Archive for January, 2012

I regularly receive emails and comments asking where to find good low-carb recipes.  I always mention that I like the cookbooks by Dana Carpender and Judy Barnes Baker the best.  We use them all the time.  (Judy’s moussaka recipe is one of my all-time favorites.)

So I was pleased to receive a copy of Judy Barnes Baker’s newest cookbook Nourished: a Cookbook for Health, Weight Loss and Metabolic Balance earlier this week.  For those of you who don’t know, this is the cookbook Judy originally pitched to the American Diabetes Association.  For awhile, they were on board … then backed out.  Can’t say I’m surprised.  They just can’t admit their dietary advice is wrong.

The book includes an opening section that explains the science of why low-carb diets are the best choice (especially for diabetics) with short chapters written by Dr. Mary Vernon, Jacqueline Eberstein (who worked with Dr. Atkins for decades as his nurse) and Dr. Richard Feinman.

But you already know that stuff.  You’ll want this book for the recipes.  Here are just a few examples of the hundreds you’ll find in the book:

  • Corned Beef Hash with Poached Eggs
  • Peanut and Chicken Soup
  • Creole Gumbo
  • Strawberry Rhubarb Parfait
  • Sautéed Cabbage
  • Barbecued Ribs
  • Herb Roasted Olives

If you think a low-carb diet is boring, it just means you don’t have enough good recipes on hand.

To celebrate the release of the book, Judy is running a prize-giveaway contest on her Carb Wars blog.  Here’s the link.

Herb Roasted Olives … mmmm…

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I’m starting to wonder if the editors of medical journals schedule a yearly Meat Causes Cancer! issue …something like their own equivalent of the Sports Illustrated Swimsuit issue.

Our cover model this year is pancreatic cancer, folks — and as you can see, she’s a hot little topic!  We don’t want to start any rumors, but we have it on good authority she’s often seen in the company of some beefy hunks.

The hot little topic made a splash in the media last week, with headlines and opening paragraphs like these:

Bacon eaters warned of cancer risk

Eating two rashers of bacon or one sausage a day can increase the risk of a deadly form of cancer by almost a fifth, according to a new study.  New research by the Karolinska Institute in Stockholm has found that eating 50g of processed meat a day can increase the risk of pancreatic cancer by 19%.

Processed Meat Could Raise Pancreatic Cancer Risk

Some possible bad news for all the bacon lovers out there.

A new review in the British Journal of Cancer suggests a link between processed meats — like bacon and sausages — and an increased pancreatic cancer risk. In particular, eating an extra 50 grams a day of processed meat — or about a sausage — is enough to raise pancreatic cancer risk by 19 percent, BBC News reported, while an extra 100 grams of processed meat a day could raise the cancer risk by 38 percent.

“The authors of this study have suggested that one of the reasons could be that some of the chemicals that are used to preserve processed meat are turned in our bodies into some really harmful chemicals which can affect our DNA and increase the chance of cancer,” Jessica Harris, health information manager at Cancer Research UK, told Sky News.

Holy jumpin’ jiminy!  A 19% increase in risk – that’s almost a fifth!  Better drop that bacon right now, Mister.  You don’t want to mutate your DNA and roll the dice with a 19% increase in the odds you’ll die of pancreatic cancer.

I tracked down the full study, and it was pretty much what I expected:  a meta-analysis of several other studies, all of them based on food-recall surveys.  So let’s put on our Science For Smart People hats (mine is cone-shaped; you can choose your own) and ask some critical-thinking questions:

Q: Was this an observational study or a clinical study?

A:  It was a meta-analysis of 11 observational studies, the kind where the researchers pool the data and crunch the numbers.

Q:  Did the researchers control the variables?

A:  No, because they couldn’t.  They were dealing with data published by other researchers who may or may not have done a good job controlling their variables.  As the authors of the current study noted:

Our study has some limitations. First, as a meta-analysis of observational studies, we cannot rule out that individual studies may have failed to control for potential confounders, which may introduce bias in an unpredictable direction. All studies controlled for age and smoking, but only a few studies adjusted for other potential confounders such as body mass index and history of diabetes. Another limitation is that our findings were likely to be affected by imprecise measurement of red and processed meat consumption and potential confounders.

Let me put that into plain English:  Our findings are meaningless. The studies we analyzed were based on food-recall surveys that are notoriously inaccurate, and most of them didn’t control for body mass index or diabetes, which essentially means they didn’t control for intake of sugars and refined carbohydrates.

Okay, folks, move along; nothing here to see.

What, you’re still here?  Then we may as well continue.

Q:  If A is linked to B, is it possible that they’re both caused by C?

A:  Yes, of course it’s possible.  As the researchers noted above, “All studies controlled for age and smoking, but only a few studies adjusted for other potential confounders.”  Since processed meats are often served with a big wallop of refined carbohydrates – pizza, burritos, deli sandwiches, etc. – it’s entirely possible that people who consume more processed meats have higher rates of pancreatic cancer (if that’s even the case) because they also consume more white flour.

Q:  If A is linked to B, do we see that connection consistently, or are there glaring exceptions?

A:  We can answer that question by looking at the charts from the full study.  This one shows the change in the relative risk of developing pancreatic cancer from consuming an additional 120 grams of red meat per day:

A relative risk of 1.0 is neutral – no change in risk.  Below 1.0 means lower relative risk and above 1.0 means higher relative risk.  The horizontal bars represent the range of values that fell within the “confidence interval,” the black squares represent the average relative risk for each study, and the white diamond in the last row represents the overall average obtained by pooling data from all the studies.

The first thing that jumped out at me is that in four of the 13 studies analyzed, the relative risk of developing pancreatic cancer was lower for the people who (supposedly) eat a lot of red meat.  I wouldn’t call that a consistent result.  If some studies show higher risk and some studies show lower risk, I’d conclude that we’re looking at the wrong variables.

But through the magic of statistical analysis, the researchers pooled the results (from studies that often failed to control the variables) and declared that consuming 120 grams of red meat per day raises your risk of developing pancreatic cancer by 13%.

Now here’s the change in relative risk from consuming an additional 50 grams of processed meat per day:

Nine studies, and in three of them the relative risk of developing pancreatic cancer was lower for people who consumed more processed meat.  Once again, that’s hardly a consistent result, but the researchers pooled the data in order to declare that processed meat raises your risk of pancreatic cancer by 19% — which leads to our final question.

Q:  What was the actual difference?

A:  Almost nothing.  That’s the short answer.  Now for the longer answer:

Scientists like to cite relative risk instead of absolute risk because relative risk sounds far more impressive.  Suppose that when I lived in sunny California, my odds of being struck by lightning were 1 in a million.  But now that I live in Tennessee, suppose the odds are 1.5 in a million.  That’s a 50% increase in relative risk … but a meaningless increase in absolute risk.  The actual difference — the change in absolute risk –  is 0.5 in a million.

According to the National Cancer Institute, the age-adjusted annual incidence rate of pancreatic cancer is 13.6 per 100,00 men and 10.3 per 100,00 women.  We’ll split the difference and call it 12.15 per 100,000 people.  Expressed as a percentage, here are the odds that you’ll be diagnosed with pancreatic cancer this year:

0.0122%

Just barely over one-hundredth of one percent.  Now … let’s set aside the fact that this meta-analysis was 1) based on observational studies that 2) used unreliable food-recall surveys and 3) produced inconsistent results.  Suppose we choose to believe that processed meat really and truly causes pancreatic cancer at the increased rate found by pooling all that data, but we keep on eating our bacon anyway.  Here are the odds, expressed as a percentage, that we bacon-eaters will be diagnosed with pancreatic cancer this year:

0.0145%

And here’s the actual difference between those two numbers:

0.0023%

Well, maybe you’d prefer to deal with lifetime odds instead of annual odds.  Okay, fine.  According the National Cancer Institute, the lifetime odds of developing pancreatic cancer in the U.S. are 1.45%.  If eating 50 grams per day of bacon or other processed meat really and truly (and all by itself) raised the rate by 19%, your lifetime odds would be 1.70%.

Here’s the actual difference between those two numbers:

0.25%

Enjoy your bacon.

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The first time we made this spinach dish, the girls snapped up their portions and then were outraged to learn they couldn’t have seconds — it was all gone.  So now we make it with two boxes of spinach.

Ingredients:

  • 2 ten-ounce boxes of frozen spinach
  • 4 TB (half a stick) of butter
  • 1/2 tsp garlic powder
  • 1/4 tsp nutmeg
  • 1/4 cup parmesan cheese
  • 1/4 cup sour cream
  • Salt to taste

Steps:

Microwave the spinach for 10 minutes, then press out most of the liquid.


Put drained spinach in a dish and stir in the butter, then stir in the parmesan so it melts.

Stir in the remaining ingredients.

Adjust the spices to taste.  Sometimes I use a little garlic salt in place of some of the garlic powder, but you can always add salt later.  I also like extra nutmeg now and then.

Enjoy.

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Dr. Robert Su posted the last of the listener-roundtable discussions that included me.  Joining us for this podcast is Drew Kime, a frequent commenter on this blog and also a blogger himself … his blog How to Cook Like Your Grandmother is dedicated to teaching people to cook real food, and his other blog Willpower Is For Fat People is dedicated to the art and science of low-carb.

You can listen to the episode here.

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Here’s part one of my interview with Jonathan Bailor, author of The Smarter Science of Slim.

Fat Head: Let’s start with the obvious question:  what inspired you to write The Smarter Science of Slim?  With all the diet books already out there, what new information did you hope to provide?

Jonathan: I’ve always been interested in science and technical topics, and as little kid, I wanted to emulate my older brother. He was heavy into athletics and working out, and so I naturally did the same. At first, I took a traditional path to health and fitness but also read all I could in popular literature because it interested me. In fact, I got so involved in health and fitness that I became a personal trainer.

Shortly after I started working with clients, I realized how ineffective traditional approaches to health and fitness were. For example, I’d work with a client for a few weeks and she’d drop a few pounds by following a traditional “eat less, exercise more” approach. But a few weeks later, that client would inevitably report how the pounds came right back. I tried all sorts of different techniques to make eating less and exercising more practical, but the results were the same:  clients would lose weight, only to find themselves heavier a few months later. This caused me to re-think what success means in terms of weight loss and health, and I realized success is not defined by short-term weight loss. Instead, it is long-term fat loss and improved health. Also, I didn’t derive much satisfaction from asking clients to feel hungry, tired, deprived, and time-crunched for the rest of their lives.

Something had to change, and I was determined to find out what that change could look like. Building on my interest in science, I started reading all the academic research on health and fitness I could find. I didn’t plan to spend a decade studying this topic; it’s just something that deeply interests me.

Immediately, I was startled by the sharp contrast between what researchers had proven about how to burn fat and boost health in the long term and what I was taught by popular literature and as a personal trainer. At that point, I was determined to get to the bottom of the disconnect between traditional assumptions regarding weight loss, diet and exercise and what scientific research had proven.

The goal of The Smarter Science of Slim is to use scientifically proven facts to show how anyone can lose fat and boost health in the long term. There aren’t many people who are going to read thousands of pages of academic research to achieve this, and I saw a great opportunity to distill what I had learned into an easy-to-read manual anyone can understand and apply.

Fat Head: A lot of so-called experts have tried to dismiss Gary Taubes as “just a journalist.”  Are you worried at all about being dismissed as “just an independent researcher”?

Jonathan: I can see how that could be a concern, but The Smarter Science of Slim has little to do with me because it is a compilation of research conducted by the scientific and academic communities’ most brilliant minds. While I’m sure some people will dismiss me because I don’t have M.D. or PhD after my name, it would seem odd for them to dismiss academically and scientifically robust research conducted by experts at The Harvard Medical School, Johns Hopkins, UCLA, The Mayo Clinic, and hundreds of other top institutions worldwide. “Biology isn’t a matter of opinion” is one of my favorite phrases. And just as it would be puzzling to try to discredit 1 + 1 = 2, the worldwide scientific community has shown it would be puzzling to try to discredit starch + body = a lot of insulin production or non-starchy vegetables + body = improved health.

Fat Head: How did you conduct your research for the book?

Jonathan: I studied more than 1,100 academic journal articles and had numerous follow-up correspondences (phone and email) with the articles’ M.D. and PhD authors. All told, it took me about 10 years to complete. I probably could have done it in less time, but I have been working full-time at Microsoft for the majority of this period.

Fat Head: You did a nice job of taking some complex science and explaining it clearly and simply, which is always a big plus for me when I’m recommending a book.  Was that difficult, or is that just how you think?  Did you ever find yourself rewriting the same paragraph dozens of times, trying to come up with a simpler explanation?

Jonathan: Oh my gosh, yes! I have a folder on my computer that contains hundreds of megabytes of Smarter Science of Slim drafts, outlines, notes, and graphics. That’s a lot of Word documents.

My editors Hillel Black, John Paine, and Mary Rose Bailor (my English professor mother) helped me strip the jargon from the science and re-explain it as concisely and simply as possible. This was a daunting task, but I’m fortunate in that taking complex information and simplifying it is what I do at Microsoft. Every day of my professional life, I collaborate with the most technical people at Microsoft and then simplify their complex technological concepts so they are useful to a non-technical audience. My experience at Microsoft was extremely influential in developing The Smarter Science of Slim, and I feel fortunate to work at such a fantastic place. The Smarter Science of Slim is really just an extension of what I do every day. The only difference is I’m simplifying biology rather than technology.

Fat Head: How did you become so interested in the topic of weight loss?  Have you ever been a fat guy who needed to lose weight?

Jonathan: I’ve always been interested in how people can improve how they look and feel though food and exercise. Chalk that one up to wanting to emulate my athletic older brother combined with my innate interest in science.

My personal situation was weighing too little rather than too much. I was the scrawny guy getting sand kicked in his face at the end of the comic book. This circumstance was instrumental in inspiring me to conduct the research that lead to The Smarter Science of Slim. I’ve since learned that I—and millions of other fortunate people—can eat and eat and eat and not gain fat because:

1. Burning fat is about more than just the quantity of food we eat and the quantity exercise we get
2. The human body is capable of burning fat, automatically, long-term.

As I progressed in my research, two questions drove me:

1. What are the key factors that affect fat gain and fat loss?
2. Is there a way for everyone to make their metabolisms work more like the metabolisms of naturally thin people?

As it turns out, researchers have answered both of these questions. These answers are described in detail in The Smarter Science of Slim.

Fat Head: One of the main points you make in The Smarter Science of Slim is that it’s highly unlikely we’ll lose weight and keep it off without first changing our set-points.  We know the body fights to maintain some of its fat mass –  much more for some than for others –  but does anyone really know exactly what a set-point is?  That is, do we know why our bodies are so determined to remain fatter than we’d like to be that they’ll burn away muscle instead of burning more body fat?

Jonathan: The simplest answer is that the set-point is an abstraction of our neural wiring and the balance of hormones in our body. The former is genetic, while the latter can be influenced by the quality (not the quantity) of our eating and exercise. The body uses this neural wiring and balance of hormones to:

  • regulate how many calories it demands
  • regulate how many calories it burns off
  • determine how it deals with excess calories
  • determine how it fuels itself when no calories are available from food

Researchers D.S. Weigle from the University of Washington, T. Kelesidis from UCLA and Harvard,  P.J. Havel from the University of California, R.E. Keesey from the University of Wisconsin, and many others have done extensive research around the set-point.

While one part of our set-point is determined before we are born, the other part is a function of what we eat and how we exercise. Changing the set-point is about food and exercise quality… it has nothing to do with simply eating less of our existing diet and doing more of traditional exercise. This is why so many hard-working people struggle with weight loss: they’ve been given a quantity-based solution (eat less, exercise more) to a quality-based problem. It’s a bit like trying to cure allergies by breathing less air in and breathing more air out.

Here’s a paraphrased excerpt of the book that may help here:

…Think about trying to remove fat from a hormonally “clogged” body like trying to drain water from a clogged sink. Eating less is like turning down the faucet. Exercising more is like scooping out the overflowing water. Both are temporary ways to deal with the symptoms of the problem. Neither does anything about the root cause. That is why they both fail long term.

The problem is the clog. The solution is clearing the clog. And clearing the clog requires thinking in terms of quality, not quantity.

Fiddling with the quantity of food we eat and the quantity of exercise we get will never clear our hormonal clog. Quality—low-quality food and low-quality exercise—is the cause of the backup. A sink does not get clogged by putting too much water into it. It gets clogged when we put the wrong stuff into it. Our body works the same way…

Fat Head: A lot of dieters who semi-starved themselves found to their great dismay that they lost weight, then gained it all back, then gained more, then had an even more difficult time losing weight.  Do you believe the severe calorie restriction raised their set-points?  If so, why?  What biochemical or hormonal changes occurred?

Jonathan: My research did not specifically cover whether severe caloric restriction raises the set point. However, it did show that depriving our bodies of nutrition (which is distinct from depriving our bodies of calories) does the following:

1. Dramatically slows down the metabolism
2 .Burns at least as much muscle as fat
3. Creates an environment that causes the body to gain more body fat than it burned as soon as possible. Researchers call this “fat super accumulation”

Item three in the list above suggests a change in the set-point. But that’s as far as I’ve found researchers take it.

The simple version of what biochemical or hormonal changes occurred is that the body is designed to prevent us from starving. If we starve ourselves, i.e., provide the body with insufficient nutrition, the body will do all it can to slow down the metabolism and burn calorie-hungry muscle before it burns body fat. Then it will predispose us to storing more fat to protect us from future starvation.

Fat Head: Some people – especially those who’ve never been fat – see obese people eating a lot and assume they’re just being gluttons.  I believe people eat when they’re hungry.  Are obese people hungrier than thin people who eat less, and if so, why?

Jonathan: Most people store excess body fat because they are experiencing what researchers call “metabolic dysregulation.” (I call this “a clog in the metabolism.”) Their hormonal balance has been compromised in such a way that their body is unable to effectively metabolize food, which causes them to over-consume food just to nourish themselves. Researchers call this condition “internal starvation.”  Here’s an excerpt from The Smarter Science of Slim that explains this process:

…Once most of the calories we eat are being stored in fat cells because insulin cannot get them into other cells, internal starvation has set in. We eat plenty of food but starve on the inside because insulin cannot effectively get that energy into any cells other than our fat cells. With excess insulin shuttling most calories into fat tissue and eliminating our ability to burn body fat, the fat metabolism system has no choice but to slow down, burn muscle tissue, and demand more food. It does what it always does when it senses starvation.

Consider Terri. She is internally starving and needs 500 calories of energy. Terri is also a yo-yo dieter and has already slowed down her metabolism and burned as much muscle as she can. Needing some calories, Terri eats 500 calories. Instead of those 500 calories getting into the cells needing it, only 250 make it in while the other 250 are ignored—thanks to insulin resistance—and stored as new body fat. Terri still needs 250 calories. She cannot slow down anymore. She cannot burn any more muscle. And thanks to all the excess insulin floating around, she does not have the ability to burn body fat. What is her only option? Overeat. Specifically, eat 250 extra calories.

So Terri snacks on 250 extra calories to keep her cells from starving. But now only a fraction of the 250 make it to the cells needing it while the rest is stored as body fat. Again, she must overeat even more. This process of overeating to keep a clogged fat metabolism system running repeats itself until Terri eats 1,000 calories to meet her need for 500 calories. Terri’s fat metabolism system is leaking calories into her fat cells and has to compensate by taking in extra calories.

Continue this “overeat to compensate for [her hormonal clog]” cycle day after day and Terri gains body fat. And on the surface it looks like she is gaining body fat because she is eating too many calories. But eating too many calories is not the cause of her new body fat. It is a symptom of a deeper problem: her hormonal clog. Terri’s high consumption of calories is not the cause of her weight gain. It is a symptom of the hormonal clog caused by low-quality calories…

Fat Head: You make the point several times that when we eat quality food, we’re less likely to overeat.  Why is that?  How does the quality of food affect our appetites?

Jonathan: Studies show that the satiety of food—how quickly it satisfies us and how long it keeps us satisfied—is a function of three primary factors:

1. How much do the calories we are eating stretch our digestive organs (our stomach, etc.)?
2. How much do the calories we are eating impact our hormone levels in the short term?
3. How much do the calories we are eating impact our hormone levels in the long term?

Researchers have proven that the more water, fiber, and protein in a food, the more it stretches our digestive organs and triggers a short-term and long-term hormonal response causing us to feel full.

Note: Natural fats also play an important role in triggering this hormonal response. However, my research shows our primary focus should be on eating more foods that contain a lot of water, fiber, and protein. If those foods naturally contain fat, that’s totally fine.

Thank you, Jonathan.  I’ll post part two of our interview next week.

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Suppose you were reading the health section of a newspaper looking for ideas on how to lose weight, and you came across an article that started like this:

Whether you are just starting a New Year’s diet or struggling to maintain a healthy weight, a provocative new study offers some timely guidance. It isn’t so much what you eat, the study suggests, but how much you eat that counts when it comes to accumulating body fat.

The findings are the latest in a string of studies to challenge claims that the secret to healthy weight loss lies in adjusting the amount of nutritional components of a diet—protein, fat and carbohydrates.

I don’t know about you, but I’d assume that provocative new study involved adjusting the nutritional components of a diet – protein, fat and carbohydrates.  Let’s check:

In the study, to be published in Wednesday’s issue of the Journal of the American Medical Association, 25 young, healthy men and women were deliberately fed nearly 1,000 excess calories a day for 56 days, but with diets that varied in the amounts of protein and fat.

Hmmm  … it appears that the provocative new study which supposedly proves the secret to healthy weight loss isn’t a matter of adjusting the ratio of protein, fat or carbohydrates is

1)  a study of people who intentionally gained weight instead of losing weight

which

2) manipulated the balance of fat and protein, but not carbohydrates.

Let’s read on:

While those on a low-protein diet—about 5% of total calories—gained less weight than those on a normal- or high-protein regimen, body fat among participants in all three groups increased by about the same amount. Typical protein consumption is about 15% of calories, while the U.S. government recommends it make up between 17% and 21% of total daily calories.

The findings suggest that it matters little whether a diet is high or low in fat, carbohydrates or protein, it’s calories that build body fat.

It matters little whether or a diet is high or low in fat, carbohydrates or protein?  I must be missing something here … did the researchers change the ratio of carbohydrates in the diet nor not?

The patients in the Pennington study ranged in age from 18 to 35 and had BMIs between 19 and 30. (Between 25 and 30 is considered overweight.)  They lived at the center’s metabolic unit for between 10 and 12 weeks and were fed the 1,000 extra calories a day for the final eight weeks of their stay. Carbohydrates were held steady at about 41% to 42% of calories while fat levels varied with the protein regimen.

Brilliant.  Study subjects were put on three different diets designed to induce weight gain, the carbohydrate ratio was virtually the same across all three groups, and yet media health reporters are telling us the provocative study proves that manipulating the fat, carbohydrate or protein content of a diet won’t help us lose weight.

After eight weeks, all participants in the study gained weight. The 16 men and nine women made similar gains. The low protein-diet group gained about seven pounds, about half the 13.3 pounds added on by the normal protein participants and 14.4 pounds put on by the high protein group.

If you read the full study (which I did), you’ll learn that the low-protein group didn’t gain as much weight because – despite overeating by 1,000 calories per day – they lost muscle mass.  The other two groups gained muscle mass, with the high-protein group gaining the most.  I’d say that’s an important difference.  Losing muscle mass is a great way to slow your metabolism.  Gaining muscle mass raises your metabolism.  The results listed in the study seem to confirm that point:

The low protein diet had 6% of energy from protein, 52% from fat, and 42% from carbohydrates. The normal protein diet had 15% of energy from protein, 44% from fat, and 41% from carbohydrates. The high protein diet had 26% of energy from protein, 33% from fat, and 41% from carbohydrates.

Overeating produced significantly less weight gain in the low protein diet compared with the normal protein diet group or the high protein diet.  Body fat increased similarly in all 3 protein diet groups and represented 50% to more than 90% of the excess stored calories. Resting energy expenditure, total energy expenditure, and body protein did not increase during overfeeding with the low protein diet.  In contrast, resting energy expenditure and body protein (lean body mass) increased significantly with the normal and high protein diets.

Elsewhere in the study, the researchers provide more details:  the low-protein group lost an average of 1.5 pounds of lean body mass, while the high-protein group gained an average of 7 pounds of lean body mass.  When you overeat by 1,000 calories per day and still lose muscle, you know it’s a lousy diet.

The effects on metabolism may not have produced significant differences in fat accumulation in the short duration (less than two months) of this study, but I suspect that since the low-protein group was losing muscle mass, we’d see more of a difference over time.  Interestingly, the researchers didn’t say exactly how much extra body fat each group gained.  They only told us the difference wasn’t significant:

The overall increase in fat mass for all 3 groups was 3.51 kg (95% CI, 3.06 to 3.96 kg) from baseline and was not significantly different between the 3 groups (P = .89), although the low protein group added on average more than 200 g of fat (about 2000 kcal).

I also found these paragraphs interesting:

With the low protein diet, more than 90% of the extra energy was stored as fat. Because there was no change in lean body mass, the 6.6% increase in total energy expenditure reflects the energy cost of storing fat and is close to the estimate of 4% to 8% for fat storage derived by Flatt. With the normal and high protein diets, only about 50% of the excess energy was stored as fat with most of the rest consumed (thermogenesis).

The extra calories in our study were fed as fat, as in several other studies, and were stored as fat with a lower percentage of the excess calories appearing as fat in the high (25%) protein diet group.

I’m confused … if the low-protein group stored 90% of their extra energy as fat, while the other groups only stored 50% of their extra energy as fat, how did they all end up gaining the same amount of body fat?

Maybe I’m just not getting the math involved, but never mind.  Even if all three groups did gain the same amount of body fat, this study doesn’t really tell us anything about how to effectively lose weight, and it certainly doesn’t prove anything one way or another about the effects of manipulating the carbohydrate content, since the carbohydrate ratios were virtually identical.

Another researcher who commented on the study in a Reuters article put it nicely:

Donald Layman, a food science researcher at the University of Illinois in Urbana, said it’s difficult to see how the findings apply to a general population that isn’t being overfed such a protein-deficient diet, in the case of the low-protein group.

“It’s an interesting scientific study, but from an obesity standpoint, I don’t think it tells us anything,” he told Reuters Health.
Bingo.  Even if the protein ratio made little or no difference on fat accumulation in an over-eating study conducted in a metabolic ward, most of us aren’t trying to get fatter.  We’re trying to get leaner.  And we don’t live in metabolic wards where our meals are prepared for us and every calorie is tabulated.  We live in the real world where we don’t (and can’t) count every calorie, and where the amount of food we eat is determined by our appetites.  Protein is satiating.  When we eat higher-protein foods, we tend to eat less.  When we eat high-carb meals, many of us find our appetites going all out of whack, and we eat more.

The lead researcher for the study was George Bray, who seems to have dedicated his career to proving that the federal government’s dietary guidelines are correct – and if he has to cleverly design studies to achieve that goal, or write conclusions that aren’t backed up by the actual data, by gosh he’ll do it.

It was Bray who conducted the study on salt restriction that I mentioned in my Science For Smart People Speech, the one in which a drastic reduction in dietary sodium produced a whopping two-point drop in blood pressure.  Based on that meaningless result, Bray concluded that sodium restriction is an effective means of controlling hypertension.  (Say what?  Two points is a meaningful reduction in blood pressure?  I don’t think so.)

Here’s Bray offering his conclusion from the latest study:

“If you over-eat extra calories, no matter what the composition of the diet is, you’ll put down more fat.”

Really, Dr. Bray?  If you wanted solid scientific evidence that the composition of the diet is meaningless, why was the ratio of carbohydrates the same in all three groups?  Since you blasted Gary Taubes in your review of Good Calories, Bad Calories, we know you’re well aware of the hypothesis that it’s carbohydrates, not protein or fat, that promote fat accumulation … so why didn’t this provocative study include a group that restricted carbohydrates?  After all, none of the low-carb diet gurus recommend anything close to a ratio of 40% carbohydrates.

I think the answer to that question can be found near the end of the study.

This study was supported in part by the US Department of Agriculture.

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