Junk Free January

Last year, Matt Lentzner organized a project called Gluten Free January, in which 546 people from around the world gave up gluten for one month.  The results were striking: a surprisingly large proportion of participants lost weight, experienced improved energy, better digestion and other benefits (1, 2).  This January, Lentzner organized a similar project called Junk Free January.  Participants can choose between four different diet styles:

1. Gluten free
2. Seed oil free (soybean, sunflower, corn oil, etc.)
3. Sugar free
4. Gluten, seed oil and sugar free

Wheat, seed oils and added sugar are three factors that, in my opinion, are probably linked to the modern "diseases of affluence" such as obesity, diabetes and coronary heart disease.  This is particularly true if the wheat is eaten in the form of white flour products, and the seed oils are industrially refined and used in high-heat cooking applications.

If you've been waiting for an excuse to improve your diet, why not join Junk Free January?

Gluten-Free January Survey Data, Part II: Health Effects of a Gluten-Free Diet

GFJ participants chose between three diet styles: a simple gluten-free diet; a "paleo light" diet diet that eliminated sugar and industrial seed (vegetable) oils in addition to gluten; and a "paleo full monty" diet that only included categories of food that would have been available to our pre-agricultural ancestors. The data in this post represent the simple gluten-free diet group, and do not represent the other two, which I'll analyze separately.

To get the data I'll be presenting below, first I excluded participants who stated on the survey that they did not adhere to the diet. Next, I excluded participants who were gluten-free before January, because they would presumably not have experienced a change from continuing to avoid gluten. That left us with 53 participants.

For each of these graphs, the vertical axis represents the number of participants in each category. They won't necessarily add up to 53, for several reasons. The most common reason is that for the questions asking about changes in health conditions, I didn't include responses from people who didn't have the condition in question at baseline because there was nothing to change.

Question #1: What is your overall opinion of the effect of gluten free January on you?

Participants had a very positive experience with the gluten-free diet. Not one person reported a negative overall experience.

Question #2: Did you note a weight change at the end of gluten free January?

And here are the data for people who described themselves as overweight at baseline:

Two-thirds of people who were overweight at baseline lost weight, and only one person out of 37 gained weight. That is striking. A number of people didn't weigh themselves, which is why the numbers only add up to 37.

Question #3: Before January 2011, did you have a problem with intestinal transit (frequent constipation or diarrhea)? If so, did your symptoms change during the month of January?


Responses are heavily weighted toward improvement, although there were a few instances where transit worsened. Transit problems are one of the most common manifestations of gluten sensitivity.

Question #4: Before January 2011, did you have frequent digestive discomfort (pain, bloating, etc.)? If so, did your symptoms change during the month of January?


Digestive discomfort was common, and the gluten-free diet improved it in nearly everyone who had it at baseline. I find this really impressive.

Question #5: Before January 2011, did you have acid reflux? If so, did your symptoms change during the month of January?

Acid reflux responded well to a gluten-free diet.

Question #6: Before January 2011, did you have a problem with tiredness/lethargy? If so, did your symptoms change during the month of January?
Lethargy was common and generally improved in people who avoided gluten. This doesn't surprise me at all. The recent controlled gluten study in irritable bowel syndrome patients found that lethargy was the most reliable consequence of eating gluten that they measured (1, 2). That has also been my personal experience.

Question #7: Before January 2011, did you have a problem with anxiety? If so, did your symptoms change during the month of January?

Anxiety tended to improve in most participants who started with it.

Question #8: Before January 2011, did you have a problem with an autoimmune or inflammatory condition? If so, did your symptoms change during the month of January?

Autoimmune and inflammatory conditions tended to improve in the gluten-free group, although one person experienced a worsening of symptoms.

Question #9: If you ate gluten again or did a gluten challenge after gluten free January, what was the effect?

Just under half of participants experienced moderate or significant negative symptoms when they re-introduced gluten at the end of the month. Two people felt better after re-introducing gluten.


Conclusion

I find these results striking. Participants overwhelmingly improved in every health category we measured. Although the data may have been somewhat biased due to the 53% response rate, it's indisputable that a large number of participants, probably the majority, benefited from avoiding gluten for a month. At some point, we're going to compile some of the comments people left in the survey, which were overwhelmingly positive. Here's a typical comment in response to the question " In your own words, how would you describe your January 2011 experience" (used with permission):

Amazing! I would recommend the experiment to anyone. I felt completely more alert, and less bloated. When I ate some gluten at the close of the experiment, I felt gross, bloated, and lethargic.

I think it's worth mentioning that some participants also eliminated other starches, particularly refined starches. Judging by the comments, the diet was probably lower in carbohydrate for a number of participants. We may try to assess that next year.

Gluten-Free January Survey Data, Part I: Demographics and Limitations

Thanks to Matt Lentzner for organizing Gluten-Free January, and everyone who participated and completed the survey, we have a nice data set illustrating what happens when a group of people stop eating gluten for a month. Janine Jagger, Matt and I have been busy analyzing the data, and I'm ready to begin sharing our findings.

GFJ had over 500 participants, 527 of which received the survey and 279 of which completed the survey at the end of the month. Of those who received the survey, 53 percent completed it. I think these are respectable numbers for a survey of this nature, and it reflects the conscientious nature of the people who participated in GFJ.

Demographics

Although respondents were primarily from the United States, I'm happy to say that the data represent 18 different nationalities:

Respondents represented a diversity of ages, the largest group being 30-39 years old, with similar numbers in the 20-29 and 40-49 year groups.
Respondents were just under 2/3 women.

Respondents represented a variety of weights, but the sample was biased toward lean people, in comparison with the general population. There were not many obese participants.
Overall, I was pleased to see that the demographics were quite diverse, particularly in the age and gender categories.

Limitations

There are a few caveats to keep in mind when interpreting the survey results:

1. GFJ participants do not represent a random cross-section of the population at large. They represent primarily health-conscious individuals who were motivated enough to make a substantial dietary change. In addition, many of the people who participated probably did so because they already suspected they had a problem with gluten.
   
2. The survey response rate was 53%. Although I think that's a reasonable number considering the circumstances, it leaves open the possibility that survey responders differ from non-responders. It's conceivable that participants with better adherence and better outcomes were more likely to complete the survey than those who did not adhere to the diet or had neutral or unfavorable outcomes, despite our efforts to encourage everyone to complete the survey regardless of adherence or outcome. So the results could be biased toward positive outcomes, meaning that we will need to see a strong effect for it to be believable.
   
3. This was a non-blinded diet trial without a control group. There's no way to know how much of the effect was due to avoiding gluten per se, how much was due to overall changes in diet patterns, and how much was a placebo effect.
   

With that in mind, what can we take from the survey data? I feel that we can use it to answer the following question: "what is likely to happen when a motivated, health-conscious person decides to avoid gluten for a month?" And I think we can also use it to generate (but not test) hypotheses about the effects of eating gluten on the general population.

Gluten-Free January Raffle Winners Selected!

Raffle winners have been selected and shirts are on their way. You know who you are. Thanks to everyone who participated and filled out the survey! For those who didn't, there's always next year.

Janine Jagger, Matt Lentzner and I are busy crunching the mountain of data we collected from the GFJ survey. We got 279 responses, which is remarkable for a survey of this nature.

Stay tuned for data!

My Gluten-Free January

I've been avoiding most gluten, particularly wheat, for over a year now. I never had obvious symptoms that I could clearly link to eating wheat, although I had my suspicions. I've made many changes to my diet over the last decade, and I feel much better than I did ten years ago, but it's hard to disentangle all the factors. I don't think I ever went an entire month without eating any gluten at all before this January. After posting Matt Lentzner's challenge to go gluten-free this January, I felt obligated to do it myself, so I signed up!

I succeeded in avoiding all gluten for the month of January, even though it was a pain at times. I felt good before January, and didn't start with any health or body weight problems, so there wasn't much to improve. I also felt good while strictly avoiding gluten this January, perhaps a little better than usual but it's hard to say.

At the end of the month, I did a blinded wheat challenge using the method I described in a previous post, which uses gluten-free bread as the placebo (1). I recorded my blood sugar at 30 minute intervals after eating the bread, and recorded how I felt physically and emotionally for three days after each challenge.

The result? I think the bread gave me gas, but that's about it. I'm not even positive that was due to the wheat. My energy level was good, and I didn't experience any digestive pain or changes in transit time. There was no significant difference in my blood glucose response between the bread and the gluten-free bread.

I decided that I didn't have any symptoms, so I celebrated by having a porter (1) with friends a few nights later. I slept poorly and woke up with mild digestive discomfort and gas. Then I ate wheat later in the week and slept poorly and got gas again. Hmmm...

Some people might say that the body adapts to any food, and wheat is no different. Go without it for a while, and the body has a tough time digesting it. But I can go for weeks without eating a potato, a chicken thigh or broccoli, and all will digest just fine when I eat them again.

I'm pretty sure I don't have a severe reaction to gluten. I think I'm going to stick with my mostly gluten-free habits, and eat it occasionally when I'm offered food in social situations.

Did anyone else do a blinded wheat challenge? Describe it in the comments!

Gluten-Free January Raffle!

Hi, Gluten-Free January participants. Matt, Janine and I have collected about 200 survey responses at this point. So far, the results are very interesting! But we want to get as many responses as possible, because the more responses we get, the more informative the data will be for all of us. So please fill out the survey Matt sent you by e-mail, no matter what your results were, and no matter whether you stuck with the diet or not! The survey is strictly about your GFJ experience, not investment opportunities, timeshares, ShamWows or anything else. It will take you less than 5 minutes, and it's totally anonymous. The deadline is Feb 15th. Big thanks to everyone who has taken it so far.

To encourage participants to complete the survey, we're organizing a raffle. Matt and I have five Gluten-Free January T-shirts we're ready to give out for free. These shirts were designed by Matt and they're really cool. I have one myself, and the print and fabric quality are top notch. Here's what the logo looks like:
If you've completed the survey and want to be included in the raffle, please e-mail Matt to let him know you've completed it. Anyone who has already e-mailed Matt to let him know they completed the survey will automatically be entered, so no need for a second e-mail. So far, very few people have written Matt, so your probability of winning a shirt is high!

Gluten-free January Participants: Take the Survey!

Matt Lentzner, Janine Jagger and I have designed a survey for participants of Gluten-free January, using the online application StatCrunch. Janine is an epidemiologist who studies healthcare worker safety at the University of Virginia; she has experience designing surveys for data collection so we're glad to have her on board. The survey will allow us to systematically gather and analyze data on the results of Gluten-free January. It will be 100 percent anonymous-- none of your answers will be connected to your identity in any way.

This survey has the potential to be really informative, but it will only work if you respond! The more people who take the survey, the more informative it will be, even if you didn't avoid gluten for a single day. If not very many people respond, it will be highly susceptible to "selection bias", where perhaps the only people who responded are people who improved the most, skewing the results.

Matt will be sending the survey out to everyone on his mailing list. Please complete it, even if you didn't end up avoiding gluten at all! There's no shame in it. The survey has responses built in for people who didn't avoid gluten. Your survey will still be useful!

We have potential data from over 500 people. After we crunch the numbers, I'll share them on the blog.

Two Wheat Challenge Ideas from Commenters

Some people have remarked that the blinded challenge method I posted is cumbersome.

Reader "Me" suggested:

You can buy wheat gluten in a grocery store. Why not simply have your friend add some wheat gluten to your normal protein shake.

Reader David suggested:

They sell empty gelatin capsules with carob content to opacify them. Why not fill a few capsules with whole wheat flour, and then a whole bunch with rice starch or other placebo. For two weeks take a set of, say, three capsules every day, with the set of wheat capsules in line to be taken on a random day selected by your friend. This would further reduce the chances that you would see through the blind, and it prevent the risk of not being able to choke the "smoothie" down. It would also keep it to wheat and nothing but wheat (except for the placebo starch).

The reason I chose the method in the last post is that it directly tests wheat in a form that a person would be likely to eat: bread. The limitation of the gluten shake method is that it would miss a sensitivity to components in wheat other than gluten. The limitation of the pill method is that raw flour is difficult to digest, so it would be difficult to extrapolate a sensitivity to cooked flour foods. You might be able to get around that by filling the pills with powdered bread crumbs. Those are two alternative ideas to consider if the one I posted seems too involved.

Blinded Wheat Challenge

Self-experimentation can be an effective way to improve one's health*. One of the problems with diet self-experimentation is that it's difficult to know which changes are the direct result of eating a food, and which are the result of preconceived ideas about a food. For example, are you more likely to notice the fact that you're grumpy after drinking milk if you think milk makes people grumpy? Maybe you're grumpy every other day regardless of diet? Placebo effects and conscious/unconscious bias can lead us to erroneous conclusions.

The beauty of the scientific method is that it offers us effective tools to minimize this kind of bias. This is probably its main advantage over more subjective forms of inquiry**. One of the most effective tools in the scientific method's toolbox is a control. This is a measurement that's used to establish a baseline for comparison with the intervention, which is what you're interested in. Without a control measurement, the intervention measurement is typically meaningless. For example, if we give 100 people pills that cure belly button lint, we have to give a different group placebo (sugar) pills. Only the comparison between drug and placebo groups can tell us if the drug worked, because maybe the changing seasons, regular doctor's visits, or having your belly button examined once a week affects the likelihood of lint.

Another tool is called blinding. This is where the patient, and often the doctor and investigators, don't know which pills are placebo and which are drug. This minimizes bias on the part of the patient, and sometimes the doctor and investigators. If the patient knew he were receiving drug rather than placebo, that could influence the outcome. Likewise, investigators who aren't blinded while they're collecting data can unconsciously (or consciously) influence it.

Back to diet. I want to know if I react to wheat. I've been gluten-free for about a month. But if I eat a slice of bread, how can I be sure I'm not experiencing symptoms because I think I should? How about blinding and a non-gluten control?

Procedure for a Blinded Wheat Challenge

1. Find a friend who can help you.

2. Buy a loaf of wheat bread and a loaf of gluten-free bread.

3. Have your friend choose one of the loaves without telling you which he/she chose.

4. Have your friend take 1-3 slices, blend them with water in a blender until smooth. This is to eliminate differences in consistency that could allow you to determine what you're eating. Don't watch your friend do this-- you might recognize the loaf.

5. Pinch your nose and drink the "bread smoothie" (yum!). This is so that you can't identify the bread by taste. Rinse your mouth with water before releasing your nose. Record how you feel in the next few hours and days.

6. Wait a week. This is called a "washout period". Repeat the experiment with the second loaf, attempting to keep everything else about the experiment as similar as possible.

7. Compare how you felt each time. Have your friend "unblind" you by telling you which bread you ate on each day. If you experienced symptoms during the wheat challenge but not the control challenge, you may be sensitive to wheat.

If you want to take this to the next level of scientific rigor, repeat the procedure several times to see if the result is consistent. The larger the effect, the fewer times you need to repeat it to be confident in the result.


* Although it can also be disastrous. People who get into the most trouble are "extreme thinkers" who have a tendency to take an idea too far, e.g., avoid all animal foods, avoid all carbohydrate, avoid all fat, run two marathons a week, etc.

** More subjective forms of inquiry have their own advantages.

Eating Wheat Gluten Causes Symptoms in Some People Who Don't Have Celiac Disease

Irritable bowel syndrome (IBS) is a condition characterized by the frequent occurrence of abdominal pain, diarrhea, constipation, bloating and/or gas. If that sounds like an extremely broad description, that's because it is. The word "syndrome" is medicalese for "we don't know what causes it." IBS seems to be a catch-all for various persistent digestive problems that aren't defined as separate disorders, and it has a very high prevalence: as high as 14 percent of people in the US, although the estimates depend on what diagnostic criteria are used (1). It can be brought on or exacerbated by several different types of stressors, including emotional stress and infection.

Maelán Fontes Villalba at Lund University recently forwarded me an interesting new paper in the American Journal of Gastroenterology (2). Dr. Jessica R. Biesiekierski and colleagues recruited 34 IBS patients who did not have celiac disease, but who felt they had benefited from going gluten-free in their daily lives*. All patients continued on their pre-study gluten-free diet, however, all participants were provided with two slices of gluten-free bread and one gluten-free muffin per day. The investigators added isolated wheat gluten to the bread and muffins of half the study group.

During the six weeks of the intervention, patients receiving the gluten-free food fared considerably better on nearly every symptom of IBS measured. The most striking difference was in tiredness-- the gluten-free group was much less tired on average than the gluten group. Interestingly, they found that a negative reaction to gluten was not necessarily accompanied by the presence of anti-gluten antibodies in the blood, which is a test often used to diagnose gluten sensitivity.

Here's what I take away from this study:

1. Wheat gluten can cause symptoms in susceptible people who do not have celiac disease.
2. A lack of circulating antibodies against gluten does not necessarily indicate a lack of gluten sensitivity.
   
3. People with mysterious digestive problems may want to try avoiding gluten for a while to see if it improves their symptoms**.
4. People with mysterious fatigue may want to try avoiding gluten.
   

A previous study in 1981 showed that feeding volunteers a large dose of gluten every day for 6 weeks caused adverse gastrointestinal effects, including inflammatory changes, in relatives of people with celiac disease, who did not themselves have celiac (3). Together, these two studies are the most solid evidence that gluten can be damaging in people without celiac disease, a topic that has not received much interest in the biomedical research community.

I don't expect everyone to benefit from avoiding gluten. But for those who are really sensitive, it can make a huge difference. Digestive, autoimmune and neurological disorders associate most strongly with gluten sensitivity. Avoiding gluten can be a fruitful thing to try in cases of mysterious chronic illness. We're two-thirds of the way through Gluten-Free January. I've been fastidiously avoiding gluten, as annoying as it's been at times***. Has anyone noticed a change in their health?


* 56% of volunteers carried HLA-DQ2 or DQ8 alleles, which is slightly higher than the general population. Nearly all people with celiac disease carry one of these two alleles. 28% of volunteers were positive for anti-gliadin IgA, which is higher than the general population.

** Some people feel they are reacting to the fructans in wheat, rather than the gluten. If a modest amount of onion causes the same symptoms as eating wheat, then that may be true. If not, then it's probably the gluten.

*** I'm usually about 95% gluten-free anyway. But when I want a real beer, I want one brewed with barley. And when I want Thai food or sushi, I don't worry about a little bit of wheat in the soy sauce. If a friend makes me food with gluten in it, I'll eat it and enjoy it. This month I'm 100% gluten-free though, because I can't in good conscience encourage my blog readership to try it if I'm not doing it myself. At the end of the month, I'm going to do a blinded gluten challenge (with a gluten-free control challenge) to see once and for all if I react to it. Stay tuned for more on that.

A Gluten-free January

Are You Gluten Sensitive?

Many people are totally unaware of the fact that they react poorly to gluten. Because they've been eating wheat, barley and/or rye products every day for virtually their entire lives, they don't know what their bodies feel like without gluten. In susceptible people, eating gluten is linked to a dizzying array of health problems that stem from an immune reaction to gliadins and other proteins in gluten (1). Are you a susceptible person? How do you know?

The gold standard way to detect a gluten sensitivity is to do a gluten "challenge" after a period of avoidance and see how you feel. People who react poorly to gluten may feel better after a period of avoidance. After a gluten challenge, symptoms can range from digestive upset, to skin symptoms, to fatigue or irritability within minutes to days of the gluten challenge.

With 2011 approaching, why not make your new year's resolution to go gluten-free for a month? A man named Matt Lentzner e-mailed me this week to ask if I would help with his (non-commercial) project, "A Gluten-free January". I said I'd be delighted. Although I don't typically eat much gluten, this January I'm going 100% gluten-free. Are you on board? Read on.

A Message from Matt Lentzner

Hi There.

My name is Matt Lentzner. I'm just some guy who lifts weights on his patio and tries to eat healthy. That's not important, but I have an idea that just might be.

I am trying to get as many people as possible to go gluten-free for one month - this January 2011.

I've considered this whole ancestral diet thing and I've come to a conclusion. If you could only do just one thing to improve your health then not eating gluten would be it. This is not to say that avoiding other nasty things like fructose or industrial vegetable oil is not important. They are, but you'd get the most bang for your buck from not eating gluten.

"Eat No Gluten" is simple and easy to remember. I think that sometimes the rules get so complicated and overwhelming and people just give up on it. We're keeping it simple here. Even at this simplified level I see that it's difficult for a lot of folks. I think people, Americans especially, tend not to pay much attention to what they're eating - what it is, where it came from, etc.

Getting people to get out of their eating ruts and think a little about what goes into their mouths is a valuable exercise. It sets the stage for better choices in the future. I hope that some success with the simple step will encourage people to further improve their diets.

I have a website at www.glutenfreejan.com. If you want to sign up just send an email with your first name, last initial, and town of residence to glutenfreejan@gmail.com. If you are on Facebook there's a community you can 'Like' called: Gluten Free January. So far I have over 120 people all over the world signed up. If you are already gluten-free then I still want you to sign up - the more the merrier. You can also use this opportunity to spread the word and sign up your family and friends.

Merry Christmas - Looking forward to a gluten-free New Year.

Matt

The China Study on Wheat

Denise Minger has just put up another great China Study post that's worth reading if you haven't already. Denise has been busy applying her statistics skills to the mountain of data the study collected. She noted in a previous post that wheat intake was strongly associated with coronary heart disease (CHD), the quintessential modern cardiovascular disease. I, and several other people, requested that she work her mathmagic to see if the association could be due to some other factor. For example, wheat is eaten mostly in the Northern regions of China, and CHD rates are generally higher at higher latitudes (vitamin D insufficiency?). This is true in Europe as well, and may be partly responsible for the purported benefits of the Mediterranean diet. You can mathematically determine if the association between wheat and CHD is simply due to the fact that wheat eaters live further North.

To make a long story short, nothing could explain the association except wheat itself, even latitude. Furthermore, she found a strong association between wheat intake and body mass index, typically a predictor of fat mass although we can't say that for sure. That finding echos a previous study in China where wheat eaters were more likely to be overweight than rice eaters (1, 2). Head over to Denise's post for the full story.

The China Study has major limitations built into its basic design, due to the fact that it was observational and pooled the blood samples of many individuals. Therefore, its findings can never prove anything, they can only suggest or be consistent with hypotheses. However, the study also has some unique advantages, such as a diversity of diets and regions, and the fact that people had presumably been eating a similar diet for a long time. I feel that Denise's efforts are really teasing out some useful information from the study that have been de-emphasized by other investigators.

There has been so little serious investigation into the health effects of wheat in the general population that I have to rely mostly on indirect evidence, such as the observation that the diseases of civilization tend to closely follow the introduction of white flour around the globe. Researchers studying celiac disease and other forms of gluten allergy, and the efforts of the paleolithic diet community in spreading that information (for example, Loren Cordain and Pedro Bastos), have been major contributors to understanding the health effects of wheat. Denise's analysis is one of the strongest pieces of evidence I've come by so far. One of these days, I'll post all of my references incriminating wheat. There are quite a few, although none of them is the smoking gun. I think there's enough indirect evidence that investigators should begin taking the idea seriously that wheat, particularly in the form of industrial flour products, may contribute to chronic disease in more than just a small subset of the population.

Real Food XI: Sourdough Buckwheat Crepes

Buckwheat was domesticated in Southeast Asia roughly 6,000 years ago. Due to its unusual tolerance of cool growing conditions, poor soils and high altitudes, it spread throughout the Northern latitudes of Eurasia, becoming the staple crop in many regions. It's used to a lesser extent in countries closer to the equator. It was also a staple in the Northeastern US until it was supplanted by wheat and corn.

Buckwheat isn't a grain: it's a 'pseudograin' that comes from a broad-leaved plant. As such, it's not related to wheat and contains no allergenic gluten. Like quinoa, it has some unusual properties that make it a particularly nutritious food. It's about 16 percent protein by calories, ranking it among the highest protein grains. However, it has an advantage over grains: it contains complete protein, meaning it has a balance of essential amino acids similar to animal foods. Buckwheat is also an exceptional source of magnesium and copper, two important nutrients that may influence the risk of insulin resistance and cardiovascular disease (1, 2).

However, like all seeds (including grains and nuts), buckwheat is rich in phytic acid. Phyic acid complexes with certain minerals, preventing their absorption by the human digestive tract. This is one of the reasons why traditional cultures prepare their grains carefully (3). During soaking, and particularly fermentation of raw batters, an enzyme called phytase goes to work breaking down the phytic acid. Not all seeds are endowed with enough phytase to break down phytic acid in a short period of time. Buckwheat contains a lot of phytase, and consequently fermented buckwheat batters contain very little phytic acid (4, 5). It's also high in astringent tannins, but thorough soaking in a large volume of water removes them.

Buckwheat is fermented in a number of traditional cultures. In Bhutan, it's fermented to make flatbreads and alcoholic drinks (6). In Brittany (Bretagne; Northwestern France), sourdough buckwheat flour pancakes are traditional. Originally a poverty food, it is now considered a delicacy.

The following simple recipe is based on my own experimentation with buckwheat. It isn't traditional as far as I know, however it is based on traditional methods used to produce sourdough flatbreads in a number of cultures. I used the word 'crepe' to describe it, but I typically make something more akin to a savory pancake or uttapam. You can use it to make crepes if you wish, but this recipe is not for traditional French buckwheat crepes.

It's important that the buckwheat be raw and whole for this recipe. Raw buckwheat is light green to light brown (as in the photo above). Kasha is toasted buckwheat, and will not substitute properly. It's also important that the water be dechlorinated and the salt non-iodized, as both will interfere with fermentation.

For a fermentation starter, you can use leftover batter from a previous batch (although it doesn't keep very long), or rice soaking water from this method (7).

Ingredients and Materials

• 2-3 cups raw buckwheat groats
• Dechlorinated water (filtered, boiled, or rested uncovered overnight)
• Non-iodized salt (sea salt, pickling salt or kosher salt), 2/3 tsp per cup of buckwheat
  
• Fermentation starter (optional), 2 tablespoons
  
• Food processor or blender

Recipe

1. Cover buckwheat with a large amount of dechlorinated water and soak for 9-24 hours. Raw buckwheat is astringent due to water-soluble tannins. Soaking in a large volume of water and giving it a stir from time to time will minimize this. The soaking water will also get slimy. This is normal.
   
2. Pour off the soaking water and rinse the buckwheat thoroughly to get rid of the slime and residual tannins.
3. Blend the buckwheat, salt, dechlorinated water and fermentation starter in a food processor or blender. Add enough water so that it reaches the consistency of pancake batter. The smoother you get the batter, the better the final product will be.
4. Ferment for about 12 hours, a bit longer or shorter depending on the temperature and whether or not you used a starter. The batter may rise a little bit as the microorganisms get to work. The smell will mellow out. Refrigerate it after fermentation.
   
5. In a greased or non-stick skillet, cook the batter at whatever thickness and temperature you prefer. I like to cook a thick 'pancake' with the lid on, at very low heat, so that it steams gently.
   

Dig in! Its mild flavor goes with almost anything. Batter will keep for about four days in the fridge.

Thanks to Christaface for the CC licensed photo (Flickr).

Fermented Grain Recipes from Around the World

In my last two posts on grains, I described how traditional food processing methods make grains more nutritious and digestible (1, 2). I promised to briefly describe a few recipes from around the world, then got distracted by other things. Here they are.

Africa: Ogi

Grain fermentation is widespread in Africa and is probably nearly as old as agriculture on the continent. The nutritional importance of fermentation is suggested by the amount of time and effort that many African cultures put into it, when they could save themselves a lot of trouble by simply soaking and cooking their grains.

Ogi is a common West African porridge that's eaten as a staple food by people of all ages. It's even used as a weaning food. It's made in essentially the same manner from corn, sorghum or millet.

Whole grain is soaked in water for one to three days. It's then wet milled, mixed with water and sieved to remove a portion of the bran. Extra bran is fed to animals, while the white, starchy sediment is fermented for two to three days. This is then cooked into a thin or thick porridge and eaten.

South America: Pozol

At first glance, some people may think I left the 'e' off the word 'pozole', a traditional Mexican stew. However, pozol is an entirely different beast, an ancient food almost totally unknown in the US, but which fueled the Mayan empire and remains a staple food in Southeastern Mexico.

To make pozol, first the corn must be 'nixtamalized': whole kernels are boiled in a large volume of water with calcium hydroxide (10% w/v). This is a processing step in most traditional South American corn recipes, as it allows a person to avoid pellagra (niacin deficiency)! The loosened bran is removed from the kernels by hand.

The kernels are then ground into dough, formed into balls and placed into banana leaves to ferment for one to 14 days. Following fermentation, pozol is diluted in water and consumed raw.

Europe: Sourdough Bread

Sourdough bread is Europe's quintessential fermented grain food. Before purified yeast strains came into widespread use in the 20th century, all bread would have been some form of sourdough.

Although in my opinion wheat is problematic for many people, sourdough fermentation renders it more nutritious and better tolerated by those with gluten/wheat sensitivity. In an interesting series of studies, Dr. Marco Gobbetti's group, among others, has shown that fermentation partially degrades gluten, explaining the ability of fermentation to decrease the adverse effects of gluten in those who are sensitive to it (3). They even showed that people with celiac disease can safely eat wheat bread that has been long-fermented with selected bacteria and yeasts under laboratory conditions (4). Rye contains about half the gluten of bread wheat, and is generally nutritionally superior to wheat, so sourdough rye is a better choice in my opinion.

To make sourdough bread, first the dry grains are ground into flour. Next, the flour is sifted through a screen to remove a portion of the bran. The earliest bread eaters probably didn't do this, although there is evidence of the wealthy eating sifted flour in societies as old as ancient Egypt and ancient Rome. I don't know what the optimum amount of bran to include in flour is, but it's not zero. I would be inclined to keep at least half of it, recognizing that the bran is disproportionately rich in nutrients.

Next, a portion of flour is mixed with water and a "sourdough starter", until it has a runny consistency. The starter is a diverse culture of bacteria and yeast that is carefully maintained by the bread maker. This culture acidifies the batter and produces carbon dioxide gas. The mixture is allowed to ferment for 8-12 hours. Finally, flour and salt are added to the batter and formed into dough balls. These are allowed to ferment and rise for a few hours, then baked.

My Experience

I've tried making ogi (millet) and pozol, and I have to admit that neither attempt was successful. Pozol in particular may depend on local populations of bacteria and yeast, as the grains' microorganisms are killed during processing. However, I do eat fermented grains regularly in the form of homemade brown rice 'uthappam' and sourdough buckwheat 'crepes'. The buckwheat crepes are tasty and easy to make. I'll post a recipe at some point.

The first two recipes are from the FAO publication Fermented Cereals: a Global Perspective (5).

The Body Fat Setpoint, Part IV: Changing the Setpoint

Prevention is Easier than Cure

Experiments in animals have confirmed what common sense suggests: it's easier to prevent health problems than to reverse them. Still, many health conditions can be improved, and in some cases reversed, through lifestyle interventions. It's important to have realistic expectations and to be kind to oneself. Cultivating a drill sergeant mentality will not improve quality of life, and isn't likely to be sustainable.

Fat Loss: a New Approach

If there's one thing that's consistent in the medical literature, it's that telling people to eat fewer calories does not help them lose weight in the long term. Gary Taubes has written about this at length in his book Good Calories, Bad Calories, and in his upcoming book on body fat. Many people who use this strategy see transient fat loss, followed by fat regain and a feeling of defeat. There's a simple reason for it: the body doesn't want to lose weight. It's extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.

Therefore, what we need for sustainable fat loss is not starvation; we need a treatment that lowers the fat mass setpoint. There are several criteria that this treatment will have to meet to qualify:

1. It must cause fat loss
2. It must not involve deliberate calorie restriction
3. It must maintain fat loss over a long period of time
4. It must not be harmful to overall health
   

I also prefer strategies that make sense from the perspective of human evolution.

Strategies: Diet Pattern

The most obvious treatment that fits all of my criteria is low-carbohydrate dieting. Overweight people eating low-carbohydrate diets generally lose fat and spontaneously reduce their calorie intake. In fact, in several diet studies, investigators compared an all-you-can-eat low-carbohydrate diet with a calorie-restricted low-fat diet. The low-carbohydrate dieters generally reduced their calorie intake and body fat to a similar or greater degree than the low-fat dieters, despite the fact that they ate all the calories they wanted (1). This suggest that their fat mass setpoint had changed. At this point, I think moderate carbohydrate restriction may be preferable to strict carbohydrate restriction for some people, due to the increasing number of reports I've read of people doing poorly in the long run on extremely low-carbohydrate diets (2).

Another strategy that appears effective is the "paleolithic" diet. In Dr. Staffan Lindeberg's 2007 diet study, overweight volunteers with heart disease lost fat and reduced their calorie intake to a remarkable degree while eating a diet consistent with our hunter-gatherer heritage (3). This result is consistent with another diet trial of the paleolithic diet in diabetics (4). In post hoc analysis, Dr. Lindeberg's group showed that the reduction in weight was apparently independent of changes in carbohydrate intake*. This suggests that the paleolithic diet has health benefits that are independent of carbohydrate intake.

Strategies: Gastrointestinal Health

Since the gastrointestinal (GI) tract is so intimately involved in body fat metabolism and overall health (see the former post), the next strategy is to improve GI health. There are a number of ways to do this, but they all center around four things:

1. Don't eat food that encourages the growth of harmful bacteria
2. Eat food that encourages the growth of good bacteria
3. Don't eat food that impairs gut barrier function
4. Eat food that promotes gut barrier health

The first one is pretty easy: avoid refined sugar, refined carbohydrate in general, and lactose if you're lactose intolerant. For the second and fourth points, make sure to eat fermentable fiber. In one trial, oligofructose supplements led to sustained fat loss, without any other changes in diet (5). This is consistent with experiments in rodents showing improvements in gut bacteria profile, gut barrier health, glucose tolerance and body fat mass with oligofructose supplementation (6, 7, 8).

Oligofructose is similar to inulin, a fiber that occurs naturally in a wide variety of plants. Good sources are jerusalem artichokes, jicama, artichokes, onions, leeks, burdock and chicory root. Certain non-industrial cultures had a high intake of inulin. There are some caveats to inulin, however: inulin and oligofructose can cause gas, and can also exacerbate gastroesophageal reflux disorder (9). So don't eat a big plate of jerusalem artichokes before that important date.

The colon is packed with symbiotic bacteria, and is the site of most intestinal fermentation. The small intestine contains fewer bacteria, but gut barrier function there is critical as well. The small intestine is where the GI doctor will take a biopsy to look for celiac disease. Celiac disease is a degeneration of the small intestinal lining due to an autoimmune reaction caused by gluten (in wheat, barley and rye). This brings us to one of the most important elements of maintaining gut barrier health: avoiding food sensitivities. Gluten and casein (in dairy protein) are the two most common offenders. Gluten sensitivity is widespread and typically undiagnosed (10).

Eating raw fermented foods such as sauerkraut, kimchi, yogurt and half-sour pickles also helps maintain the integrity of the upper GI tract. I doubt these have any effect on the colon, given the huge number of bacteria already present. Other important factors in gut barrier health are keeping the ratio of omega-6 to omega-3 fats in balance, eating nutrient-dense food, and avoiding the questionable chemical additives in processed food. If triglycerides are important for leptin sensitivity, then avoiding sugar and ensuring a regular source of omega-3 should aid weight loss as well.

Strategies: Micronutrients

As I discussed in the last post, micronutrient deficiency probably plays a role in obesity, both in ways that we understand and ways that we (or I) don't. Eating a diet that has a high nutrient density and ensuring a good vitamin D status will help any sustainable fat loss strategy. The easiest way to do this is to eliminate industrially processed foods such as white flour, sugar and seed oils. These constitute more than 50% of calories for the average Westerner.

After that, you can further increase your diet's nutrient density by learning to properly prepare grains and legumes to maximize their nutritional value and digestibility (11, 12; or by avoiding grains and legumes altogether if you wish), selecting organic and/or pasture-raised foods if possible, and eating seafood including seaweed. One of the problems with extremely low-carbohydrate diets is that they may be low in water-soluble micronutrients, although this isn't necessarily the case.

Strategies: Miscellaneous

In general, exercise isn't necessarily helpful for fat loss. However, there is one type of exercise that clearly is: high-intensity intermittent training (HIIT). It's basically a fancy name for sprints. They can be done on a track, on a stationary bicycle, using weight training circuits, or any other way that allows sufficient intensity. The key is to achieve maximal exertion for several brief periods, separated by rest. This type of exercise is not about burning calories through exertion: it's about increasing hormone sensitivity using an intense, brief stressor (hormesis). Even a ridiculously short period of time spent training HIIT each week can result in significant fat loss, despite no change in diet or calorie intake (13).

Anecdotally, many people have had success using intermittent fasting (IF) for fat loss. There's some evidence in the scientific literature that IF and related approaches may be helpful (14). There are different approaches to IF, but a common and effective method is to do two complete 24-hour fasts per week. It's important to note that IF isn't about restricting calories, it's about resetting the fat mass setpoint. After a fast, allow yourself to eat quality food until you're no longer hungry.

Insufficient sleep has been strongly and repeatedly linked to obesity. Whether it's a cause or consequence of obesity I can't say for sure, but in any case it's important for health to sleep until you feel rested. If your sleep quality is poor due to psychological stress, meditating before bedtime may help. I find that meditation has a remarkable effect on my sleep quality. Due to the poor development of oral and nasal structures in industrial nations, many people do not breathe effectively and may suffer from conditions such as sleep apnea that reduce sleep quality. Overweight also contributes to these problems.

I'm sure there are other useful strategies, but that's all I have for now. If you have something to add, please put it in the comments.


* Since reducing carbohydrate intake wasn't part of the intervention, this result is observational.

It's Time to Let Go of The Glycemic Index

The glycemic index (GI) is a measure of how much an individual food elevates blood sugar when it's eaten. To measure it, investigators feed a person a food that contains a fixed amount of carbohydrate, and measure their blood glucose response over time. Then they determine the area under the glucose curve and compare it to a standard quickly digesting food such as white bread or pure glucose.

Each food must contain the same total amount of carbohydrate, so you might have to eat a big plate of carrots to compare with a slice of bread. You end up with a number that reflects the food's ability to elevate glucose when eaten in isolation. It typically depends on how quickly the carbohydrate is absorbed, with higher numbers usually resulting from faster absorption.

The GI is a standby of modern nutritional advice. It's easy to believe in because processed foods tend to have a higher glycemic index than minimally processed foods, high blood sugar is bad, and chronically high insulin is bad. But many people have criticized the concept, and rightly so.

Blood sugar responses to a carbohydrate-containing foods vary greatly from person to person. For example, I can eat a medium potato and a big slice of white bread (roughly 60 g carbohydrate) with nothing else and only see a modest spike in my blood sugar. I barely break 100 mg/dL and I'm back at fasting glucose levels within an hour and a half. You can see a graph of this experiment here. That's what happens when you have a well-functioning pancreas and insulin-sensitive tissues. Your body shunts glucose into the tissues almost as rapidly as it enters the bloodstream. Someone with impaired glucose tolerance might have gone up to 170 mg/dL for two and a half hours on the same meal.

The other factor is that foods aren't eaten in isolation. Fat, protein, acidity and other factors slow carbohydrate absorption in the context of a normal meal, to the point where the GI of the individual foods become much less pronounced.

It's time to put my money where my mouth is. Researchers have conducted a number of controlled trials comparing low-GI diets to high-GI diets. I've done an informal literature review to see what the overall findings are. I'm only interested in long-term studies-- 10 weeks or longer-- and I've excluded studies using subjects with metabolic disorders such as diabetes.

The question I'm asking with this review is, what are the health effects of a low-glycemic index diet on a healthy normal-weight or overweight person? I found a total of seven studies on PubMed in which investigators varied GI while keeping total carbohydrate about the same, for 10 weeks or longer. I'll present them out of chronological order because they flow better that way.

Study #1. Investigators put overweight women on a 12-week diet of either high-GI or low-GI foods with an equal amount of total carbohydrate. Both were unrestricted in calories. Body composition and total food intake were the same on both diets. The reason became apparent when they measured the subjects' glucose and insulin response to the high- and low-GI meals, and found that they were the same!

Study #2. Investigators divided 129 overweight young adults into four different diet groups for 12 weeks. Diet #1: high GI, high carbohydrate (60%). Diet #2: low GI, high carbohydrate. Diet #3: high GI, high-protein (28%). Diet #4: low GI, high protein. The high-protein diets were also a bit higher in fat. Although the differences were small and mostly not statistically significant, participants on diet #3 improved the most overall in my opinion. They lost the most weight, and had the greatest decrease in fasting insulin and calculated insulin resistance. Diet #2 came out modestly ahead of diet #1 on fat loss and fasting insulin.

Study #3. At 18 months, this is by far the longest trial. Investigators assigned 203 healthy Brazilian women to either a low-GI or high-GI energy-restricted diet. The difference in GI between the two diets was very large; the high-GI diet was double the low-GI diet. Weight loss was a meager 1/3 pound greater in the low-GI group, a difference that was not statistically significant at 18 months. Insulin resistance and fasting insulin decreased in the high-GI group but increased in the low-GI group, also not statistically significant.

Study #4. The FUNGENUT study. In this 12-week intervention, investigators divided 47 subjects with the metabolic syndrome into two diet groups. One was a high-glycemic, high-wheat group; the other was a low-glycemic, high-rye group. After 12 weeks, there was an improvement in the insulinogenic index (a marker of early insulin secretion in response to carbohydrate) in the rye group but not the wheat group. Glucose tolerance was essentially the same in both groups.

What makes this study unique is they went on to look at changes in gene expression in subcutaneous fat tissue before and after the diets. They found a decrease in the expression of stress and inflammation-related genes in the rye group, and an increase in stress and inflammation genes in the wheat group. They interpreted this as being the result of the different GIs of the two diets.

I have a different interpretation. I believe wheat is a uniquely unhealthy food, that promotes inflammation and general metabolic havoc over a long period of time. This probably relates at least in part to its gluten content, which is double that of rye. Dr. William Davis has had great success with his cardiac patients by counseling them to eliminate wheat. He agrees based on his clinical experience that wheat has uniquely damaging effects on the metabolism that other sources of starch do not have.

Study #5. This is the only study I've seen that has found a tangible benefit for glycemic index modification. Investigators divided 18 subjects with elevated cardiovascular disease risk markers into two diets differing in their GI, for 12 weeks. The low-glycemic group lost 4 kg (statistically significant), while the high-glycemic group lost 1.5 kg (not statistically significant).  In addition, the low-GI group ended up with lower 24-hour blood glucose measurements.  This study was a bit strange because of the fact that the high-GI group started off 14 kg heavier than the low-GI group, and the way the data are reported is difficult to understand.  Perhaps these limitations, along with the study's incongruence with other controlled trails, are what inspired the authors to describe it as a pilot study.

Study #6. 45 overweight females were divided between high-GI and low-GI diets for 10 weeks. The low-GI group lost a small amount more fat than the high-GI group, but the difference wasn't significant. The low-GI group also had a 10% drop in LDL cholesterol.

Study #7. This was the second-longest trial, at 4 months. 34 subjects with impaired glucose tolerance were divided into three diet groups. Diet #1: high-carbohydrate (60%), high-GI. Diet #2: high-carbohydrate, low-GI. Diet #3: "low-carbohydrate" (49%), "high-fat" (monounsaturated from olive and canola oil). The diet #1 group lost the most weight, followed by diet #2, while diet #3 gained weight. The differences were small but statistically significant. The insulin and triglyceride response to a test meal improved in diet group #1 but not #2. The insulin response also improved in group #3. The high-GI group came out looking pretty good. 

[Update 10/2011-- please see this post for a recent example of a 6 month controlled trial including 720 participants that tested the effect of glycemic index modification on body fatness and health markers-- it is consistent with the conclusion below]

Overall, these studies do not support the idea that lowering the glycemic index of carbohydrate foods is useful for weight loss, insulin or glucose control, or anything else besides complicating your life. 

Further reading:

The Fructose Index is the New Glycemic Index

How to Eat Grains

Our story begins in East Africa in 1935, with two Bantu tribes called the Kikuyu and the Wakamba. Their traditional diets were mostly vegetarian and consisted of sweet potatoes, corn, beans, plantains, millet, sorghum, wild mushrooms and small amounts of dairy, small animals and insects. Their food was agricultural, high in carbohydrate and low in fat.

Dr. Weston Price found them in good health, with well-formed faces and dental arches, and a dental cavity rate of roughly 6% of teeth. Although not as robust or as resistant to tooth decay as their more carnivorous neighbors, the "diseases of civilization" such as cardiovascular disease and obesity were nevertheless rare among them. South African Bantu eating a similar diet have a low prevalence of atherosclerosis, and a measurable but low incidence of death from coronary heart disease, even in old age.

How do we reconcile this with the archaeological data showing a general decline in human health upon the adoption of agriculture? Humans did not evolve to tolerate the toxins, anti-nutrients and large amounts of fiber in grains and legumes. Our digestive system is designed to handle a high-quality omnivorous diet. By high-quality, I mean one that has a high ratio of calories to indigestible material (fiber). Our species is very good at skimming off the highest quality food in nearly any ecological niche. Animals that are accustomed to high-fiber diets, such as cows and gorillas, have much larger, more robust and more fermentative digestive systems.

One factor that reconciles the Bantu data with the archaeological data is that much of the Kikuyu and Wakamba diet came from non-grain sources. Sweet potatoes and plantains are similar to the starchy wild plants our ancestors have been eating for nearly two million years, since the invention of fire (the time frame is debated but I think everyone agrees it's been a long time). Root vegetables and starchy fruit have a higher nutrient bioavailibility than grains and legumes due to their lower content of anti-nutrients and fiber.

The second factor that's often overlooked is food preparation techniques. These tribes did not eat their grains and legumes haphazardly! This is a factor that was overlooked by Dr. Price himself, but has been emphasized by Sally Fallon. Healthy grain-based African cultures typically soaked, ground and fermented their grains before cooking, creating a sour porridge that's nutritionally superior to unfermented grains. The bran was removed from corn and millet during processing, if possible. Legumes were always soaked prior to cooking.

These traditional food processing techniques have a very important effect on grains and legumes that brings them closer in line with the "paleolithic" foods our bodies are designed to digest. They reduce or eliminate toxins such as lectins and tannins, greatly reduce anti-nutrients such as phytic acid and protease inhibitors, and improve vitamin content and amino acid profile. Fermentation is particularly effective in this regard. One has to wonder how long it took the first agriculturalists to discover fermentation, and whether poor food preparation techniques or the exclusion of animal foods could account for their poor health.

I recently discovered a paper that illustrates these principles: "Influence of Germination and Fermentation on Bioaccessibility of Zinc and Iron from Food Grains". It's published by Indian researchers who wanted to study the nutritional qualities of traditional fermented foods. One of the foods they studied was idli, a South Indian steamed "muffin" made from rice and beans. Idlis happen to be one of my favorite foods.

The amount of minerals your digestive system can extract from a food depends in part on the food's phytic acid content. Phytic acid is a molecule that traps certain minerals (iron, zinc, magnesium, calcium), preventing their absorption. Raw grains and legumes contain a lot of it, meaning you can only absorb a fraction of the minerals present in them.

In this study, soaking had a modest effect on the phytic acid content of the grains and legumes examined (although it's generally more effective). Fermentation, on the other hand, completely broke down the phytic acid in the idli batter, resulting in 71% more bioavailable zinc and 277% more bioavailable iron. It's safe to assume that fermentation also increased the bioavailability of magnesium, calcium and other phytic acid-bound minerals.

Fermenting the idli batter also completely eliminated its tannin content. Tannins are a class of molecules found in many plants that are toxins and anti-nutrients. They reduce feed efficiency and growth rate in a variety of species.

Lectins are another toxin that's frequently mentioned in the paleolithic diet community. They are blamed for everything from digestive problems to autoimmune disease, probably with good reason. One of the things people like to overlook in this community is that traditional processing techniques such as soaking, sprouting, fermentation and cooking, greatly reduce or eliminate lectins from grains and legumes. One notable exception is gluten, which survives all but the longest fermentation and is not broken down by cooking.

Soaking, sprouting, fermenting, grinding and cooking are the techniques by which traditional cultures have been making the most of grain and legume-based diets for thousands of years. We ignore these time-honored traditions at our own peril.

Sugar, Hydrogen, Bacteria and Maldigestion

There are several ways to cause a nutrient deficiency. The first is to eat too little of a nutrient. Another way is to burn through your body's nutrient stores at an accelerated rate, for example, what omega-6 vegetable oils do to vitamin E, and what wheat bran does to vitamin D. A third way is to eat enough nutrients but fail to absorb them efficiently.

A good way to reduce your absorption of nutrients is to lower your stomach's acidity. This will protect you from those pesky nutrients protein, vitamin B12, and iron (and probably others as well). The stomach is one tough organ. When it receives food, a healthy stomach lowers its pH to roughly 2.0 by secreting hydrochloric acid. That's more acidic than lemon juice and more than 10 times more acidic than vinegar. This begins to break food down, and will kill most bacteria and other pathogens. Stomach acidity is basically the body's way of "cooking" food before further digestion. At the same time, the stomach secretes pepsin, which is an acid-stable enzyme that digests protein.

Insufficient stomach acidity promotes bacterial overgrowth in the small intestine and allows undigested proteins into the intestine. The gastrin knockout mouse, which is incapable of producing stomach acid, suffers from bacterial overgrowth, inflammation, damage and precancerous polyps in its intestines. The same thing happens when you treat mice with a drug that inhibits stomach acidification.

There are a few different ways to reduce your stomach's acidity level. The most straightforward is to take an antacid, or any number of drugs that lower stomach acidity (as in the mouse study above). But can we do it naturally? Sure, all it takes is a little Helicobacter pylori infection! Luckily, most people already have one.

H. pylori is a bacterium that's the main proximal cause of stomach ulcers. Antibiotics are now the standard treatment for ulcers, and they're effective. Treating an asymptomatic H. pylori infection with antibiotics increases stomach acidity, suggesting that H. pylori is capable of suppressing the secretion of stomach acid. In another study, eradicating H. pylori with antibiotics improved nearly all patients suffering from hypochlorhydria (insufficient stomach acid).

Like any organism, H. pylori likes to stay well-fed. Its favorite food is hydrogen gas (H2), and the more it gets, the more it grows. It's not the only bacterium to like H2. Salmonella, of food poisoning fame, requires H2 to become pathogenic. Clostridium bacteria are also associated with elevated H2. H2 is produced by the fermentation of food by bacteria in the digestive tract. It's very small so it diffuses around the body, reaching the stomach lining where it's eagerly gobbled up by H. pylori. It may be equally good food for a number of other parasites around the body.

Now let's stop beating around the bush and get to the meat of this post. It's all summed up in a beautiful title: Fructose Intake at Current Levels in the United States May Cause Gastrointestinal Distress in Normal Adults. Dr. Richard W. McCallum et al. fed doses of isolated fructose to 15 normal adults. Can I say it any better than the abstract?

More than half of the 15 adults tested showed evidence of fructose malabsorption after 25 g fructose and greater than two thirds showed malabsorption after 50 g fructose... Fructose, in amounts commonly consumed, may result in mild gastrointestinal distress in normal people.

Here's where it gets really interesting. One of the measures of malabsorption they used was H2 on the breath. Both the 25g and the 50g doses caused a large increase in H2, especially the 50g dose (5-fold increase). This is the same thing you see in people who are lactose intolerant. Bacterial fermentation is the only significant source of H2 in the human body. That means the fructose was hanging around in the small intestine for long enough to be decomposed by the local bacteria, who took advantage of it to proliferate.

Certain types of fiber also promote H2 production. Resistant starch, as well as certain non-caloric sweeteners, are readily fermented into H2 in some people. Cellulose, the predominant fiber in vegetables and grains, does not increase H2. The large difference in fiber content of rural vs. urban Mexican diets doesn't seem to correlate with H2 production by intestinal bacteria. Interestingly, both white and whole wheat bread increase H2 production.

Let's put those doses of fructose into perspective. One medium banana contains about 7 grams. A 16-ounce bottle of apple juice contains about 30 grams. A slice of cake contains about 12. One "child-size" 12 ounce cup of Coca-Cola from McDonald's contains 17 grams (as long as you don't get a refill!). One large 32 ounce Coca-Cola contains 47 grams. Your H. pylori will be VERY pleased if you drink one of those, especially if you use it to wash down the white flour bun on your hamburger.

I do think it's important to mention that the study described above used isolated fructose. It's not clear that other sources of fructose would behave the same. For example, the presence of glucose enhances fructose absorption. Fruit, table sugar and high-fructose corn syrup all contain glucose. It's also not clear what the effect would be of eating fructose with a meal rather than in isolation. None of this has been studied to my knowledge, so we're left extrapolating from studies that used pure fructose.

Now let's connect the dots. Excessive fructose, certain types of fiber, and wheat cause bacterial overgrowth and H2 production (if you believe the fructose-H2 connection). Elevated H2 causes overgrowth of H. pylori and possibly other pathogenic bacteria in the body. H. pylori lowers stomach acid, causing further overgrowth of bacteria in the small intestine. This causes inflammation and increases the risk for digestive cancers.

Decreased stomach acid also causes malabsorption of protein, B12, iron and perhaps other nutrients. It allows undigested protein to travel into the small intestine. This could potentially be very important. For example, many people are allergic to the casein in milk. It's one of the two most common alleriges, along with gluten. Both casein and gluten are proteins. A normally functioning stomach at the proper pH should completely digest casein. You can't be allergic to casein if there's none around. I don't know if the same applies to gluten.

Robust digestion may explain why many healthy non-industrial groups do very well eating dairy, sometimes to the exclusion of nearly everything else, yet many people in modern societies do better without dairy protein (butter is typically well tolerated). This phenomenon could also go a long way toward explaining the fact that allergies are becoming more and more common in industrial nations as we consume more sugar.

Thanks to Peter and Matt Stone for some of the ideas I incorporated into this post. Thanks to pbo31 for the CC photo.

Gluten Sensitivity: Celiac Disease is the Tip of the Iceberg

Celiac disease is a degeneration of the lining of the small intestine caused by a sensitivity to gluten. Gluten is the protein portion of wheat, rye, barley, and wheat relatives (spelt, kamut, emmer, einkorn and triticale). I found an interesting paper recently on the impact of celiac disease on nutrient status and bone density. Researchers compared 54 Northern Italian children with untreated celiac disease to 60 presumably healthy children. The celiac patients had extremely poor vitamin D status, with a deficiency rate of 35.18% compared to 5% in the control group. This was using the lenient cut-off point of 20 ng/mL. Average serum 25(OH)D3 in celiac patients was less than half the level of the control group. The celiac patients also had low serum calcium and magnesium, and elevated parathyroid hormone. Celiac children had lower bone mineral density. All parameters returned to normal after 6 months on a gluten-free diet.

This confirms what has been shown numerous times before: celiac disease interferes with nutrient status, including the all-important fat-soluble vitamins. It's not surprising, since it flattens the villi, finger-like structures necessary for efficient nutrient absorption in the small intestine. But wait, the overwhelming majority of our vitamin D comes from the effect of sunlight on our skin, not through our small intestine! So gluten sensitivity must be doing something besides just flattening villi. Perhaps it does. Feeding wheat bran to "healthy" volunteers caused them to burn through their vitamin D reserves at an accelerated rate. I think this underlines what I've come to believe about wheat: it's problematic for a large proportion of the population, perhaps the majority.

Approximately 12% of Americans can be diagnosed as gluten sensitive using blood antibody tests (anti-gliadin IgA or IgG). A subset of these have full-blown celiac disease. The vast, vast majority are undiagnosed. Gluten sensitivity associates with a dizzying array of diseases, including autoimmune disorders, cancer, and neurological problems. The problem with the blood tests is they aren't very sensitive. The most common blood tests for celiac disease look for a class of antibody called IgA. IgA is produced by the mucosa, including the gut. Unless gut damage is already extensive, the majority of IgA stays in the gut. This may cause the assay to overlook many cases of gluten sensitivity. A negative blood antibody test does not rule out gluten sensitivity!

I recently discovered the work of Dr. Kenneth Fine of EnteroLab. He has developed an assay that detects anti-gliadin IgA in stool. Gliadin is one of the problematic proteins in gluten that is implicated in gluten sensitivity. Dr. Fine has been conducting informal research using his fecal anti-gliadin IgA test (data here). He has found that:

• 100% of untreated celiac patients are antigliadin IgA positive by fecal test, compared to only 76% by blood (n= 17).
• 76% of microscopic colitis (a type of chronic diarrhea) patients are positive by the fecal test, compared to 9% by blood (n= 57).
• 57% of symptomatic people (digestive problems?) are positive by the fecal test, compared to 12% by blood (n= 58).
• 62% of people with autoimmune disease are positive by the fecal test.
• 29% of asymptomatic (healthy) people are positive by the fecal test, compared to 11-12% by blood (n= 240).
• Baby and cow feces are 0% positive by the stool assay.

It gets worse. Gluten sensitivity is determined in large part by genetics. A gene called HLA-DQ is intimately involved. It encodes a protein that is expressed on the surface of cells, that serves to activate immune cells when certain foreign substances are present. Different versions of the gene are activated by different substances. HLA-DQ2 and HLA-DQ8 are classically associated with celiac disease. Roughly 42% of the US population carries DQ2 or DQ8. According to Dr. Fine, every allele except DQ4 has some association with gluten-related problems! Only 0.4% of the U.S. population carries HLA-DQ4 and no other allele.

Not everyone who is genetically susceptible will end up developing health problems due to gluten, but it's impossible to estimate how many of the problems we attribute to other causes are in fact caused or exacerbated by gluten.

The immune system can be divided into two parts: innate and adaptive. The innate immune system is a nonspecific, first-line reaction to a perceived threat. The adaptive immune system is a more sophisticated, but slower system that produces a powerful response by particular cell types to a very specific threat. Antibody production is part of the adaptive immune system. Thus, if your gluten sensitivity test is looking for antibodies, it could still be missing an immune reaction to gluten mediated by the innate immune system!

This question has been addressed in a preliminary study. Researchers took gut biopsies from celiac patients and asymptomatic controls. Five out of six asymptomatic controls showed elevated interleukin-15, a marker of innate immune activation, upon exposure to gliadin. An activated innate immune system (commonly called 'inflammation') is associated with a wide array of chronic diseases, from obesity to cancer to cardiovascular disease. Inflammatory cytokines are elevated in celiac patients and may play a role in their bone pathology. What I would like to see is some negative controls-- would the gut biopsies have produced interleukin-15 in response to benign foods or is it truly specific to gluten?

I don't intend to imply that everyone has gluten sensitivity, but I do think the totality of the data are thought-provoking. They also include the association between the introduction of wheat to non-industrial populations and the development of widespread health problems. Another thing to keep in mind is that traditional sourdough fermentation breaks down a portion of gluten, possibly explaining the rise in gluten sensitivity that has paralleled a shift to quick-rise yeast breads. I believe that gluten sensitivity is behind many modern ills, and should be on the short list of suspects in the case of unexplained health problems. This is particularly true of digestive, autoimmune and neurological disorders. Gluten sensitivity is easy to address: stop eating gluten for a few weeks. See how you feel. Reintroduce gluten and see what happens. You might learn something about yourself.