must be bad and therefore needs to be reduced or outright expunged from the diet. That is one big difference I’ve noticed between studies cited by writers who want to condemn the entire diet consumed by Americans vs those who look at it with a more in depth eye and realize that certain components are the problem not the whole diet across the board.

    • It’s *really* tough to study this stuff properly, especially compared to studying things blood pressure lowering pills, which are complex in their own right, but MUCH easier to control in a study. Here’s the good new: this CAN be done and we will get it done.

  2. Comment
    Consumer reports publishes that which they are paid to publish. Case in point…they recently reported that olive oil is not good for you because it does not contain omega 6. And…sunflower and soybean oil are better. Pulp fiction!!!

        • The current sponsors for the former ADA, now the Academy of Nutrition and Dietetics: Coca-Cola, Pepsi, Hershey’s, Aramark, Mars, General Mills and Kellogg’s.

          The American Diabetes Association’s biggest supporters include: Eli Lilly, Merck, Novo Nordisk, and Sanofi as the ‘elite’ sponsors.

          Do you think the Academy’s supporters want to hear that if you eliminate their products you will no longer need to rely on the products provided by the biggest supporters of the Diabetic Association?

        • The point has clearly been made, but I can not resist adding to this. In my field, the American Academy of Pediatric Dentistry Foundation accepted a $1 million dollar grant from Coca Cola!

    • Dr. Gambina, Dr. Attia: no, Consumer Reports accepts *no* corporate money whatsoever; that didn’t play into it.

      The main criticism I’d have for this analysis, Dr. Attila, is that while WW does indeed cut carbs, it does so in the context of also cutting fat and Calories (which of course you note): you’re not accounting for the fact that other, lower-carb diets (in both absolute and relative terms) were ranked more poorly, which is (surely) the issue.

      Marilyn, a commenter on p. 3, has a good point about some plans (including WW) having the advantage of group support, which I think is a very major confounder.

      Stylistically, Dr. Attia, I’d suggest that you have here and in several places bitten off too much at once: you analyze many different kinds of problems at once, which tends to make the post as a whole a bit rambling; I’d suggest finding one issue at a time and breaking it down. Eg, the criticism of the Ornish Lifestyle Heart Trial is excellent (and I LOVED the kitten-stroking quip), and really could and should have stood alone. Any time you feel compelled to say ,”Ok, back to the Consumer Reports “best diet” list I started this discussion around”, you probably have too much digression 😉 .

      • Michael, I agree with you…sometimes I just get carried away and write too much. This post was really two posts in one. But, hey, consider it bonus material! To you point about ranking, the main reason a diet like Atkins does poorly on this is because of the component of the ranking that depends on adherence to dietary recommendations, which obviously run counter to Atkins.

    • Perhaps Consumer Reports *doesn’t* accept any “corporate money” – who really knows?

      They still lost all credibility (with me anyway) when in the late nineties they intentionally altered test conditions to create the results they wanted on an automobile report for a car they didn’t like: The Suzuki Samurai.

      Pretty much solely because of their report, Suzuki was forced to eventually withdraw the Samurai from production in the US although they later won the lawsuit that was filed as a result of the forged report by showing videos from the actual testing of the car conducted by CR. In these videos, CR reps were shown *forcing* the vehicle to roll by altering the test conditions far beyond that required of any other vehicle. In fact, it was so bad that the “professional drivers” could NOT get the vehicle to roll and refused to alter their driving to make it happen. It took one of the producers of CR to don a helmet and force the vehicle to roll. Why? Because that’s what they wanted.

      Ironically, the fact that CR had to admit it was faked somehow wasn’t plastered all over their magazines and the front pages of a bunch of newspapers.

      At that point, everything they publish became suspect and may as well line a birdcage somewhere.

  3. Peter, I have a coworker who has recently lost 80lbs over the course of a year on weight watchers. It is wonderful to watch these people glow once they have found some sort of solution to their weight problem. After short diologue with her on the particulars of her daily intake I quickly realized her consumption of carbohydrate was significantly reduced and eliminated almost all fructose. Not that I wish any harm to her but my question is to what happens post weight loss goals? Do they rapidly regain the stored adipose? I recall hearing Gary talking about his discussion with a participant from the Biggest loser on Larry King and the rapant weight gain after the show. I admit, I get fired up watching Gary trying to make points to Jilian Michaels. Anything that helps these people I agree with you is well intentioned, yet lacks educating the persons what might have taken place inside their bodies instead of for example counting “points.” Do they even know? Keep up the great work!

    • John, I point this out at the bottom of my post (not that I can blame you for not reading the whole thing…it’s a bit long). Sadly, virtually all folks (I’ve read stats anywhere from 80-95%) on these diets gain all the weight back once they leave the program and try to re-integrate into their normal eating pattens. Why? Probably because these diets don’t actually help people understand WHY they worked, so the helpless person is now trying to eliminate fat (or whatever else they think got them fat in the first place).

      • Exactly, it’s the WHY that is missing. I’ve done WW more times than I care to admit, and I’d always lose 20lbs, look better, feel lighter, but be miserable and starving. Why? Because my body couldn’t handle the “low-points” carbs I was feeding it. Now, I must point out that WW has changed it’s points system to be harder on carbs and easier on fat and protein, but they also made fruit a “free” item. Not a great idea. The one great thing that came out of my last WW adventure was that they did change the points system, and all my low points carbs, like bran cereal and small tortillas went up dramatically, so I eliminated them, and after a few days without any wheat realized that I felt terrific! No more wheat for me, it’s been over a year now. The thing is, it is possible to eliminate wheat and still eat way too many carbs (can we say ice cream?). So after actually losing another 5 lbs after quitting WW, just by cutting out wheat, I started to carb drift upwards, and gained 15lbs in just a few months. So after watching FatHead a couple of times I made the decision to try Atkins instead of WW this time – BEST decision I’ve ever made (well, other than marrying my husband!). I’m now happily in ketosis, and the best part is, I know the WHY of weight loss now, how totally liberating and hope giving. After 40 years of being fat, I have hope that the next 40 years will be quite different.

  4. Hi Peter,

    Great post!

    A question on fatty acids, as this is relevant to the diets described here: In Belgium, where I live the reference values for omega 3/omega 6 ratio is 0,28 – 0,45 while LA/DGLA is <7 and DGLA/AA is 0.10. What is your take on this?

    Finally any thoughts on Krill oil vs Fish oil vs Cod liver oil (fermented?).

    Looking forward to your next post, and of course people's comments for the current one!

  5. It’s sad how often you see a study stating a conclusion that isn’t actually supported by the data in the study. And given the fat-phobia brainwashing that we’ve received for the past several decades, maybe it’s not surprising that the actual data in the studies is almost irrelevent, since we already KNOW that the “correct” conclusion is that anything bad in the study was caused by saturated fat, and anything good was caused by whole grains.

    Sometimes I think/hope that the tide is turning, and the truth will start to gain some mainstream traction. But realistically, I think we’re going to have to wait for a lot of the current crop of “experts” to get old and die before the saturated-fat-is-bad lie will be exposed by the mainstream media in any significant amount.

    Anyway, it’s nice to discover someone who takes the Taubes viewpoint on things, and also takes the time to actually post online about it with some frequency, so thanks!

    • Anthony, I’m a bit more optimistic that we don’t need to wait that long. Also, don’t underestimate the importance of “normal” people like us who are fed up with fed bad science. Not confusing the hypothesis that people like me and Gary have about carbs/fat, the REAL issue is getting rid of amateur-hour science and joining the 21st century like all other scientific disciplines. Thanks for your support!

  6. Great post! One of my favorite things to say to people who are scared of saturated fat is that even on an entirely plant based diet, (ala Ornish Diet), if they are restricting their caloric intake, their bodies will be running on the saturated (animal) fat that they have stored on themselves. A bit trite perhaps, but I think the point is an important one. Nobody debates that weight loss is good, but nobody seems to talk about the fact that if we are losing weight, our bodies are almost invariably going to be running on saturated fat.

    • This assertion doesn’t make sense to me. The human body doesn’t store saturated fat. It takes saturated fat you eat and disassembles it with enzymes into it’s component fats. So, even when you’re metabolizing body fat, you’re not running on saturated fat unless you’re actually eating it.

      Did I take you too literally?

      • Sorry if I was unclear. Human body fat is saturated fat. Otherwise our fat cells would be liquid, and we would be very sloshy. So when our bodies release FFAs from our fat cells, those FFAs are saturated, and our body is essentially running on saturated fat.

        • It’s actually a bit more complicated than that. For example the degree of unsaturated fatty acids in our membrane bilayer probably plays a role in our insulin sensitivity, just as one example. This is highly variable from cell to cell and person to person. As an anecdote, when making pemmican out of beef, the solidity of the meal at room temperature is highly dependent on where you’ve harvested the fat from the animal. The more peripheral the fat source, the more polyunsaturated, the less solid; the more central the fat source, the more saturated, the more solid.

        • Oh absolutely, I was mostly referring to the fact that most of the excess carbs we eat are converted to palmitic acid, which is a SFA. I found the thought of a sloshy person funny, though, so I thought I’d throw it in. I like to imagine that if we stored all PUFAs we’d be like waterbeds.

  7. Great post, Peter. The literature is virtually endless with bad ‘science’ when it comes to diet studies. The recent study by Bray in the AJCN is another great example. The conclusion was essentially that “when it comes to weight loss, how much you eat matters more than the proportion of fat, carbohydrate, and protein in your foods,” according to Marion Nestle. This coming from the author of “Why Calories Count,” so take it with a grain of [hypertenstion-inducing-heart-disease-causing] salt.

    The study looked at four different diets…except that it didn’t.

    There was an (1) average protein, low fat group (65% CHO), (2) High protein, low fat group , (3) Average protein, high fat, and (4) high protein, high fat (35% CHO).

    All data was self-reported which brings about another host of limitations.

    When you look at the self-reported data, the difference between the supposed ‘low fat’ group and ‘high fat’ group was a tablespoon of olive oil.

    In other words, the proportions of fat, carbohydrate, and protein were not much different between subjects and the results in terms of weight loss were not much different, either

    Many times when looking at the efficacy of an “Atkins” diet, the long-term (2 years) results will lead the investigators to conclude that the diet doesn’t work in the long term. But what you find is the subjects progressively increase their consumption of carbohydrates; and if you are testing the carbohydrate hypothesis (and not steeped in the calories-in/calories-out paradigm), you would expect this to happen and you wouldn’t conclude the diet doesn’t work.

    And the investigators will defend their views by saying they were looking at what happens when you ‘prescribe’ a diet, not the diet itself, and then that gets into intention-to-treat analysis, which is another can of worms.

    The ‘science’ really is questionable, to put it diplomatically.

    Again, illuminating post, Peter. Invariably, when anyone goes on a ‘diet,’ they switch from regular soda to diet soda, they ditch the twinkies, and so on…

    • Thanks very much, Bob, both for the kind comments and for sharing the other data with folks. We can solve this problem! We just need to be disciplined and patient enough to start doing good science.

    • “Many times when looking at the efficacy of an “Atkins” diet, the long-term (2 years) results will lead the investigators to conclude that the diet doesn’t work in the long term. But what you find is the subjects progressively increase their consumption of carbohydrates; and if you are testing the carbohydrate hypothesis (and not steeped in the calories-in/calories-out paradigm), you would expect this to happen and you wouldn’t conclude the diet doesn’t work.”

      I don’t understand this comment. What long-term result from an “Atkins” diet would lead researchers to conclude that the diet doesn’t work:
      . weight loss?
      . improved compliance rate?
      . reduction in blood triglycerides?
      . increase in HDL?
      . reduction in amount of small, dense LDL particles?
      . decrease in fasting blood glucose?
      . decrease in HbA1C?
      . decrease in CRP?

      Do you mean the decrease in carbohydrates eaten? That’s not a result — that’s an input. Besides, all you’d have to do is define “Atkins” as carbs constituting 20% or less of a diet, with no grains, no processed sugar, and less than “x” g of fructose/day.

      Also, what does “…saying they were looking at what happens when you ‘prescribe’ a diet, not the diet itself, and then that gets into intention-to-treat analysis, which is another can of worms.” mean?

    • @[email protected] – I’m one of those former Atkins adherents from the 90s. I had a wonderful outcome, with trouble maintaining a few years out because I reverted to my old habits. I would just like to clarify a couple points for those who may not be as familiar with the details of Dr. Atkins’ plan. First, it is truly low carb whatever your ratios, the initial phase is 25g with increases of 5g daily in weekly increments. Second, adherents are supposed to cap at levels that prevent weight gain, for me that would be 50g (at least back then). So even in the lifetime maintenance phase, you are still low carb, some would say very low carb. The problem with execution is that a person must maintain impeccable process for self monitoring. If this were something I had a natural talent for, I would not have a weight problem in the first place. Add to this a cultural environment that says your way of eating is not only indulgent, but unhealthy, and I think remaining within the parameters becomes nearly impossible.

      Today, my hope is that with works like Peter’s and Gary’s and soon NuSI, we can turn this thing around. In closing, I’d like to say that I am low carb again, and only 10 lbs over my Atkins low. Know that there are thousands, maybe tens of thousands, of people with similar histories to mine that will benefit immensely from your efforts in the near term.

      Best, L.

  8. Thanks for this post! Great explanations. I have tried WW in the past-and did not have much success.
    Since going low-carb in September, I have been tempted to track my ‘points’ using the WW system (just for fun). My daily ‘points’ consumed would far outweigh my recommended ‘points,’ yet I am still losing weight. For example, if I had 30 ‘points’ to use per day, I am probably consuming about 50 points a day because of how they weigh fat/protein in the system.
    It is also interesting to note that although they allow ‘unlimited’ fruit with the new system, they note that if your weight stalls, you should reduce your fruit consumption.
    I’m not sure it will ever be in WW’s interest to concede it is the reduction in carbs that makes the difference.
    Although I wonder if there is enough of a shift in society’s thinking about carbs, will WW follow? Only if it benefits the bottom line I guess.

    • The only way “mainstream” nutrition will be able to change is when the medical establishment begins to use real science to study the impact of food composition on health. Until we do that, folks like me and many others who disagree with Current Dogma will be marginalized.

  9. Once again, a terrific post. I thoroughly appreciate the work and attention to detail you put forth. Hate to sound like a tin foil hat-wearer, but this is just another reason I can’t believe most of what I read, hear, or even see. Keep up the good work! And yes, Denise’s breakdown of the china study is awesome.

  10. Hi Peter: Excellent post! If you look at healthy populations around the world, ie Japan and France that have different macro nutrient compositions you note several things: No eating of junk food, and the carb intake even with the rice eating Japanese is considerably less that what you see with the Standard American Diet. On top of which most to all eating is done at meal time; snacking like in the US is virtually absent.
    Esselstyn is an Ornish acolyte with no fat mantra and has shown plaque regression, but if you look closely at the book(which i browsed)all who experience regression, or almost all were on statins.
    For me a whole food diet is the way to go with emphasis on animal products some fruits veggies and starch in form of potatoes and some rice.
    Look forward to your review of Polys. As you know the med profession is on the bandwagon of the Mediteranean diet with emphasis on poly’s. Not sure what Medit diet is by the way.

  11. Thanks for the great post. There are two points with the plant based diet that I can’t seem to get over. The first is that a whole foods plant based diet is not nutritionally complete for humans. Mainly because it lacks B12, but also is very low in other essential nutrients. So to be a healthy vegan you have to take a man-made vitamin.

    Also, how could whole grains and legumes be the perfect foods for humans when no one had much access to them until 10,000 years ago? Even after the invention of agriculture, many people didn’t, and still don’t have any access to these products. It doesn’t add up that we are perfectly suited to consume foods we never ate for over 100,000 years.

    • Helga, I do ask myself the same question. When I watch my cat tackle and devour mice and birds effortlessly, I can’t seem to understand why I would ever force him to eat a diet of zero animal products. Isn’t evolution supposed to be smarter than us?

    • “So to be a healthy vegan you have to take a man-made vitamin.” To be a healthy low-carber/paleo eater, you have to take man-made vitamins, too. Grok the caveman didn’t, because his environment was relatively clean. Ours isn’t, so we have to compensate. Nor do we get out in the sun much. If you’re not taking with at least an omega-3 supplement, vitamin C, D, and K2, you’re not getting the amount of these nutrients you need to cope with the toxic environment in which we live.

      • I actually disagree with this, mainly because I find the whole RDI ‘science’ suspect.

        Vitamins and minerals as quantifiable RDI values are a rather modern concept. Their ‘discovery’ is what, 100 years old or so, and the science on which the RDI’s are based is NOT based on cultures eating carnivorous or ‘paleo’ diets. Recommended intakes are derived from deficiency levels ascertained within the context of a modern agricultural diet.

        We cannot conclude that these RDI numbers apply as some kind of ‘absolute’ objective human essential.

        For example, our supposed Vitamin C ‘requirements’: Since Vit C competes with glucose (same receptors) for entry into cells, the modern RDI tells me nothing about how much I need if I don’t eat carbs. If I eat a SAD diet maybe I need the RDI’s 60mg to prevent deficiency.
        But if I don’t eat carbs, my requirement for Vit C may in fact be MUCH smaller and easily thus available in sufficient levels from animal sources.

        Considering also how grains and other agricultural foods contain all sorts of anti-nutrients like phytates, lectins, oxalates etc which bind to and prevent absorption of many minerals, it is not surprise that RDI levels based on modern diets are so high that it ‘seems’ like animal foods alone don’t have enough to provide the ‘correct’ levels every day.

        But without the modern foods the levels of these vitamins and minerals in animal products is just fine to prevent deficiencies.

  12. I only recently realized that when I initially lost my weight – 80 pounds about 23 years ago – I was on a low-carb diet. I went to WW, but modified it by leaving out the bread servings. I did this knowing, frankly, the diet was too many calories for me, and – this was before the big food pyramid change – that I needed my protein, and starch was fattening.

  13. Another nice post, Peter. I will reread it when I have more time. Purely-constructive criticism here… I think you may have tackled two subjects at once though – the reason other diets sometimes work, and the typical flaw in many diet studies. Each would warrant its own post and may be easier to digest on its own. Love the kittens analogy – very effective.

    • Very fair point, Matt. I definitely experienced some “scope creep” on this one. Don’t worry, I’ve got lots of planned writing on the “bad science” issue…This will be a full course!

  14. Great post, excellent insights about what actually gets eliminated with most of these diets!

    When I first came upon your blog, I mentioned that I can’t “like” you on Facebook because I’ve got “hard science-y” friends (e.g. a planetary climatologist) who jump all over me whenever I post something about the poor science behind the saturated fat scare. Recently I posted a couple of excerpts from a Harvard School of Public Health article which quoted this result from a large review study:

    “There is insufficient evidence from prospective epidemiologic studies to conclude that dietary saturated fat is associated with an increased risk of CHD, stroke, or CVD.”

    They then go on to say that replacing saturated fat with refined carbohydrates is bad for your heart. Hurrah! Progress!

    Not so fast… A little further down you’ll find:

    “The net effect is as bad for the heart as eating too much saturated fat…

    But wait, I thought you said… Oh, nevermind.

    My pointing out on Facebook of this bizarre disconnect resulted in the usual accusations of “cherry picking” and not understanding science, etc. But I think I scored some points when I noted that the article also cites PIZZA as one of the main sources of saturated fat in the American diet, so there are plenty of confounding variables when trying to determine exactly what it is that is so unhealthy.

    I look forward to your post about PUFAs, especially since one of the main takeaways of the Harvard article is that we should now replace saturated fats with corn and soybean oils…

    http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/fats-full-story/

      • BTW, what’s a healthy light-flavored oil to use for homemade mayonnaise? Extra-virgin olive oil has too strong a flavor when I’m making a base for something like sesame mayo to go with salmon teriyaki. Is peanut oil a good choice?

    • I like to use Avocado oil as a nice light oil when olive oil is too strong. I also have a lighter version of olive oil that doesn’t have the strong flavor regular olive oil has.

  15. Peter,
    This is a truly outstanding post. In addition to explaining why many diets seem to work it will hopefully help many people understand how research works (or doesn’t work)and why we sometimes need to have the courage to try something based on anecdotal evidence only. You have been a great role model for that. I believe it takes courage to change the world and it seems we don’t have too much time looking at the health crisis in the developed world and our overburdened health care system. You have the rare gift to analyze complicated issues to where the average American (with some college education) can understand them.
    Cheers,
    Birgit

    • Thanks so much for such kind comments. I’ve very optimistic that a change in afoot. If we (the “normal” people) start to demand real science, the truth will come out. Then we can begin to course correct (assuming the current path is incorrect, which I personally believe it is).

  16. Peter — on your graphic, the red numbers (e.g. “203 gm carboydrates”), are those supposed to be calories (i.e. “203 kcal from carbs”)?

  17. One thing I don’t see mentioned here – but I believe you mentioned it elsewhere – is the hormonal aftermath of low-calorie diets. You know, the new study finding that leptin levels remain at least one-third lower for an entire year after a dieter loses weight on a low-calorie diet? So this is part of the reason Weight Watchers people gain their weight back 95% of the time, right? After a successful low-calorie intervention, they go on to face lower leptin levels – and an attendant compulsion to overeat – until they return to their former caloric intake (and thus their former weight). Or so I gather.

    I have two questions:

    1) Do you think this study is legit? Was it methodologically rigorous enough to accept the claim that low-calorie diets have this chain of hormonal effects?

    2) Are there comparable studies showing that low-carb diets don’t have these effects? My own low-carb experience has been free of cravings, but I wonder if anyone has measured hormonal impact the way this study did.

    • “the new study finding that leptin levels remain at least one-third lower for an entire year after a dieter loses weight on a low-calorie diet”

      Do you have a link for that?

      I watched Dr. Lustig’s presentation to the Ancestral Health Symposium and it was fascinating to see how people reached a weight-loss plateau after losing a certain amount of weight (whether by toughing it out through hunger or taking an appetite suppressant)due to leptin deficiency. When leptin was restored, weight loss resumed.

      I get pretty annoyed when I think about how much further ahead we could have been with this research if we hadn’t taken a thirty year detour through sloth-and-gluttony land!

    • NO, I meant this one:

      Sumithran, P., Prendergast, L.A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., Proietto, J. (2011). Long-term persistence of hormonal adaptations to weight loss. New England Journal of Medicine, 365, 1597-1604.

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