Diets don't work for you? How about fasting?

I was interested to see this new study in the American Journal of Clinical Nutrition which found that an alternate day fasting technique helped people lose weight and improve their cholesterol profiles.

I've talked about the pros and cons of modified fasting for weight loss before and in the last year I've been experimenting with this technique for some of my nutrition counseling clients. This study confirms my own observation: For some people, eating very little some of the time is easier than eating a little less all of the time.

In this particular study, the participants ate whatever they wanted every other day. On the days in between, they ate a single mid-day meal which provided about 25% of their normal calorie needs. At the end of eight weeks, the participants had lost about ten pounds a piece, lowered their body fat by about 6%, and also lowered their total and bad cholesterol.

Is fasting easier than dieting?

Here's what's especially interesting to me: The subjects were able to stick to the diet just as well when they were on their own as they were when their fast-day meals were provided as part of the study.  

What do you think? Would it be easier for you to cut way back on calories every second day if you knew you could basically eat what you wanted the next day?  It seems to be an effective way for overweight people to drop a significant amount of weight.

Modified fasting could also be adapted as a long-term maintenance strategy as well. You might find, for example, that you can avoid regaining the weight by fasting one day a week and eating ad libitum the rest of the days.

Your thoughts?

How much fructose can you safely eat?

Q. I'm confused by conflicting things I've read about fructose.

[In this article], I read that:

When large amounts of fructose are ingested, they do "provide a relatively unregulated source of carbon precursors for hepatic lipogenesis." In other words, if you eat too much fructose, the liver can make the excess into fat. 

But later in the same article, another scientist is quoted as saying:

There is no evidence that reasonable consumption of fructose in a typical diet has any adverse effect on the liver or that it produces more body fat than sucrose or glucose.

I'm confused. Should we be concerned about fructose actually being stored as fat?  And how much fructose would a typical person have to eat for fat conversion to begin?

A. Notice that whenever the negative effects or dangers of fructose are discussed, it's always in regard to  "large amounts of fructose" or "too much fructose" or "when fructose is consumed in excess."

If you eat too much of ANY nutrient, the excess will be stored as fat. Fructose may be converted to fat more efficiently than glucose but these fat stores are readily mobilized when energy is needed. Over the long term, body fat accumulates because we take in more energy than we spend.

Here's an analogy I used in a recent episode of my weekly podcast: 

Your body stores energy (or calories) in a variety of formats and places in your body. You store a little bit in your blood, a little bit in your muscles, some in your liver, and the rest you store as body fat. It’s a little like storing your money in a number of places. You probably have some in your wallet, possibly some more in your dresser drawer, some in a checking account, and maybe the rest is in a money market account. 

Your body alternately makes and burns body fat all day long, transferring fuel in and out of its various accounts.  When you eat, energy is stockpiled in your body's accounts. As you go through your daily activities, you draw down these reserves. Which account you withdraw energy from will probably depend on how much you need and how fast you need it.

But just like with your money, regardless of which account you withdraw from, you’re still spending the same amount. If you spend less than you deposit, your net worth goes up. And when you burn fewer calories than you take in, you’re going to gain body fat.

Is fructose really the problem?

While it's true that our consumption of fructose has gone up dramatically, it has simply paralleled the increase in our intake of sugar (and calories). Even with the increased use of high fructose corn syrup, the proportion of sugar consumed as fructose has not changed significantly.  So, regardless of what happens when you feed huge quantities of pure fructose to lab rats, I think it's a little silly to say that  the negative effects of too eating much sugar are because of fructose.

How much fructose can you safely eat?

In my opinion, if your intake of added sugar is not excessive and your total calorie intake is appropriate to your needs, you probably don't need to worry about consuming too much fructose.

What's excessive? The World Health Organization recommends limiting added sugars to 10% of calories (something in the neighborhood of 50g/day).  More recently, the American Heart Association has recommended limiting added sugars to 5% of calories. Both are well below the threshold where fructose consumption would be a concern.

What's an added sugar? The WHO defines added sugar as concentrated sugars (white sugar, brown sugar, honey, maple syrup, etc.) that are used in processed foods and beverages, recipes, or at the table.  The naturally occurring sugars in fruits and dairy are not considered added sugars.

Can you eat too much fruit?  You can eat too much of anything. But no-one is claiming that excessive fruit intake is behind the rise in obesity or diabetes (although fruit juice might be another story). Reasonable intake in the context of a typical diet is two to four servings of whole fruit a day.

P.S. The entire article is well-worth reading.

Metabolic mysteries: why some people can't lose weight even when they eat less

It's a familiar complaint: "I simply can't lose weight, no matter how little I eat."

As a nutritionist, I've worked with patients who fail to lose weight even when their food diaries show that they are being diligent about their diets.  They assure me that they are accounting for every bite of food and correctly estimating portion sizes.  They're convinced that a faulty metabolism makes it impossible for them to lose weight.

Yet a recent study suggests another possibility. In a 12-month weight maintenance study (other details of which are being discussed in this recent post), the subjects kept diet diaries, which were examined by the researchers at regular intervals. However, the researchers report that "it was apparent that, on average, women in both study groups had underestimated their food intake."

And not by a little bit.  On average, the women reported having consumed 1370 calories per day.  The researchers calculated that their actual calorie intake was 2044 calories per day. That discrepancy of 674 calories a day adds up to over 5 pounds a month!

The men, on the other hand, were spot on: They reported average intake of 1765 calories, the researchers estimated actual intake at 1771.

Anyone have any theories as to why women would be so much less accurate at recording what they eat, despite the fact that they traditionally do more of the cooking and food shopping and are presumably familiar with the weights and measures involved?

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High and low carb diets equally effective...as long as someone else is in charge

We've been talking a lot on the blog lately about quality vs. quantity of calories.  On one end of the spectrum are those who insist that weight loss (or gain) is simply a matter of quantity: It doesn't matter whether you eat protein, fat, complex carbs, or sugar; if you simply eat fewer calories than you burn, you will lose weight. 

On the other end are those who believe that quality is the key: you can eat as many calories as you want without gaining weight as long as they are the right kind of calories (i.e. protein and fat rather than refined carbohydrates).  

Those in the second camp spend a lot of time talking about how refined carbohydrates stimulate insulin release which promotes fat storage, while protein increases thermogenesis and fat-burning.  But I think the magnitude of these metabolic effects is greatly over-stated. 

I suspect that the real "magic" of the low-refined-carb diet is that it tends to regulate calorie intake.

Refined carbohydrates tend to stimulate appetite and lead to over-consumption. But what if you take appetite out of the equation.  What happens when someone else decides what and how much you eat? Consider this recent study: 

After losing an average of 36 pounds on a weight loss program, obese subjects were put on one of two weight maintenance regimens: one was high protein and the other high in carbs.  A year later, both groups were equally successful in maintaining their weight loss. The researchers concluded that "the protein or carbohydrate content of the diet has no effect on successful weight-loss maintenance."  

When calories and macronutrients are "tightly controlled," the metabolic magic of the low-carb diet is undetectable.  This would seem to support my suspicion: The primary advantage of the low-refined-carb diet is not that it recalibrates the body's metabolism and tendency to store or burn fat, but that it reins in appetite, thereby reducing calorie intake. Nothing wrong with that!

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Do overweight people eat less than thin people (or do they just think they do)?

A lot of people are excited about Gary Taubes' book Good Calories, Bad Calories, which claims that weight loss or gain has nothing to do with how many calories you eat but how much refined carbohydrate you eat. I heard Taubes present his ideas at a conference last year and he makes some great points. Ultimately, I agree with his conclusion--over-consumption of refined carbohydrates is a primary cause in today's epidemic of "diabesity."

But I think he over-argues his case--and some of his arguments about how and why carbohydrates lead to obesity are flawed.

For example, as proof that excess calories are not the cause of weight gain, Taubes cites studies showing that that overweight people eat the same or less than thin people. Here's the problem: The studies he cites use self-reported intake records. We know that overweight people consistently under-report the number of calories they eat. (Here's yet another study measuring this.) The more overweight you are, the more you tend to under-report.

In fact, when you put overweight people into controlled (i.e. in-patient) settings and feed them the number of calories they think or say they are eating, they reliably lose weight--regardless of whether they are eating refined carbohydrates or not. (Whether this weight loss is sustainable in the real world is another question).

I think it's more accurate to say that refined carbohydrates seduce us into eating more calories than we need.  They taste good, you can consume a lot of calories before you get full, and you're hungry again sooner than you would have been had you eaten proteins, fats, or non-refined carbs. Excess calories = weight gain.

Eliminating or reducing refined carbohydrates may help realign your appetite regulation systems with your actual energy needs.  Reduced calories = weight loss.

Tropical Oils: A better saturated fat?

Shelly posted the following comment on a recent post on dietary fats:

"I've been reading some information that says coconut oil does not cause plaque build-up like other saturated fats because it is a medium-chain fatty acid, which apparently means it is digested more like a carb and doesn't have a chance to become plaque. I'd like to find more sources of this information, just to build some confidence. (When I relay this information about coconut, people look at me as though I'm from Mars.)"

Before I had a chance to respond, Dave posted a comment in response to Shelly's question:

"Short-chain fatty acids do take a different route than most fats. Most fats we eat are packaged up by the small intestine in large lipo-protein molecules called chylomicrons, which take a leisurely route through the lymphatic system before being dumped into circulation several hours after a meal. Short-chain fatty acids, by contrast, get a ride straight to the liver. The liver utilizes mostly fats for energy, so this probably frees up other energy sources for the body (the liver has high energy requirements), giving a quick-energy boost much like carbohydrates."

I love it when you guys do my work for me!  All I would add to Dave's little seminar on fatty acid metabolism is that the upshot of this is still largely hypothetical.  It might seem that medium and short chain fatty acids would be less likely to be stored as fat and/or form arterial plaques because they are metabolized differently. But there is very little research on what effect replacing other dietary fats with tropical fats has on weight or heart disease risk. (What research there is is contradictory.)

What's the take-home?

Shelly's question seems pretty straight-forward but there are actually a number of issues entwined in the tropical oil question. Here's my take on a few of them:

1. The role of dietary fat in obesity has been over-estimated in the past. But I think the pendulum may now have swung a bit too far in the other direction.The role of dietary fat in obesity is now being underestimated in some quarters.  In other words: Fat doesn't make you fat--but it probably doesn't make you thin either.

2. The role of dietary fat (and saturated fat in particular) in heart disease has probably been over-estimated. See also Steve Parker's post "Diet-Heart Disease Hypothesis: RIP".  My own pet theory is that the effect of dietary fats on health depends a lot on the quantity and quality of carbohydrates in the diet. Any study that fails to look at that interaction (which is most of them) is likely to reach unreliable conclusions.

3. Tropical oils are probably no more dangerous than animal saturated fats--which, as I noted above may not be as dangerous as we thought. 

4. Unrefined (extra virgin) tropical oils also contain some valuable antioxidants and phytonutrients.

5. Buyer beware: Many of the health claims being made for coconut oil these days are unsubstantiated and/or exaggerated. (See also my recent podcast on coconut oil.)

Genetics of obesity: Why we're never going to find one diet that's right for everyone

Any regular reader of this blog knows that we spend a lot of time debating the merits of various dietary theories. One of the reasons I sometimes find this debate frustrating (even tiresome) is that so many of the arguments boil down to this:

"Diet X has completely cured my diabetes (heart disease, weight problem, gout, wobbly upper arms, etc.).  Based on my experience, I'm convinced that Diet X is the one and only road to optimal health."

The problem is that "Diet X" may be a low-carb diet, a Paleo diet, a vegan diet, a raw diet, or any number of other mutually exclusive systems. At that point, the conversation starts to resemble discussions of religion or politics. Everyone spends a lot of energy proving their own point of view and trying to disprove alternate views. Some arguments are more articulate and compelling than others.  But in the end, few minds are changed.

In Defense of Wishy-Washiness

Perhaps you think I've been wishy-washy because I don't endorse one side or the other. After all, I've read the arguments and evidence. And I keep saying things like "Do What Works for You" and "One Size Doesn't Fit All." Shouldn't I have reached some sort of conclusion, even tentative, about which approach is "right," or at least "better"?

I really don't think there is one dietary prescription that is right for everyone. Part of this is simply pragmatic: It's a waste of time pitching a caveman diet to a committed vegan. But we're also beginning to see that genetics plays a big role in eating patterns.

Is it the carbs making my jeans so tight? Or my genes?

For example, some argue that eating carbohydrates disrupts the body's ability to regulate appetite and signal satiety (fullness)--leading to overeating and obesity.  As elegant as some of these diet/disease theories are, I don't think that the phenomenon of obesity (or its absence) can be fully explained by nutritional biochemistry alone. 

Recent research suggests that genetic variation also plays a significant role in how much we eat and whether or not we gain weight, or develop diabetes or heart disease. Here's a recent review article on the work in this field. (Subscription or library access required to view the entire article.)

The smart money now is on mapping out these genetic variations so that we can better predict who will fare well on what type of dietary prescription.  And here's a perfect example: This study suggests that a low-fat diet may be the best choice for people with a certain "obesity" gene.  Those with a double copy of the FTO gene are 2.5 times more likely to be obese. However, a low-fat diet neutralizes the effect of the gene.

In the meantime, people may need to try different eating patterns to find the one that is a good fit with their lifestyle and personal preferences.but allows them to maintain a healthy body weight over the long term.

Whither the Food Pyramid?

Many have questioned the validity of the U.S. Food Pyramid and Dietary Guidelines. But most simply want to replace them with pyramids and guidelines which better represent their own dietary dogma.  However, as nutritional genomics matures, one-size-fits-all efforts like the Food Pyramid and Dietary Guidelines may become less and less relevant.

Your thoughts?

Is Paleo the new Mediterranean?

The Mediterranean Diet has been king of the hill for the last several years. While low-carb and low-fat camps continue to trade jabs, each amassing roughly the same number of studies in its favor, the Mediterranean diet (which is neither) has risen above the fray, trumping every diet it's compared with in study after study.

Just last week, for example, I noted a study finding that the Mediterranean diet helped diabetics lose more weight and use fewer medications than a low-fat diet.

But I sense a shift of power (or at least of focus) in the works.  The "Paleo Diet" has been garnering a larger and larger share of popular attention and support as the latest Solution To All Our Problems.  And now the research community is beginning to test the theory, designing studies that pit the Paleo diet against other dietary prescriptions.

The caveman versus the shepherd

While the Mediterranean Diet hearkens back a couple of thousand years ago to a pre-industrial, agrarian era, the Paleo diet turns the clock back by ten thousand years and attempts to replicate a pre-agricultural, hunter/gather diet.  Grains, dairy, legumes, and oils--mainstays of the Mediterranean Diet--are off the table in the Paleo diet, which is based on lean meat, fish, fruits, vegetables, eggs, and nuts.

The two went head to head in a small study of patients with heart disease. Paleo pinned Mediterranean to the mat, yielding greater improvement in glucose tolerance and greater decrease in waist size. Have the cavemen knocked the shepherds off the hill? Not yet. 

Studies are one thing; real life is another

For one thing, I wonder about the long-term practicality of the Paleo diet. Diets which depart dramatically from the cultural norm often lead to dramatic weight loss. This may be partly due to the metabolic "magic" put forth by proponents. But I think it's also at least in part behavioral and practical: when whole categories of food are off limits, you tend to eat less and weight loss ensues.

Paleo and other dietary theorists have compelling stories to tell, but what are the realities on the ground?  What are the subjects in the study going to eat when the study is over? History has shown that, while purists and zealots may succeed in renouncing grains, carbs, dairy, etc. for life, mere mortals eventually find these diets too difficult to maintain and lapse back into prior eating habits. 

And while cutting fat and calories and getting more exercise may seem hopelessly old-fashioned in an era of "good calories, bad calories," let's not ignore the fact that millions of people continue to lose weight and keep it off doing nothing more exotic than that.

Do what works

A change in diet only really improves health outcomes if it's sustainable. And sustainability involves practicality, logistics, economics, personal preferences and beliefs, as well as social conditioning and cultural norms. By all means, let's use what we're learning in the research lab to to nudge our social and cultural norms and public health and food policies in the right direction.

But changing cultural norms takes time. Right now, I think the Mediterranean diet may have a practical advantage over the more extreme Paleo approach.  Fortunately, we don't all need to agree on the same solution. If what you're doing isn't producing results, try a different approach. If you've found what works for you, keep doing it. But don't assume that what works for you is the (only) solution for everyone.

Do sugar substitutes hurt or help with weight loss?

The whole idea of zero-calorie sweeteners is that they save calories. But evidence against the usefulness of artificial sweeteners as a weight-control tool seemed to be stacking up.

It's been noted that consumption of diet sodas is linked obesity.  Studies have suggested that the hyper-sweet flavor may increase the desire for sweets.  Or that the stimulation of sugar taste sensors combined with lack of calories may induce an unintended hormonal or metabolic response.  Or, simply that the idea that one is "saving calories" by using sugar substitutes may lead one to over-consume other foods in compensation. 

(See also my previous post "Sugar-Free Doesn't Get You Off Scot--Free" and this recent episode of the Nutrition Diva Podcast)

There's also new brain-mapping research from the Utrecht University and University of Birmingham (Britain) showing that the brain can distinguish caloric beverages from calorie-free ones, even when the taste-buds can't. Researchers wonder whether this leads people to subconsciously replace those calories with other foods. (See this article from the Chicago Tribune for more details.)

So what are we to make of this latest study, from the International Journal of Obesity, which found that the use of artificial sweeteners was an effective strategy for weight maintenance.  The report also notes a 2002 finding that people who used artificial sweeteners lost more weight than those who didn't.

For now, I think the bottom line is that using artificial sweeteners doesn't automatically lead to a reduction in calorie intake.  For those who closely monitor their calorie intake, including artificially-sweetened beverages may make sticking to the budget just a bit easier.

High fat diet increases insulin resistance?

I was just re-reading Tara Parker Pope's article in the NY Times on the now-famous rat study which found that high-fat meals impaired cognitive and athletic performance. Predictably, the study was dissed and dismissed by the low-carb and pro-fat bloggerati.

(By the way, for those who dismissed the study because it involved rodents, data from a parallel human study are still being analyzed but appear to line up with the original findings.)

Whatever the merits and implications of this particular study, I was struck by the following quote from Pope's article:

It’s not clear why fatty foods would cause a short-term decline in cognitive function. One theory is that a high-fat diet can trigger insulin resistance, which means the body becomes less efficient at using the glucose, or blood sugar, so important to brain function.

This, of course, is exactly the opposite of what low-carb/high-fat advocates are always telling us The story is that a high carbohydrate diet is the culprit (and a low-carb diet is the cure) for insulin resistance.

Specifically, ingestion of carbohydrates (especially high glycemic carbs) sends blood sugar soaring, which triggers insulin secretion. Over time, cells become less sensitive to the effects of all that insulin and blood sugar levels creep dangerously higher.  Next stop: obesity, Type 2 Diabetes, and heart disease. Cutting down on carbs reverses the whole cycle.

So what's all this about a high-fat diet triggering insulin resistance? 

In a long discussion, Mark Jenkins, MD, suggests that while carbohydrates may raise insulin levels, high insulin levels do not cause cells to become insulin resistant. Further, he suggests that obesity leads to insulin resistance and not the other way around.

Here are a few of his observations, which some may find surprising:

• High fat stores [in obese individuals] down-regulate insulin receptors and cause a resistance to circulating insulin.
• It has been repeatedly shown in the medical literature that...insulin sensitization is accomplished by aerobic exercise, low-fat / high-carbohydrate diet, and reduction of excessive body fat. Conversely, obesity and high fat diets have been shown to induce insulin resistance. 
• It is important that the high carbohydrate diet have predominantly complex carbohydrates and also have a high fiber content.  Overly refined, simple sugars do not appear to have the same effect as complex carbos. 

Please see Jenkins' entire discussion here and selected references here.

Maybe the problem is not the fat in our foods but the fat in our bodies

Jenkins' arguments don't separate the effects of diet composition from the effects of body weight or weight loss. In the studies he cites, those with insulin resistance aren't just eating a high fat diet; they're also obese. Those who see increased insulin sensitivity aren't just eating a low-fat diet, they're also exercising and losing weight. One wonders: Does a high fat diet lead to insulin resistance in normal weight people? Does a low-fat diet improve insulin resistance if the subjects don't lose weight? What if they lose weight on a high fat diet?

The epidemiological argument?

I find it interesting that both sides of this debate invoke epidemiological evidence. The pro-fat folks (the Weston Price gang, for example) claim that atherosclerosis and diabetes were "unheard of" in traditional cultures which had high fat, grain-free diets.  Jenkins, on the other hand, says:

If one looks at epidemiological data, the traditional diet of many third world countries consists of high complex carbohydrate content, very low fat, and high fiber. Atherosclerotic disease was virtually unheard of until the introduction of the high fat Western diet. 

Obviously the ratio of fats to carbohydrates does not tell the whole story.  Jenkin's observation about the difference between complex and simple carbohydrates is one key.

Maybe we can't blame the modern epidemic of obesity, heart disease, and diabetes on fat OR carbohydrates--but on a toxic combination of fat AND refined carbohydrates (with over-consumption and sedentary lifestyles playing significant supporting roles).

Your thoughts?