Why You Should Arm Your Bullshit Alarm Before Reading Diet News.

In the fight over best diet for health and weight loss, it's protein lovers vs. vegetarian zealots. So far, a clear winner has not emerged. Only one loser: you, the victim of biased research. Here is an example of why you should keep your bullshit alarm on high alert when reading about weight loss diets.  

[tweet this].

Ellen M. Evans and colleagues wanted to know whether overweight men and women differ in their body composition responses to different weight loss diets [1]. So they enrolled 58 men and 72 women with a BMI greater than 26, and randomized them into two diet groups.
One group was instructed to follow a high-protein low-carbohydrate diet, which delivered 1.6 g of protein per kg bodyweight per day. The high-carb group  received only half that amount of protein, and both groups' fat intake was capped at 30% of total energy intake. Both diets contained the same amount of fiber. Women received a daily total of 1700 calories, men 1900 calories. The intervention lasted for 4 months, followed by an 8-months weight maintenance period. Fast forward to the 12-months results:

Both diet groups and both genders lost about 10% of their body weight. But expressing weight loss in kilos of body weight can be a deceptive thing. Ideally we want that loss to be fat loss rather than loss of lean mass, that is, muscle mass. In the study at hand, for men on the high-carb diet, a little over one third of their weight loss came from lean body mass. Meaning, of the 14 kilos, which they lost on average, 5 Kilos came from a reduction in muscle tissue. The high-protein guys maintained their muscle mass to a greater extent: only 20% of their weight loss came from wasted muscle. For the women the picture looked almost identical: muscle mass contributed 37% to the weight loss of the high-carb women, compared to 23% in the high-protein group. 

You would be forgiven if you now agreed with the authors' statement that the high-protein diet "...was more effective in reducing percent body fat...". Or in other words, a high-protein diet is superior to a high-carb alternative, as losing lean mass isn't a good thing in weight loss. I'll get to that point shortly in a little more detail. 

Before we go there, let me state, that, being a firm supporter of the high-protein low-carb dietary philosophy, I loved to read this study. But I'm an equally firm supporter of proper scientific methods. And they have been prostituted in this case, which is why I love this study a lot less than its results. 

Here is why: When I read the tables in which the authors present the results, I was impressed by the fact that both groups not only managed to rescue the 4-months weight loss to the 12-months finish line, but even increased this weight loss a little. When you have read literally hundreds of studies on weight loss interventions, as I have done, you'll find this observation to be in stark contrast to what we typically see: a reversal of weight loss. That is, at least a partial post-intervention regain of the weight lost during the dietary period. 

We find the explanation for this miraculous exception in the number of participants. Or rather in the number of disappearing participants. Of the 66 participants who started in the high-carb group, only 30 made it to the finish line 12 months later. That's a drop-out rate of more than 50%!  And of the 64 participants in the high-protein group 23, or 36%, had dropped out by month 12. 

High drop-out rates are nothing unusual in weight loss trials, but it is good practice for researchers to tell their readers, how they accounted for these drop outs in the statistics, with which they interpret the data. Nothing of that in this paper. So, we don't know whether the drop-outs simply did not show up for their measurements, or whether the researchers did not consider the data of those participants, who failed to achieve some arbitrary weight loss threshold. The latter is an absolute no-no. It enables researchers to skew the results every which way they want. And the former is reason to investigate whether the drop-outs differed in some way significantly from the adherent participants. Such differences often affect the interpretation of the results. 

One interpretation emerges right away, when checking the differences of relative fat loss while considering the drop-out rates:  the smaller relative loss of muscle mass in the high-protein diet is not significantly different from the loss observed in the high-carb group. That does not mean, there is no difference between these two diet types. It only means, the study was underpowered to detect such difference, if there was any. And if it was underpowered to detect the difference between diet groups, it was certainly underpowered to differentiate between men and women in this respect. 

If you still want the final verdict on high-carb vs. high-protein, I'm afraid I can't give it to you, even though I'm heavily leaning in favor of the high-protein version. I base my judgment on a 2009 systematic review of all randomized controlled trials, which were performed between 2000 and 2007, and which had pitted high-carb vs. high-protein strategies [2]. This review demonstrated that high-protein diets are more effective with respect to weight loss and probably with respect to cardiovascular risk factors than high-carb diets. At least over observation periods of 6 to 12 months. 

Only long-term observations, comparing hard endpoints, can decide which diet may be better. Those studies are a long way off. To complicate matters, we might find that different people react differently to the same type of dietary strategy. Until we know better, we need to go with what we know: 

The preservation of lean body mass certainly is a key aspect. Muscle tissue is an important endocrine organ, which, when exercised, produces potent anti-inflammatory substrates and hormones. These are the key elements of physical activity's protection against the initiating step of heart disease: atherosclerosis. Muscle tissue is also the body's primary site to store dietary carbohydrate in the form of glucose. The other site being the liver. With a high-carb diet, these storage sites are easily overwhelmed, which leads to conversion of carbs to fat. When, ironically, a high-carb diet nibbles away at the body's carb storage sites, you can imagine what this means to the body's relative fat content. Another aspect is that muscle tissue consumes energy, even at rest. The loss of this "burner" during weight loss makes weight rebound more likely.

So, if all these matters are known and understood, why perform a study, which is underpowered and fraud with questionable interpretations? Why produce the food equivalent of a scientology propaganda piece?  

Beats me. Maybe because part of the study's funding came from the National Cattlemen's Beef Association and The Beef Board. Both of which are, of course, entirely neutral to the outcome of research funded by them, and unbiased to its interpretation. 

It also beats me, why a respected journal and its peer reviewers facilitate the publication of such a study. Maybe because its senior author, Professor DK Layman, is a leading researcher in nutrition science, and... 

...the Egg Nutrition Center's director of research. 

As much as my dietary preferences place me in the protein camp of this contest, my bullshit alarm is set to high-sensitivity. And so should yours be. 

[tweet this].

  

1. Evans, E., et al., Effects of protein intake and gender on body composition changes: a randomized clinical weight loss trial. Nutrition and Metabolism, 2012. 9(1): p. 55.

2. Hession, M., et al., Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obesity Reviews, 2009. 10(1): p. 36-50.

Evans, Ellen, Mojtahedi, Mina, Thorpe, Matthew, Valentine, Rudy, Kris-Etherton, Penny, & Layman, Donald (2012). Effects of protein intake and gender on body composition changes: a randomized clinical weight loss trial Nutrition and Metabolism : doi:10.1186/1743-7075-9-55

Hession, M., Rolland, C., Kulkarni, U., Wise, A., & Broom, J. (2009). Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities Obesity Reviews, 10 (1), 36-50 DOI: 10.1111/j.1467-789X.2008.00518.x

How to get those vegetarian zealots off your back.

Does red meat kill you? Only in a vegetarian's dream!

Red meat is the favorite enemy of nutritionists nowadays. Their studies and publications are often (ab-)used by those evangelical vegetarian types who would love to impose their no-meat religion on the rest of us. Don't buy it. Now let me show you how you can profess your love for steak AND support it with the data from the same studies which the zealots use for their vegetarian crusades.

Earlier this year Pan et al. published a study titled "Red meat consumption and mortality" [1]. They had pooled the data of two large prospective studies, the Nurses' Health Study and the Health Professionals' Follow-up Study. Collectively these studies had followed 121,000 people, who were free of cardiovascular diseases at baseline, for more than 20 years. Altogether, the participants accumulated close to 3 million person years for observation. During the observation period close to 24,000 deaths occurred of which 6,000 were of cardiovascular causes, that is heart attack, stroke, heart failure.

The researchers discovered that for every increase of 1 serving of unprocessed red meat per day the hazard ratio of dying from any cause was 1.13 and the hazard ratio of dying from a cvd-cause was 1.2. That means for every increase of a serving of red meat per day the chances of dying from any cause and from a cvd-cause increased by 13% and 20% respectively. Those rates were a little higher for processed red meat. To put this into perspective the researchers also calculated that if all participants had eaten less than half a serving of red meat per day (42g/d), 9% of deaths in men and 7.6% of deaths in women could have been prevented. Wonderful. Sounds impressive, but it isn't for one simple reason:

Unreliable data acquisition. Just ask one question: how did the researchers know how much red meat those people ate? This question cuts to the heart of many, if not most, studies on diet-disease associations. Data on food consumption are typically acquired through food frequency questionnaires (FFQ). These FFQs ask you about your consumption of food items over the past days, weeks or even months. And as you can imagine, such recall can be terribly unreliable. So much so, that other researchers wanted to quantify this effect. So they used FFQs and compared the results with objective quantitative measurement of energy intake and protein intake [2]. And lo and behold, they discovered that if relative risks (such as the hazard ratio mentioned above) were calculated from FFQs they overestimate the true diet-disease association very severely. In fact so severe, that a hazard ratio of, say, 2 would in reality be around 1.3.

What does that mean for a hazard ratio which is, as in the study of Pan and colleagues, less than 1.3 to begin with? It means possibly nothing. You certainly can't conclude from these data that red meat kills you. That's what it means.  And mind you, this inaccuracy of FFQs shows up with recall periods of a few weeks. Pan and colleagues had to rely on FFQs which were conducted YEARS apart. In fact,  data acquisition based on FFQs is so flawed, that the question been raised "is it time to abandon the food frequency questionnaire?" [3]. And the authors state: "We should be very circumspect about analyses of current studies that have used FFQs for dietary assessment." That was 7 years ago. We still have those FFQs and you  still have the media telling you  how bad red meat is for you.

And I'm going to have a real nice steak now. How about you?

1.           Pan, A., et al., Red Meat Consumption and Mortality: Results From 2 Prospective Cohort Studies. Archives of Internal Medicine, 2012: p. archinternmed.2011.2287.

2.           Kipnis, V., et al., Structure of dietary measurement error: results of the OPEN biomarker study. American Journal of Epidemiology, 2003. 158(1): p. 14-21; discussion 22-6.

3.           Kristal, A.R., U. Peters, and J.D. Potter, Is it time to abandon the food frequency questionnaire? Cancer Epidemiology, Biomarkers and Prevention, 2005. 14(12): p. 2826-8.

Are fat people just lazy?

Are fat people just lazy? Or is it in their genes?

Let's look at an unlikely place for the answer: an AA meeting. If you get up and say "My name is Jane, and I'm not really an alcoholic, I don't drink that much..." they throw you out. They welcome you back, once you say "My name is Jane and I'm an alcoholic". The same should be true for fat people. And I'm using this politically incorrect term deliberately. Because unless you wake up to the reality, you won't be able to change that reality.

 AA have long ago realized that fact. And they have a 50% long-term success rate. That is, half the alcoholics who join AA stay dry for the rest of their lives. That's way more than what public health, clinical and commercial weight loss programs achieve with obese participants. We are happy if 10% of those who enter these programs achieve a 10% weight loss AND keep it for more than 2 years. It's that bad. Is it because of the genes? A study published recently in Nature Genetics, might supply another excuse to some overweight people. But before we look at this study, let's look at some other facts first.

One thing we all know for sure: if you are overweight, you obviously have taken in more calories than you have expended. Over quite some time, because it takes a while to accumulate all those energy reserves on your waist and hips. Boils down to one of the tenets of a universal law of physics that says: Energy can neither be destroyed nor miraculously created. Not even on your hips.

Now I know all the objections raised by so many overweight people, like "But, I hardly eat anything. How can I be fat? Even my friends say, from what you eat nobody can get fat." Believe me, I've heard them all.  And my heart sinks, when I do, because I know there goes the hopeless case. The Jane who goes to AA and tells them she is different. The study published in Nature Genetics might just deliver her the next excuse. Not because the researchers tell her so, but because some media genius might just read it the wrong way. As they often do. So, let's look a what the researchers say.

The researchers conducted a meta-analysis of some 14 genome wide association studies involving altogether 14,000 children, one third of which were obese. They found 7 genetic markers which correlated with obesity and which also turned out to correlate with obesity in adults. The beauty of looking at genetics in kids is, that they haven't been exposed to decades of lifestyles which may obscure such links. 

So, the results clearly point into the direction of some genetic signature predisposing a person to become obese. But having this signature doesn't mean you'll inevitably become obese. Because most kids who have the signature are not obese. It's only that this signature shows up a little more often in the obese kids than in their non-obese peers.  And there is one more thing, you need to keep in mind. Over the past 20 years the human genetic make-up hasn't changed at all. But the obesity rate in US kids has. In fact it has tripled during that period. And health behavior has changed, too. And so did our environment.

What makes me always frustrated in all this debate about genes vs. environment vs. behavior is my scientist colleagues' and the media's inability to educate their audience about the complete picture. Genes make up the blueprint to your organism. True. But they don't make that organism. Genes make proteins, but whether they make them or whether they are silenced into not making them, that depends on epigenetics, on the interaction with your environment, and on your behavior, which again is influenced by all the others. It is a very complex relationship, and I'm afraid, genetics will not help us, to solve the obesity epidemic. But neither will the stigmatization of the obese. 

What we need, is a way to help those who recognize their fatness as a resolvable reality, resolve it. That's why I'm working on the GPS tochronic health, because I know that once the health behaviors put you on track to chronic health and longevity, your overweight problem will resolve automatically. As a side effect. But only if the obese person works with us. 

So did that answer the question? You decide for yourself.   

The three hidden barriers to chronic health, weight loss and weight maintenance.

Into The Age of Chronic Health

The most amazing thing about modern health care systems is that they let most of us die from chronic diseases which we know how to prevent. So why don't we?

As a public health scientist I have devoted the past 15 years of my life to answering this question. Many of my colleagues outdo each other with doom and gloom predictions of aging societies buckling under the economic burden of aging related diseases. I believe that the age of chronic health and longevity is about to begin. With you. And with a radically new approach to make the prevention of heart attacks, strokes diabetes and cancers finally work.     

Because, until now, it doesn't. But don't just take my word for it, let's look at some of the facts first:

You have probably heard that obesity is the new smoking. In fact for every American who stopped smoking in 2011 another one became obese.   

Today, for the first time in human history there are more overfed than malnourished people walking this planet. And their lifestyles of too much food and too little exercise have become the number one risk factor for the number one chronic disease and killer: cardiovascular disease with its most well-known end points - heart attack, stroke and heart failure. With nasty other diseases on the side: diabetes, kidney failure and certain cancers.

You probably also heard about major studies, like the U.S. government funded Diabetes Prevention Program, and the Look AHEAD trial, which proudly, and correctly, report weight loss and major reductions in cardiovascular risk factors among participants in the lifestyle arms of these trials. What you don't hear so often, is that within 3-4 years after enrollment, most participants will have regained not only most of their weight but also all their risk factors.

Ok then, lifestyle change prevents disease. But what prevents lifestyle change?

Why is it that over the last 30 years of public health efforts we have not seen a demonstration of any program that results in a clinically meaningful weight loss that can be maintained for more than 2-3 years in the majority of participants and at low cost?  That's the question which Dr. Richard Khan threw at an assembly of public health advocates, who had gathered earlier this year under the event's message "Prevention works!".  Dr. Khan, who teaches medicine at the University of North Carolina, was the chief scientific officer of the American Diabetes Association for 25 years. The man certainly knows what he is talking about. 

Now think about the implication. If you chose a lifestyle of which you know might increase risk of disease and premature death, then you make that choice either willingly or it is not your free will which makes that choice.

My money is on the latter. Because how else could we explain that an obese child maintains her fattening habits despite experiencing the same psychological agony as a child with cancer? How else could we explain that obese adults maintain their bulk when it significantly reduces their chances of getting an academic education, a job and a mate? How else could we explain that over the past 20 years the obesity rate in the US went up by 60% when, during the same period, Americans doubled their spending on weight loss products to US$ 60 billion annually? They WANT to lose weight, but they don't. The explanations are called addiction, hormones and hyperbole.  

Food addiction

The neurohormonal architecture which drives an addict to crave and consume his drug, despite knowing and hating the consequences, is exactly the same architecture that keeps us going for the sweet, fatty and salty stuff in restaurants, hawker centers and vending machines. Does that explain, why the food industry adds sugars to so many foods in which you least expect it? You bet. In fact we shouldn't be afraid of calling ourselves food addicts, because this is what Mother Nature intended us to be all along. With this addiction she drove our ancestors for millions of years to what is naturally sweet in the natural human habitat: fruits. They deliver not only the carbohydrates for which we have very little storage capacity in our bodies and without which our brain can't function. Fruits also pack a punch of essential micronutrients. Unlike the cokes and cakes and cookies which deliver more sugar than we need and no other nutrients with it.  

Hormones

Once you have changed your figure into the shape of a beached whale, you will also have changed the way the hormones of your gut and of your fat tissue work. It's a rather complicated picture unfolding in the labs of biomedicine, but one emerging theme is a colossal malfunction of the satiety and appetite signaling pathways. Instead of feeling full, you are now ready to add a tiramisu to a lunch that would have satiated a family of four in rural Bangladesh.

Hyperbole

Actually it's called hyperbolic discounting, and it's a simple mathematical formula, which behavioral scientists have found to neatly describe why we will still grab that tiramisu tomorrow even though we swear today that we won't. It has to do with how we more steeply discount the relatively larger but more distant reward of staying healthy against the relatively smaller but immediate reward of enjoying the tiramisu. It doesn't operate only in humans. The behaviors of rats, pigeons and apes, for example, follow the same formula. Which means, Mother Nature must have found out early during evolution that this principle is a recipe for survival in her species. We simply inherited this survival tool.   

With all these issues stacked in favor of an ever expanding population of chronically ill people, why do I believe that we might be close to the age of chronic health and longevity? For three reasons: Because Wall Street is getting into the act, because we can outfox our brain, and because biomedical science has got the tools ready.

How we will enter the age of chronic health is the subject of the next episode, so stay tuned!

In the meantime, visit my crowd funding campaign, watch the videos, recommend the campaign to your friends and, if you like what you see, participate in our chronic health project: www.indiegogo.com/adiphea

What weight loss?
You have probably heard one or the other diet guru claiming that manipulating the nutrient composition of your diet will make you lose weight. Well, for those of you, who stubbornly cling to the notion that excess weight is simply a matter of too many calories-in vs. too few calories-out, here is the good news: You are right, after all. It really doesn't matter.


In an exemplary 2-year study New Zealand researchers compared the effectiveness of a low-fat high-protein diet with an equally low-fat but high-carb diet http://www.springerlink.com/content/c5krn1t1104nuk3k/. Not only was there no difference at all between the diet groups into which the participants had been randomized. Their mean weight loss was a paltry 4 Kilos. Nothing to scream about when you look at the mean starting BMI of 36 and a mean body weight north of 100 Kilos.

The primary outcome parameters, that is blood sugar and HbA1c, which is what you are really after, when you try to lose weight as an overweight diabetic, didn't improve a bit. Well, there was some improvement after 6 months, but by 24 months the participants were back to square 1. Does that sound familiar?

Now, let's not get ahead of ourselves and let's look at what makes this study exemplary. First the researchers took in 419 overweight, diabetic participants for 24 months (which is really a large number and a long duration relative to what is typically the case for such dietary intervention studies). These participants were randomized into one of the two dietary groups. Each participant received individualized dietary advice on how to achieve a daily 500 kcal energy deficit. In the first year each participant was given 18 dietician-led group meetings with no more than 12 people per group. Follow-up measurements of body weight, waist circumference, diet composition and a host of biomarkers were done at baseline and at 6, 12 and 24 months. And then what happened?

30 Percent of participants dropped out right away in the first year. While HbA1c and blood glucose had dropped slightly but with statistical significance in the first 6 months, these markers remained deep in the red danger zone with > 7.7% and 7.9 mmol for HbA1c and glucose respectively. Which emphasizes the point I always like to make: there is a difference between statistical significance and clinical relevance. The latter wasn't there at 6 months and certainly not at 24 months when both had come back to their baseline levels. All the other biomarkers, which you probably know from your personal risk profile, such as cholesterol, triglycerides and blood pressure, didn't show any improvement at all. Neither was there a difference between the diet groups.

So, are we, and the researchers, right to claim that it is only calories which count, and not the macronutrients which deliver them? In my view, the study doesn't really answer the question. The weight loss was possibly too small to detect any difference. From personal experience (as a diet guinea pig and as one who does research with overweight people), replacing carbs with protein does have an effect on body weight. But comparing the typical energy density of a lean piece of meat with that of, say, bread, the differential weight effect might well come from the fewer calories the meat delivers in a meal of equal weight. Which would, again, make it an issue of calories, not of macronutrients. I also have some misgivings about randomizing diabetics into any high-carb diet.

My personal reading of this study? Well, I admit I'm biased against any weight loss attempt that is purely based on diet without physical activity as a component to achieve a calorie deficit. I'm also biased against calorie counting, which really is only for masochists and for those who mistakenly believe that they can estimate their calories reliably. But more on that another day. Which is why in our health science lab we have developed that tool for people to train a 6th sense for calorie balance. It really is the simplest way of getting your weight where you want it to be in an intuitive, playful and amazingly low-effort way. Try it out here: apps.facebook.com/adiphea Maybe you won't fall for those gurus any more. And maybe, just maybe, you'll know how to deal with the calorie cartel.

Cheers

 Lutz