Celiac.com 07/25/2020 - Drs. Michael and Mary Dan Eades are physicians and health researchers from Boulder, Colorado who co-wrote the best selling Protein Power in the late 1990s.  The book sets forth, in the words of the authors, “not a high protein diet” but “an adequate protein diet.”

For this reason that I am not a big fan of the “Protein Power” phrase, though I suppose that the alternate titles Adequate Protein or Fat Power would not have helped with book sales.

The subject of this review is the sequel The Protein Power Lifeplan (Grand Central Publishing, 2001) in which the Eades take “the opportunity to answer readers’ queries, to include information on the many far-ranging benefits of the regimen, and to offer, at last, a comprehensive  plan for living what we think of as a Protein Powered life.”  This is not just your run of the mill diet book. It is a comprehensive plan for health.  One that is well worth reading - not just for celiacs and the gluten intolerant, although they do address us directly, but for all those who wish to lead a healthier and fuller life.

The Protein Power Lifeplan is composed of fifteen chapters, the cornerstone chapter being a section called “Man the Hunter,” in which the Eades lay out the evolutionary foundation for their lifestyle recommendations.  The chapters that follow address varied topics such as insulin, dietary fats, cholesterol, antioxidants, sweets, as well as iron, magnesium, sunshine, along with mental and physical exercise.  The book ends with practical advice on how to implement their nutritional plan.  

Man the Hunter

This chapter sets the foundation for the rest of the book.  It lays out the historical basis for, not just what our ancestors ate, but how they exercised, what types of minerals they obtained in their diets, and how much sunshine they got (no, they didn’t have sunscreen).

The gist of the message – a point I’ve made in my other articles for this newsletter – is that while we’ve only been consuming the fruits of agriculture and ranching for at most 10,000 years, we were hunter gatherers for at least two and a half million years before that.  What did we eat?  Well, certainly not grains in any form (inedible grass seeds), no beans, no dairy, no refined sugars.  Only a diet of “nutrient-dense foods – meat, fish, and poultry, rich in protein and good-quality essential fats; fruits, berries, and vegetables, rich in antioxidants and cancer fighting substances….”

Brief Summaries of Some Non-gluten Chapters
Before we get to the subject that’s probably of most interest to the readers of this newsletter – the impact of gluten on the human gut -- let’s briefly touch on a few of the other interesting topics in this book:

Insulin – this key hormone “lies at the root of heart disease, diabetes, hypertension, cholesterol, and triglyceride elevations….”  This is an important subject for the gluten intolerant as we tend to replace foods that contain gluten and are high in carbohydrate with non gluten foods that are also high in carbohydrate.  In doing so we’ve solved the primary problem of autoimmune reactions to foreign proteins but we continue to set ourselves up for what is variously called Syndrome X, Metabolic Syndrome, or Hyperinsulinemia/Insulin-Resistance Syndrome.

Fats – the low fat dietary recommendations made by the health establishment in the past few decades have been an abject failure.  Healthy, unadulterated fats were a staple of our ancestors’ diets.  While there is a shifting perspective with a newfound emphasis on Omega 3 and monounsaturated fats like olive oil, it is a shame of the highest order to have demonized what was to our ancestors a primary macronutrient.

Cholesterol – another unnecessary demonization has been directed at this “naturally occurring and necessary substance.”  Yes, there is such a thing as “bad” cholesterol, the subfraction of LDL called “small, dense.”  But taking drugs to reduce it is akin to demanding that bandages be removed from the scene of an auto accident.  High bad cholesterol is a symptom of a dietary issue rather than a problem in and of itself.  And, gasp, no correlation has ever been established between the consumption of cholesterol and high blood cholesterol.

Sunshine – “We recommend regular sunbathing as a necessary step back to the natural lifestyle we were meant to live.”  Huh?  Haven’t we been told to avoid the sun at all costs, to slather on layer after layer of sunscreen to avoid the deadly rays from above?  Like us, our ancestors would certainly have avoided sunburn when possible.  But sunlight is a natural source for vitamin D and will “protect us from weak bones, sad moods, a slow metabolism, and cancers….”   It is not to be avoided but enjoyed.

The Leaky Gut

Perhaps of most interest to celiacs and the gluten intolerant, The Protein Power Lifeplan contains a tour de force of a chapter entitled “The Leaky Gut: Diet and the Autoimmune Response.”  If you were to read nothing else in the book, you have to read this one chapter.

The substance of the Eades’ argument in this chapter is this:

1. We only began to consume grains as an important food source after the change from a hunter gatherer to farmer.  This occurred about 10,000 years ago at the most.  (Some groups made this shift much more recently!)
2. The purpose of the human intestinal tract is to “break down the foods we eat and absorb nutrients from them.”
3. Eating grains causes not just direct damage to the digestive system, in the case of celiac disease, but also results in cellular inflammation of the gut lining.  This inflammation then leads to intracellular gaps that allow incompletely digested plant proteins access to the bloodstream.
4. Once in the bloodstream, “these plant proteins… cause trouble because their structure is so similar to the structure of body proteins; some of them are like the proteins in joint surface tissues, others like the filtering apparatus of the kidneys, and still others like the covering of nerves.”
5. It’s not just grains that cause this problem.  Lectins from beans can also cause intracellular gaps in the gut and the autoimmune issues above.

Conclusion

By taking us back to our ancestral diet and habits that formed over millions of years, The Protein Power Lifeplan is an excellent resource for discovering why it is that we have issues with gluten-containing grains.  But, as you can see, this book is more than just a warning against wheat, rye, and barley.  It’s a refreshing, common-sense antidote to much of our recent dietary wisdom.  Highly recommended reading.

Celiac.com 07/17/2020 - I am saddened by the recent deaths of affected pets and the trauma this has caused their owners. However, this is the absolute best thing that could happen to the pet food companies. I could not be more excited about the potential for seeing the much-needed changes in pet food manufacturing that may finally come about as a result of this “scandal” in which Menu Foods has recalled a portion of the dog and cat food it manufactured between December 3, 2006 and March 6, 2007. This recall should serve as a huge and important warning. 

The latest information is that 14 pet deaths have been linked directly to the recalled foods. Six of them were cats that died in the studies conducted by Menu Foods to confirm that their food was the culprit. Mortality and morbidity rates have shown that cats are more susceptible to the effects of this food. This makes sense since cats are more strict carnivores than dogs, and would be less adapted to eating foods derived from grains. The FDA, as of this date, still holds that they do not know what the exact culprit is while the company itself has been quoted as saying that they believe it is the wheat gluten acquired from a new supplier. According to one report I read, the company has replaced the gluten and gone back to the previous formula. If that’s true, they must be convinced that the wheat gluten is the problem.

Gluten can cause these health problems and more. Gluten, in sensitized individuals, can induce both chronic and acute kidney failure. This form of kidney failure is typically what we call an IgA nephropathy, in which antibodies and immune complexes formed against gluten are deposited in the kidneys, which leads to damage and ultimately failure. Again, this can be chronic leading to persistent blood (microscopic) and protein in the urine or it can be acute.

In most cases of the “tainted” food deaths, the pets had been eating these foods for months before succumbing to its effects. You may have seen the emotion-charged interviews on national news that dealt with owners who thought they were doing the right thing by feeding their pets these foods. They have now learned that they were poisoning their dogs and cats.

First, is it a “tainted food -one that contains a poison or a toxin? Or is it one that simply contains a form of gluten that is too powerful for pets’ (or human) consumption? I can easily believe the latter, and that they will find that this new source of gluten came from some genetically modified (GMO) or hybrid wheat that is unsuitable for human consumption and hence, cheaper.  That would explain why it was chosen to replace the company’s old source of gluten. 

It could be the old Starlink (CRY9C) corn story all over again. You remember that one, right? This occurred in 2000 and Taco Bell became the poster child when they had to recall taco shells suspected of having this GMO corn that was intended only for animal feed. Of course that story died quickly (like I am trying to keep this one from doing) and the public never heard about the millions of dollars spent to rid our food supply of this transgenic maize (GMO corn). They recalled over 350 brands of corn products in their attempt to fix this situation. Who knows whether they were really effective?  Corn allergies in humans have risen as I certainly believe they have in pets. The expressed concern was that it may cause “allergic reactions.” Well, if you call immune-mediated reactions like rheumatoid arthritis, lupus, and asthma “allergic reactions” then that might be accurate.

The story of this recall, and the underlying cause, should be sending shock waves through the public and veterinary communities. But the response thus far has been limited to concern similar to that seen in an E. coli outbreak. However, if we knew that it was the wheat gluten, and if we knew what wheat gluten was capable of (like we who study celiac disease know) then we should be seeing the bigger picture here: This is just the tip of the iceberg. Dogs and cats have been dying from this stuff all along and we just haven’t known it. We need to wake up to the fact that dogs and cats should not be eating these grains to begin with, regardless of the extent to which Humankind has genetically modified these foods.

The startling but well established fact is that the lectins of gluten (wheat, barley, rye) dairy products (e.g. casein, lactalbumin) soy, and corn are all capable of inducing serious health issues in those (sensitized) individuals consuming them. I am of the firm belief that these “big 4” are not healthy foods for anyone. They are simply more harmful to some individuals than others.  It is a matter of when, not if, they will cause a problem. That’s why I lovingly call them the “four horsemen of the apocalypse”. 

You may wonder why the problems caused by these proteins do not happen immediately. That is a great question and one that sometimes keeps people from seeing the truth about these harmful glycoproteins/lectins. The fact is that the onset of the lectin-related disorder, whether it be rheumatoid arthritis, type-one diabetes, lupus, etc., is usually preceded by another event such as viral or bacterial infection. Vaccines can also act as triggers. The result of such secondary events is a sudden influx and attachment of these inflammatory proteins to various cells in the body, ushering in what we often refer to as “autoimmune” disorders.  I hate that term because it implies an immune system that has gone haywire, attacking the body for no reason. Our bodies and immune systems never make that kind of mistake! These things happen for a reason and these food proteins are often the cause. Viruses also play a role, as described on my web site.

All one needs to do is study celiac disease (gluten intolerance) to see how all of this works and appreciate the health implications that accompany this extremely common condition. It does occur in dogs and cats. That has become painfully obvious over the past 7 years I have been studying this issue. The Irish setter is the only known breed to suffer from gluten intolerance but it is clear that gluten is affecting many other breeds of dogs and cats. Why wouldn’t it? It is affecting us and we have had millennia to adapt to eating wheat. Our pets have only been eating wheat-based pet foods for about 20 years now.

The fact is that wheat gluten can cause kidney failure. With the relatively small number of deaths that have occurred, gluten is the most likely culprit. Wheat gluten can cause an IgA nephropathy that can either result in chronic or acute kidney failure. There does not have to be another toxin involved. In fact, mold toxins primarily affect the liver and the amount of other toxins that could be present would have to be much higher to cause kidney damage. If so, many more individuals would have been affected. 

Thus, the FDA is correct in pointing the finger at gluten but very wrong in saying that wheat gluten cannot cause kidney failure.

This leads to my final point (other than the fact that many of you are up in arms about so many of your “quality pet foods” being made by one big company in Canada): Are your pet foods really formulated “scientifically”? I used to think so. Hey, I used to parrot what I was taught - that the pet food companies spend millions of dollars and years of intense research coming up with balanced and nutritious foods. I used to warn people not to add any table food so that they did not upset this “balance”. I was one of their biggest fans...patsies. 

Then I woke up and wrote “Gluten Intolerance and Your Pet”. Why are we feeding dogs and cats with wheat, barley, soy, and corn (and now dairy products...again...after having removed them 20 years ago)? The manufacturers of pet foods either don’t have a clue as to what they are doing or they know better and are doing the wrong thing anyway. If I were in the pet food industry, I’d rather claim ignorance, but I’ll let readers decide for themselves. 

If the research and development departments of these companies that are starting to use dairy products again truly think that lactose is the culprit (rather than the lectins of casein, lactalbumin, etc), then the executives in charge need to fire the entire lot of them and start afresh. If they really don’t know what gluten can do to the kidneys, joints, intestinal tracts, brains and other organs of our beloved pets, then they all need to go back to school or find another line of work.

DO NOT let this story die. It does not matter whether they ever tell us that wheat gluten caused these deaths. The fact is that it can, and does. Thus, gluten has no place in pet food. The gluten found in the non-recalled dry food versions of these foods is only incrementally better, causing sub-clinical issues that shorten our pet’s lives. 

Do you really want to know why the average dog’s life is 12 years and that of the cat is 13 years (in the USA) when the former can live to be nearly thirty and the latter to 40? Look no further than what we put in their bowls. In a study done in Europe, pets that were fed table scraps lived an average of 3 years longer than those fed commercial diets alone. Why? Highly processed foods cannot possibly contain all of the essential nutrients found in fresh meats, fruits and vegetables. If our veterinarians can’t understand that, then they too need a refresher course.

The combination of these foods is woefully deficient in nutrients and the fact that they are downright harmful is an abomination. It is time to change this! Let this recall story be a warning sign but please do not let it die. This increased awareness of the pet food industry and how it works is actually good news for the pets and may also awaken many people to the hazards posed to humans.

Celiac.com 07/16/2020 - Iron deficiency is sometimes considered the most common sign of untreated celiac disease (1) so it may be surprising to learn that iron overload can also signal the presence of untreated celiac disease. I recently spoke at a support group in Comox, B.C. A member of the audience approached me afterward asking whether there is a link between celiac disease and hemochromatosis (iron overload). He has hemochromatosis, which is a genetic condition in which so much iron is stored in the body that it becomes toxic to organs such as the liver and kidneys. He also has celiac disease. In his case, a gluten-free diet seems to reduce his iron absorption which has led him to suspect that intestinal inflammation played a role in his excessive absorption of iron. He recently stated:  “I was diagnosed with hemochromatosis in 1980 and had phlebotomies regularly until 2005 when I began a gluten free diet.  It was the sudden drop in my ferritin level after going gluten free that made me begin to relate the two conditions because of the co-incident timing.” 

In my own experience where celiac disease and hemochromatosis have struck the same person, the opposite seems to happen. These patients only develop iron overload after their celiac disease has been diagnosed and they have adopted a gluten-free diet. However, when I began to search through the literature, I discovered that the gentleman in Comox is not alone. 

Geier et. al. reported in World Journal of Gastroenterology, that their 65 year old female patient, who was previously treated for almost ten years with regular phlebotomies (blood lettings) to dispose of excess iron (2) had developed celiac disease. The lady in question did eventually become anemic due to celiac disease. However, if one accepts the notion that celiac disease is a life-long illness, her celiac disease and hemochromatosis coexisted for many years, and her iron overload occurred in the context of untreated celiac disease. 

The authors of this paper argue that the intestinal damage caused by untreated celiac disease works against iron overload to establish something of a balance in iron metabolism that masks celiac disease. While this may or may not be true in some cases, it does not appear to apply to the case these authors offer as support for their argument. After all, for almost ten years, this patient underwent regular blood lettings to divest herself of excess iron. Since her celiac disease was undiagnosed and untreated during this same period this patient’s history may well suggest support for the notion that gluten ingestion may, in the context of hemochromatosis, somehow induce increased iron absorption.  As this patent’s intestinal damage worsened, she eventually reached a point where she lost the capacity to absorb excessive, even adequate quantities of iron. However, during the years leading up to this stage, she was clearly absorbing and retaining too much iron. 

Since most intestinal damage, in the context of celiac disease, is to the region where most iron is absorbed, the issue may not be as simple as it appears. Geier and colleagues reported large shifts in the transport mechanisms that move iron across the intestinal barrier. The protein for absorbing ferrous iron (divalent metal transporter 1) was significantly reduced before beginning a gluten free diet but it rebounded quickly after treatment with the diet. It was not long before these proteins were more plentiful than is considered normal. Thus, the patient may soon have to undergo regular phlebotomies again.  Understandably, the authors did not supply us with that information but it may provide data for a future publication.  

On the other hand, perhaps this patient will be like the gentleman I met in Comox. She, too, may be able to avoid phlebotomies if she carefully follows her gluten-free diet. Only time will tell. And it might prove very valuable to other celiacs if the authors publish this information in a follow-up article. 

Sources: 

1. Freeman, Hugh James. “Hepatobiliary and pancreatic disorders in celiac disease” World J Gastroenterol  2006 March 14;12(10):1503-1508
2. Geier A, Gartung C, Theurl I, Weiss G, Lammert F, Dietrich C, Weiskirchen R, Zoller H,  Hermanns B, Matem S. “Occult celiac disease prevents penetrance of hemochromatosis” World J Gastroenterology 2005;11(21): 3323-3326

Celiac.com 07/10/2020 - Gluten-free cookies are easy to prepare and the payoff is huge!  But sometimes, baking disasters occur. Expressions such as: that’s the way the cookie crumbles, one tough cookie or cookie monster can, at times, have double meanings for the gluten-free baker. 

Questions such as:  Why does a cookie batch turn out one time and the next time fail?  Why do my cookies spread so much?  My cookies are dry and hard, what am I doing wrong? What happened?   It’s time to put on the oven mitts and baker’s hat and find some cookie cures. 

First of all, subtle changes in a cookie recipe can bring varied results.  Inferior ingredients (or different brands), inaccurate measurements, differences in baking equipment, variations between ovens (inaccurate temperature), oven rack position, baking times and even weather conditions can have an effect on the outcome of gluten-free cookies.

To fine-tune your cookie-baking skills and minimize cookie disasters, here are a few suggestions. 

What to Do If:

1) Cookies Spread Too Much

Start with butter at “room temperature” not squishy but malleable (still feeling firm). To determine if butter is at “room temperature”, insert an instant read thermometer in the center of the stick of butter.  It should read 65 to 68 degrees F.

Use a combination of vegetable shortening and butter.  Cookies made with butter have an outstanding taste, but those made with shortening hold their shape better.  You can control spread by using a combination of butter and shortening.  Diet margarine or whipped spreads are not suitable for baking.  These products contain too much water.

Reduce the amount of sugar in the dough.  Measure accurately: use the “spoon in and level off” method.

Use a higher-protein flour mix.  The greater the protein value in the flour mix, the more liquid it will absorb. Examples of protein flours include brown rice, sorghum, bean, almond meal and others.  Use suggested flour mix given in the recipe since the recipe was developed and tested with that particular flour mixture.

Use less liquid in the dough. Use the correct size egg given in the recipe and measure accurately with proper measuring cup.  For liquids, use a measuring cup that has a spout.

Always drop dough portions on a cool cookie sheet. Use 2-3 identical cookie sheets, while one is baking, another is cooling and the third one is ready to be placed in the oven.  For a quick cool-down, place cookie sheet in refrigerator for a few minutes.

Bake at correct oven temperature.  A too-low temperature may lead to spreading. Preheat oven at least 15 minutes and check oven accuracy by using free-standing oven thermometer. 

Over-greased cookie sheets. Consider lining cookie sheets with parchment paper.  It reduces spread, promotes even baking and reduces cleanup.

2) Cookies Are Dry and Hard

Used too much flour/gluten-free oats.   Measure accurately.  Stir flour in container to aerate; use spoon to fill dry measuring cup and level off with knife.

Hard and stale brown sugar.  Use fresh, soft, moist brown sugar.

Hard and very dry dried fruit.  Soak dried fruit in water (or other liquid) to absorb some moisture so it won’t take it from the dough.  Drain fruit, pat dry and then stir into dough.

Overmixed dough.  Stop mixing when dough is just incorporated.

Too-hot oven temperature. Keep free-standing oven thermometer in oven to check oven accuracy.

Overbaked cookies. Check cookies at the minimal baking time.  Bake one “test” cookie to make adjustments for your oven.  Cookies continue to bake on the cookie sheet once they are removed from the oven.  Oven may be hotter than the temperature the dial reads.  Purchase an oven thermometer and keep in oven to ensure accurate temperature.
 
Improperly stored cookies.  GF cookies are best when eaten within 2 days or placed in the freezer in airtight containers for extended storage. 

Cookies Crumble. Forgot to add xanthan gum to dough.  Xanthan gum acts as a binder with other ingredients in gluten-free baking.  It is a necessary ingredient in most gluten-free baking.
 
Used diet margarine or whipped spreads as the fat. Diet margarines and whipped spreads are full of air and water which makes them unacceptable for baking.  Use stick butter (unsalted preferred), shortening or oil.  Measure accurately.

3) Cookies Break When Removed From Cookie Sheet

Cookies still too warm. Let cookies cool on cookie sheet for specified time given in recipe before transferring them to wire racks to cool completely.  For delicate cookies, bake them on parchment paper-lined cookie sheet.  When baked, slide the parchment paper off cookie sheet to a wire rack to cool. 

For the best results

Watch your cookies very carefully until you know how a particular recipe bakes in your oven and on your cookie sheets. Be consistent: use the same “brand” ingredients and stick with them, measure the same way, preheat oven for at least 15 minutes and check oven accuracy by keeping thermometer in oven.   Bake one or two “test” cookies first so adjustments can be made without ruining the whole batch.  Keep cookie dough refrigerated until ready to bake especially if kitchen is hot, humid or dough is soft. Always place dough on cool cookie sheets.

If All Else Fails

Use cookie disasters for future crumb crusts.  Freeze the cookies then put them in a food processor and make cookie crumbs.  Store the crumbs in the freezer and use them when you make desserts with crumb crusts.    Your cookie disasters may end up as wonderful crust creations! 

Happy Baking!

Triple Chocolate Bliss

This recipe is from the cookbook, Gluten-Free Cookies (What No Wheat Enterprises, 2008) by Jeanne Basye, The Gluten-Free Cookie Lady.

Ingredients:

• 2 tablespoons gluten-free flour mix
• 1/8 teaspoon xanthan gum
• 1/8 teaspoon baking powder
• 1/8 teaspoon salt
• 4 (1 oz.) squares semisweet chocolate, coarsely chopped
• 2 tablespoons unsalted butter
• ½ cup granulated sugar
• ½ teaspoon pure vanilla extract
• 1 large egg
• ½ cup coarsely chopped macadamia nuts
• ¼ cup each semisweet chocolate chips, milk chocolate chips and white chocolate chips

Directions:
1.  Preheat oven to 350 degrees F.  Line cookie sheets with parchment paper.
2.  Sift flour, xanthan gum, baking powder and salt in bowl; add nuts and flavored chips;
     stir.  Set aside.
3.  Put chocolate squares and butter in large microwave-safe bowl.  Microwave, uncovered,        on High (100 percent power) in 30 second intervals until melted.  Stir after each interval.  Cool 5 minutes.  Stir in sugar, vanilla and egg.  Gradually stir in flour mixture.
4.  Measure dough in 1 ½ tablespoon portions; drop 3 inches apart on prepared cookie sheet.
5.  Bake 11 to 12 minutes or until tops are glossy and centers are soft.  Cool 4 minutes on cookie sheet then transfer to wire rack to cool completely.
6.  Store in airtight container up to 2 days or freeze up to one month.

Makes 15 (2 ½-inch) cookies
 

Celiac.com 12/28/2019 - Nothing is better than a homemade warm cookie right from the oven, and this easy recipe makes FOUR different (gluten and dairy free) delights! These tender, flavorful treats from my new Baking Cookbook are sure to be a hit with you and your family.

Since so many gluten-free recipes use a high percentage (sometimes 60-70%) of highly refined starches -- which are correlated with diabetes, obesity and heart disease -- I was motivated to develop recipes using primarily healthy, whole grain flours. After careful testing, I’ve developed this versatile cookie recipe that features the ‘whole’ grain flours from sorghum and brown rice. 

These cookies call for walnut or sunflower oil, or your favorite butter substitute. I like the lighter taste and texture of cookies made with oils rather than with saturated fats, so when choosing a butter substitute, I look for one made from monounsaturated fats.  As in most gluten-free recipes, an acid is added to balance the pH and to boost the leavening action. Cream of tartar serves that purpose in this recipe.

3 Gluten-free Cookie Tips

1. Unlike gluten-based dough which can get rock-hard when over-beaten, beating the gluten-free dough makes it more ‘airy’ and lighter.  
2. If baking right after mixing the dough, let it sit about 5 minutes before forming balls to bake. Gluten-free flours are dry, and this helps it to absorb the moisture, to create a better end-result.
3. Gluten-free flours do not usually contain preservatives and can go rancid easily. Store them in the freezer if possible. If they smell ‘off’, throw them away. 

A year and a half ago, I started working on the Baking Cookbook. Each recipe started with a blank sheet of paper and all were developed with the goal of making delicious baked goods with the most whole grain flours possible. Saving time (and money) is emphasized. Wet and dry ingredients are separated so you can pre-make ‘dry mixes’ and then mix the ‘wet’ ingredients so you can make homemade baked goods in minutes. For more information, please visit www.alternativecook.com.  

8 Tips for Making the Perfect Cookie

1. Let dry and wet ingredients come to room temperature before mixing dough.
2. Aerate the flours before measuring. Use ‘scoop-able’ cups, measure and scrape off the top with a dull knife edge. 
3. Cookies bake best on a silicone baking pad available at cooking or department stores.  
4. Try to make all cookies the same size so they bake uniformly.  
5. Ovens vary in temperature, so it is a good idea to have a thermometer to check the actual temperature. Oven thermometers are inexpensive and available at cooking or department stores. 
6. If your oven has a ‘hot spot’, turn sheet half way through baking time, otherwise keep oven door closed while baking. If you want to peek, and if your oven has a window, turn on oven light to check on them.
7. Remove cookies from the oven and let them sit on the baking sheet a few minutes before removing from the pan.  (I know, this is hard to do–but they’ll ‘set up’ and be less likely to break.) 
8. Double or triple the recipe when you make a batch and freeze the dough to make a variety of fast, tasty cookies in a matter of minutes. 

Gluten-Free Sugar Cookie Recipe

Excerpted from Gluten-Free, Dairy-Free, (GFCF) Baking Cookbook by Jean Duane, Alternative Cook, LLC.  © 2009, Alternative Cook, LLC.

Preheat oven to 350F.

Wet Ingredients:

• ½ cup walnut, sunflower oil, OR butter substitute
• 1 cup organic cane sugar
• 2 tsp.  vanilla
• 3 egg whites
• 1/3 cup rice, nut or seed milk

Dry Ingredients:

• 1¼ cup whole grain sorghum flour
• 1¼ cup whole grain brown rice flour
• ½ cup cornstarch or sweet rice flour
• 1 tsp.  cream of tartar
• 1 tsp.  baking soda
• 1 tsp.  baking powder
• 2 tsp.  xanthan gum
• ½ tsp.  salt

Directions:

1. In a stand mixer, combine wet ingredients. In a separate bowl, whisk dry ingredients together and add to wet ingredients. Mix until incorporated.  
2. Follow directions below depending on the variation you choose.
3. Bake 10 to 12 minutes.  

Nutritional Information Per Serving: Servings 48 .  Calories 74 .  Fat 3g  .  Protein 1g .  Carbohydrates 12g .  Cholesterol 0mg .  Sodium 63mg .  Fiber 0g

Four Variations on the Basic Cookie

Snickerdoodles:  Make the Sugar cookie dough. Form the cookies into 2” balls and place on a baking sheet. Using the bottom of an oiled glass, press the cookies until they are about ½” thick and 3-4” wide. Make a cinnamon and sugar topping by placing 2 TBS of sugar and 1 tsp.  of cinnamon in a bowl. Sprinkle each cookie with the cinnamon and sugar topping. Bake according to the above directions.

Cutout Cookies:   Make the Sugar Cookie dough and refrigerate it for 2 hours. Roll out the dough about ½” thick on an oiled baking surface. Cut out with cookie cutters. (Note: if using a silicone baking surface, use plastic cutters.)  Carefully remove the dough around the cutouts. Bake according to the above directions and ice with your favorite icing when cooled.  3 Tips for Cutout Cookies:  1) Chilling the helps the dough to hold its shape when rolling out and cutting into shapes, and prevents over-spreading when baking. 2) Oil your fingers, the rolling pin and the baking rolling surface (if not using a silicone pad) with the same oil called for in the recipe before working with the dough. This will help your cookies brown nicely, and will keep the dough from sticking to you and surfaces. 3) To avoid breaking or stretching out the cut out dough, roll the dough out on a Silpat (a non-stick baking mat) cut shapes with a plastic cutter, and remove dough around the shapes.

Jammie Sammies:  Make the Sugar Cookie dough and refrigerate it for 2 hours. Roll out dough about ½” thick on an oiled baking surface. Using a round, fluted-edge cookie cutter, cut into circles. Carefully remove the dough around the cutouts. Sprinkle sugar on top. Bake according to the above directions. Cool. Smear one cookie with your favorite fruit preserves and place another cookie on top to make a ‘sandwich’.

Pressed Cookies:  Make the Sugar Cookie dough. If you like, you can color the dough with some food coloring from the natural food store (made with natural ingredients / no chemicals). Place in a cookie press and press shapes on a baking surface. Decorate with sprinkles. Bake according to the above directions.

Celiac.com 07/17/2009 - The globe-spanning presence of wheat and its exalted status among secular and sacred institutions alike differentiates this food from all others presently enjoyed by humans.  Yet the unparalleled rise of wheat as the very catalyst for the emergence of ancient civilization has not occurred without a great price.  While wheat was the engine of civilization’s expansion and was glorified as a “necessary food,” both in the physical (staff of life) and spiritual sense (the body of Christ), those suffering from celiac disease are living testimony to the lesser known dark side of wheat.  A study of celiac disease may help unlock the mystery of why modern man, who dines daily at the table of wheat, is the sickest animal yet to have arisen on this strange planet of ours.

The Celiac Iceberg

Celiac disease (celiac disease) was once considered an extremely rare affliction, limited to individuals of European origin.  Today, however, a growing number of studies indicate that celiac disease is found throughout the US at a rate of up to 1 in every 133 persons, which is several orders of magnitude higher than previously estimated.   

These findings have led researchers to visualize celiac disease as an iceberg.  The tip of the iceberg represents the relatively small number of the world’s population whose gross presentation of clinical symptoms often leads to the diagnosis of celiac disease. This is the classical case of celiac disease characterized by gastrointestinal symptoms, malabsorption and malnourishment. It is confirmed with the “gold standard” of an intestinal biopsy.  The submerged middle portion of the iceberg is largely invisible to classical clinical diagnosis, but not to modern serological screening methods in the form of antibody testing. This middle portion is composed of asymptomatic and latent celiac disease as well as “out of the intestine” varieties of wheat intolerance.  Finally, at the base of this massive iceberg sits approximately 20-30% of the world’s population – those who have been found to carry the HLA-DQ locus of genetic susceptibility to celiac disease on chromosome 6.

The “Celiac Iceberg” may not simply illustrate the problems and issues associated with diagnosis and disease prevalence, but may represent the need for a paradigm shift in how we view both celiac disease and wheat consumption among non-celiac disease populations.

First let us address the traditional view of celiac disease as a rare, but clinically distinct species of genetically-determined disease, which I believe is now running itself aground upon the emerging, post-Genomic perspective, whose implications for understanding and treating disease are Titanic in proportion. 

It Is Not the Genes, But What We Expose Them To

Despite common misconceptions, monogenic diseases, or diseases that result from errors in the nucleotide sequence of a single gene are exceedingly rare. Perhaps only 1% of all diseases fall within this category, and Celiac disease is not one of them.  In fact, following the completion of the Human Genome Project (HGP) in 2003 it is no longer accurate to say that our genes “cause” disease, any more than it is accurate to say that DNA is sufficient to account for all the proteins in our body. Despite initial expectations, the HGP revealed that there are only 30,000-35,000 genes in human DNA (genome), rather than the 100,000 + believed necessary to encode the 100,000 + proteins found in the human body (proteome).

The “blueprint” model of genetics: one gene → one protein → one cellular behavior, which was once the holy grail of biology, has now been supplanted by a model of the cell where epigenetic factors (literally: “beyond the control of the gene”) are primary in determining how DNA will be interpreted, translated and expressed.  A single gene can be used by the cell to express a multitude of proteins and it is not the DNA itself that determines how or what genes will be expressed.  Rather, we must look to the epigenetic factors to understand what makes a liver cell different from a skin cell or brain cell.  All of these cells share the exact same 3 billion base pairs that make up our DNA code, but it is the epigenetic factors, e.g. regulatory proteins and post-translational modifications, that make the determination as to which genes to turn on and which to silence, resulting in each cell’s unique phenotype. Moreover, epigenetic factors are directly and indirectly influenced by the presence or absence of key nutrients in the diet, as well as exposures to chemicals, pathogens and other environmental influences. 

In a nutshell, what we eat and what we are exposed to in our environment directly affects our DNA and its expression.

Within the scope of this new perspective even classical monogenic diseases like Cystic Fibrosis (CF) can be viewed in a new, more promising light.  In CF many of the adverse changes that result from the defective expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene may be preventable or reversible, owing to the fact that the misfolding of the CFTR gene product has been shown to undergo partial or full correction (in the rodent model) when exposed to phytochemicals found in turmeric, cayenne, and soybean  Moreover, nutritional deficiencies of seleniun, zinc, riboflavin, vitamin e, etc. in the womb or early in life, may “trigger” the faulty expression or folding patterns of the CFTR gene in Cystic Fibrosis which might otherwise have avoided epigenetic activation. This would explain why it is possible to live into one’s late seventies with this condition, as was the case for Katherine Shores (1925-2004). The implications of these findings are rather extraordinary: epigenetic and not genetic factors are primary in determining disease outcome. Even if we exclude the possibility of reversing certain monogenic diseases, the basic lesson from the post-Genomic era is that we can’t blame our DNA for causing disease. Rather, it may have more to do with what we choose to expose our DNA to.

Celiac Disease Revisited

What all of this means for celiac disease is that the genetic susceptibility locus, HLA DQ, does not determine the exact clinical outcome of the disease. Instead of being the cause, if the HLA genes are activated, they are a consequence of the disease process. Thus, we may need to shift our epidemiological focus from viewing this as a classical “disease” involving a passive subject controlled by aberrant genes, to viewing it as an expression of a natural, protective response to the ingestion of something that the human body was not designed to consume.

If we view celiac disease not as an unhealthy response to a healthy food, but as a healthy response to an unhealthy food, classical celiac disease symptoms like diarrhea may make more sense.  Diarrhea can be the body’s way to reduce the duration of exposure to a toxin or pathogen, and villous atrophy can be the body’s way of preventing the absorption and hence, the systemic effects of chronic exposure to wheat. 

I believe we would be better served by viewing the symptoms of celiac disease as expressions of bodily intelligence rather than deviance.  We must shift the focus back to the disease trigger, which is wheat itself.

People with celiac may actually have an advantage over the apparently unafflicted because those who are “non-symptomatic” and whose wheat intolerance goes undiagnosed or misdiagnosed because they lack the classical symptoms and may suffer in ways that are equally or more damaging, but expressed more subtly, or in distant organs.  Within this view celiac disease would be redefined as a protective (healthy?) response to exposure to an inappropriate substance, whereas “asymptomatic” ingestion of the grain with its concomitant “out of the intestine” and mostly silent symptoms, would be considered the unhealthy response insofar as it does not signal in an obvious and acute manner that there is a problem with consuming wheat. 

It is possible that celiac disease represents both an extreme reaction to a global, species-specific intolerance to wheat that we all share in varying degrees. celiac disease symptoms may reflect the body’s innate intelligence when faced with the consumption of a substance that is inherently toxic.  Let me illustrate this point using Wheat Germ Agglutinin (WGA), as an example. 

WGA is glycoprotein classified as a lectin and is known to play a key role in kidney pathologies, such as IgA nephropathy.  In the article: “Do dietary lectins cause disease?” the Allergist David L J Freed points out that WGA binds to “glomerular capillary walls, mesangial cells and tubules of human kidney and (in rodents) binds IgA and induces IgA mesangial deposits,” indicating that wheat consumption may lead to kidney damage in susceptible individuals.  Indeed, a study from the Mario Negri Institute for Pharmacological Research in Milan Italy published in 2007 in the International Journal of Cancer looked at bread consumption and the risk of kidney cancer.  They found that those who consumed the most bread had a 94% higher risk of developing kidney cancer compared to those who consumed the least bread.  Given the inherently toxic effect that WGA may have on kidney function, it is possible that in certain genetically predisposed individuals (e.g. HLA-DQ2/DQ8) the body – in its innate intelligence – makes an executive decision: either continue to allow damage to the kidneys (or possibly other organs) until kidney failure and rapid death result, or launch an autoimmune attack on the villi to prevent the absorption of the offending substance which results in a prolonged though relatively malnourished life.  This is the explanation typically given for the body’s reflexive formation of mucous following exposure to certain highly allergenic or potentially toxic foods, e.g. dairy products, sugar, etc?  The mucous coats the offending substance, preventing its absorption and facilitating safe elimination via the gastrointestinal tract.   From this perspective the HLA-DQ locus of disease susceptibility in the celiac is not simply activated but utilized as a defensive adaptation to continual exposure to a harmful substance.  In those who do not have the HLA-DQ locus, an autoimmune destruction of the villi will not occur as rapidly, and exposure to the universally toxic effects of WGA will likely go unabated until silent damage to distant organs leads to the diagnosis of a disease that is apparently unrelated to wheat consumption. 

Loss of kidney function may only be the “tip of the iceberg,” when it comes to the possible adverse effects that wheat proteins and wheat lectin can generate in the body.  If kidney cancer is a likely possibility, then other cancers may eventually be linked to wheat consumption as well.  This correlation would fly in the face of globally sanctioned and reified assumptions about the inherent benefits of wheat consumption. It would require that we suspend cultural, socio-economic, political and even religious assumptions about its inherent benefits.  In many ways, the reassessment of the value of wheat as a food requires a William Boroughs-like moment of shocking clarity when we perceive “in a frozen moment….what is on the end of every fork.”  Let’s take a closer look at what is on the end of our forks.

Our Biologically Inappropriate Diet

In a previous article, I discussed the role that wheat plays as an industrial adhesive (e.g. paints, paper mache’, and book binding-glue) in order to illustrate the point that it may not be such a good thing for us to eat.  The problem is implicit in the word gluten, which literally means “glue” in Latin and in words like pastry and pasta, which derives from wheatpaste, the original concoction of wheat flour and water which made such good plaster in ancient times. What gives gluten its adhesive and difficult-to-digest qualities are the high levels of disulfide bonds it contains. These same sulfur-to-sulfur bonds are found in hair and vulcanized rubber products, which we all know are difficult to decompose and are responsible for the sulfurous odor they give off when burned. 

There will be 676 million metric tons of wheat  produced this year alone, making it the primary cereal of temperate regions and third most prolific cereal grass on the planet.  This global dominance of wheat is signified by the Food & Agricultural Organization’s (FAO) (the United Nation’s international agency for defeating hunger) use of a head of wheat as its official symbol.  Any effort to indict the credibility of this “king of grains” will prove challenging.  As Rudolf Hauschka once remarked, wheat is “a kind of earth-spanning organism.” It has vast socio-economic, political, and cultural significance.   For example, in the Catholic Church, a wafer made of wheat is considered irreplaceable as the embodiment of Christ. . 

Our dependence on wheat is matched only by its dependence on us. As Europeans have spread across the planet, so has this grain.  We have assumed total responsibility for all phases of the wheat life cycle: from fending off its pests; to providing its ideal growing conditions; to facilitating reproduction and expansion into new territories.  We have become so inextricably interdependent that neither species is sustainable at current population levels without this symbiotic relationship.  

It is this co-dependence that may explain why our culture has for so long consistently confined wheat intolerance to categorically distinct, “genetically-based” diseases like “celiac.”  These categorizations may protect us from the realization that wheat exerts a vast number of deleterious effects on human health in the same way that “lactose intolerance” distracts attention from the deeper problems associated with the casein protein found in cow’s milk.  Rather than see wheat for what it very well may be: a biologically inappropriate food source, we “blame the victim,” and look for genetic explanations for what’s wrong with small subgroups of our population who have the most obvious forms of intolerance to wheat consumption, e.g. celiac disease, dermatitis herpetiformis, etc.   The medical justification for these classifications may be secondary to economic and cultural imperatives that require the inherent problems associated with wheat consumption be minimized or occluded.

In all probability the celiac genotype represents a surviving vestigial branch of a once universal genotype, which through accident or intention, have had through successive generations only limited exposure to wheat.  The celiac genotype, no doubt, survived through numerous bottlenecks or “die offs” represented by a dramatic shift from hunted and foraged/gathered foods to gluten-grain consumption, and for whatever reason simply did not have adequate time to adapt or select out the gluten-grain incompatible genes. The celiac response may indeed reflect a prior, species-wide intolerance to a novel food source: the seed storage form of the monocotyledonous cereal grasses which our species only began consuming 1-500 generations ago at the advent of the Neolithic transition (10-12,000 BC).  Let us return to the image of the celiac iceberg for greater clarification.

Our Submerged Grain-Free Metabolic Prehistory

The iceberg metaphor is an excellent way to expand our understanding of what was once considered to be an extraordinarily rare disease into one that has statistical relevance for us all, but it has a few limitations. For one, it reiterates the commonly held view that Celiac is a numerically distinct disease entity or “disease island,” floating alongside other numerically distinct disease “ice cubes” in the vast sea of normal health.  Though accurate in describing the sense of social and psychological isolation many of the afflicted feel, the celiac iceberg/condition may not be a distinct disease entity at all. 

Although the HLA-DQ locus of disease susceptibility on chromosome 6 offers us a place to project blame, I believe we need to shift the emphasis of responsibility for the condition back to the disease “trigger” itself: namely, wheat and other prolamine rich grains, e.g. barley, rye, spelt, and oats. Without these grains the typical afflictions we call celiac would not exist.  Within the scope of this view the “celiac iceberg” is not actually free floating but an outcropping from an entire submerged subcontinent, representing our long-forgotten (cultural time) but relatively recent metabolic prehistory as hunters-and-gatherers (biological time), where grain consumption was, in all likelihood, non-existent, except in instances of near-starvation.

The pressure on the celiac to be viewed as an exceptional case or deviation may have everything to do with our preconscious belief that wheat, and grains as a whole are the “health foods,” and very little to do with a rigorous investigations of the facts.

Grains have been heralded since time immemorial as the “staff of life,” when in fact they are more accurately described as a cane, precariously propping up a body starved of the nutrient-dense, low-starch vegetables, fruits, edible seeds and meats, they have so thoroughly supplanted (c.f. Paleolithic Diet).  Most of the diseases of affluence, e.g. type 2 diabetes, coronary heart disease, cancer, etc. can be linked to the consumption of a grain-based diet, including secondary “hidden sources” of grain consumption in grain-fed fish, poultry, meat and milk products.

Our modern belief that grains make for good food, is simply not supported by the facts.  The cereal grasses are within an entirely different family: monocotyledonous (one leaf) than that from which our body sustained itself for millions of years: dicotyledonous (two-leaf).  The preponderance of scientific evidence points to a human origin in the tropical rain forests of Africa where dicotyledonous fruits would have been available for year round consumption.  It would not have been monocotyledonous plants, but the flesh of hunted animals that would have allowed for the migration out of Africa 60,000 years ago into the northern latitudes where vegetation would have been sparse or non-existent during winter months. Collecting and cooking grains would have been improbable given the low nutrient and caloric content of grains and the inadequate development of pyrotechnology and associated cooking utensils necessary to consume them with any efficiency.  It was not until the end of the last Ice Age 20,000 years ago that our human ancestors would have slowly transitioned to a cereal grass based diet coterminous with emergence of civilization.   20,000 years is probably not enough time to fully adapt to the consumption of grains. Even animals like cows with a head start of thousands of years, having evolved to graze on monocotyledons and equipped as ruminants with the four-chambered fore-stomach enabling the breakdown of cellulose and anti-nutrient rich plants, are not designed to consume grains.  Cows are designed to consume the sprouted mature form of the grasses and not their seed storage form.  Grains are so acidic/toxic in reaction that exclusively grain-fed cattle are prone to developing severe acidosis and subsequent liver abscesses and infections, etc. Feeding wheat to cattle provides an even greater challenge:

“Beef:  Feeding wheat to ruminants requires some caution as it tends to be more apt than other cereal grains to cause acute indigestion in animals which are unadapted to it. The primary problem appears to be the high gluten content of which wheat in the rumen can result in a "pasty" consistency to the rumen contents and reduced rumen motility.”
(source: Ontario ministry of Agriculture food & Rural affairs)

Seeds, after all, are the "babies" of these plants, and are invested with not only the entire hope for continuance of its species, but a vast armory of anti-nutrients to help it accomplish this task: toxic lectins, phytates and oxalates, alpha-amalyase and trypsin inhibitors, and endocrine disrupters. These not so appetizing phytochemicals enable plants to resist predation of their seeds, or at least preventing them from "going out without a punch."  

Wheat: An Exceptionally Unwholesome Grain

Wheat presents a special case insofar as wild and selective breeding has produced variations which include up to 6 sets of chromosomes (3 genomes worth!) capable of generating a massive number of proteins each with a distinct potentiality for antigenicity. Common bread wheat (Triticum aestivum), for instance, has over 23,788 proteins cataloged thus far.  In fact, the genome for common bread wheat is actually 6.5 times larger than that of the human genome!

With up to a 50% increase in gluten content of some varieties of wheat, it is amazing that we continue to consider “glue-eating” a normal behavior, whereas wheat-avoidance is left to the “celiac” who is still perceived by the majority of health care practitioners as mounting a “freak” reaction to the consumption of something intrinsically wholesome.

Thankfully we don’t need to rely on our intuition, or even (not so) common sense to draw conclusions about the inherently unhealthy nature of wheat.  A wide range of investigation has occurred over the past decade revealing the problem with the alcohol soluble protein component of wheat known as gliadin, the glycoprotein known as lectin (Wheat Germ Agglutinin), the exorphin known as gliadomorphin, and the excitotoxic potentials of high levels of aspartic and glutamic acid found in wheat. Add to these the anti-nutrients found in grains such as phytates, enzyme inhibitors, etc. and you have a substance which we may more appropriately consider the farthest thing from wholesome. 

The remainder of this article will demonstrate the following adverse effects of wheat on both celiac and non-celiac populations: 1) wheat causes damage to the intestines 2) wheat causes intestinal permeability 3) wheat has pharmacologically active properties 4) wheat causes damage that is “out of the intestine” affecting distant organs  5) wheat induces molecular mimicry 6) wheat contains high concentrations of excitoxins.

1. Wheat Gliadin Creates Immune Mediated Damage To The Intestines
   Gliadin is classified as a prolamin, which is a wheat storage protein high in the amino acids proline and glutamine and soluble in strong alcohol solutions.  Gliadin, once deamidated by the enzyme Tissue Transglutaminase, is considered the primary epitope for T-cell activation and subsequent autoimmune destruction of intestinal villi.  Yet gliadin does not need to activate an autoimmune response, e.g. Celiac disease, in order to have a deleterious effect on intestinal tissue.

In a study published in GUT in 2007 a group of researchers asked the question: “Is gliadin really safe for non-coeliac individuals?”   In order to test the hypothesis that an innate immune response to gliadin is common in patients with celiac disease and without celiac disease, intestinal biopsy cultures were taken from both groups and challenged with crude gliadin, the gliadin synthetic 19-mer (19 amino acid long gliadin peptide) and 33-mer deamidated peptides.   Results showed that all patients with or without Celiac disease when challenged with the various forms of gliadin produced an interleukin-15-mediated response.  The researchers concluded: “The data obtained in this pilot study supports the hypothesis that gluten elicits its harmful effect, throughout an IL15 innate immune response, on all individuals [my italics].”

The primary difference between the two groups is that the celiac disease patients experienced both an innate and an adaptive immune response to the gliadin, whereas the non-celiacs experienced only the innate response.   The researchers hypothesized that the difference between the two groups may be attributable to greater genetic susceptibility at the HLA-DQ locus for triggering an adaptive immune response, higher levels of immune mediators or receptors, or perhaps greater permeability in the celiac intestine. It is possible that over and above the possibility of greater genetic susceptibility, most of the differences are from epigenetic factors that are influenced by the presence or absence of certain nutrients in the diet.  Other factors such as exposure to NSAIDs like naproxen or aspirin can profoundly increase intestinal permeability in the non-celiac, rendering them susceptible to gliadin’s potential for activating secondary adaptive immune responses.  This may explain why in up to 5% of all cases of classically defined celiac disease the typical HLA-DQ haplotypes are not found. However, determining the factors associated greater or lesser degrees of susceptibility to gliadin’s intrinsically toxic effect should be a secondary to the fact that it is has been demonstrated to be toxic to both non-celiacs and celiacs.

• Wheat Gliadin Creates Intestinal Permeability
  Gliadin upregulates the production of a protein known as zonulin, which modulates intestinal permeability. Over-expression of zonulin is involved in a number of autoimmune disorders, including celiac disease and Type 1 diabetes.  Researchers have studied the effect of gliadin on increased zonulin production and subsequent gut permeability in both celiac and non-celiac intestines, and have found that “gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules.”10   These results indicate, once again, that a pathological response to wheat gluten is a normal or human, species specific response, and is not based entirely on genetic susceptibilities.  Because intestinal permeability is associated with wide range of disease states, including cardiovascular illness, liver disease and many autoimmune disorders, I believe this research indicates that gliadin (and therefore wheat) should be avoided as a matter of principle.
• Wheat Gliadin Has Pharmacological Properties
  Gliadin can be broken down into various amino acid lengths or peptides. Gliadorphin is a 7 amino acid long peptide: Tyr-Pro-Gln-Pro-Gln-Pro-Phe which forms when the gastrointestinal system is compromised.  When digestive enzymes are insufficient to break gliadorphin down into 2-3 amino acid lengths and a compromised intestinal wall allows for the leakage of the entire 7 amino acid long fragment into the blood, gl idorphin can pass through to the brain through circumventricular organs and activate opioid receptors resulting in disrupted brain function. There have been a number of gluten exorphins identified: gluten exorphin A4, A5, B4, B5 and C, and many of them have been hypothesized to play a role in autism,  schizophrenia, ADHD and related neurological conditions.   In the same way that the celiac iceberg illustrated the illusion that intolerance to wheat is rare, it is possible, even probable, that wheat exerts pharmacological influences on everyone. What distinguishes the schizophrenic or autistic individual from the functional wheat consumer is the degree to which they are affected.

Below the tip of the “Gluten Iceberg,” we might find these opiate-like peptides to be responsible for bread’s general popularity as  a “comfort food”, and our use of phrases like “I love bread,” or  “this bread is to die for” to be indicative of wheat’s narcotic properties.  I believe a strong argument can be made that the agricultural revolution that occurred approximately 10-12,000 years ago as we shifted from the Paleolithic into the Neolithic era was precipitated as much by environmental necessities and human ingenuity, as it was by the addictive qualities of psychoactive peptides in the grains themselves.

The world-historical reorganization of society, culture and consciousness accomplished through the symbiotic relationship with cereal grasses, may have had as much to do with our ability to master agriculture, as to be mastered by it.   The presence of pharmacologically active peptides would have further sweetened the deal, making it hard to distance ourselves from what became a global fascination with wheat.

An interesting example of wheat’s addictive potential pertains to the Roman army.  The Roman Empire was once known as the “Wheat Empire,” with soldiers being paid in wheat rations.  Rome’s entire war machine, and its vast expansion, was predicated on the availability of wheat.  Forts were actually granaries, holding up to a year’s worth of grain in order to endure sieges from their enemies.  Historians describe soldiers’ punishment included being deprived of wheat rations and being given barley instead.   The Roman Empire went on to facilitate the global dissemination of wheat cultivation which fostered a form of imperialism with biological as well as cultural roots.

The Roman appreciation for wheat, like our own, may have had less to do with its nutritional value as “health food” than its ability to generate a unique narcotic reaction. It may fulfill our hunger while generating a repetitive, ceaseless cycle of craving more of the same, and by doing so, enabling the surreptitious control of human behavior.  Other researchers have come to similar conclusions.  According to the biologists Greg Wadley & Angus Martin:  “Cereals have important qualities that differentiate them from most other drugs. They are a food source as well as a drug, and can be stored and transported easily. They are ingested in frequent small doses (not occasional large ones), and do not impede work performance in most people. A desire for the drug, even cravings or withdrawal, can be confused with hunger. These features make cereals the ideal facilitator of civilisation (and may also have contributed to the long delay in recognising their pharmacological properties).”

• Wheat Lectin (Wga) Damages Our Tissue

  Wheat contains a lectin known as Wheat Germ Agglutinin which is responsible for causing direct, non-immune mediated damage to our intestines, and subsequent to entry into the bloodstream, damage to distant organs in our body. Lectins are sugar-binding proteins which are highly selective for their sugar moieties. It is believed that wheat lectin, which binds to the monosaccharide N-acetyl glucosamine (NAG), provides defense against predation from bacteria, insects and animals.  Bacteria have NAG in their cell wall, insects have an exoskeleton composed of polymers of NAG called chitin, and the epithelial tissue of mammals, e.g. gastrointestinal tract, have a “sugar coat” called the glycocalyx which is composed, in part, of NAG.  The glycocalyx can be found on the outer surface (apical portion) of the microvilli within the small intestine.

There is evidence that WGA may cause increased shedding of the intestinal brush border membrane, reduction in surface area, acceleration of cell losses and shortening of villi, via binding to the surface of the villi. WGA can mimic the effects of epidermal growth factor (EGF) at the cellular level, indicating that the crypt hyperplasia seen in celiac disease may be due to a mitogenic reponse induced by WGA.  WGA has been implicated in obesity and “leptin resistance” by blocking the receptor in the hypothalamus for the appetite satiating hormone leptin.  WGA has also been shown to have an insulin-mimetic action, potentially contributing to weight gain and insulin resistance.   And, as discussed earlier, wheat lectin has been shown to induce IgA mediated damage to the kidney, indicating that nephropathy and kidney cancer may be associated with wheat consumption.

• Wheat Peptides Exhibit Molecular Mimicry
  Gliadorphin and gluten exporphins exhibit a form of molecular mimicry that affects the nervous system, but other wheat proteins effect different organ systems. The digestion of gliadin produces a peptide that is 33 amino acids long and is known as 33-mer which has a remarkable homology to the internal sequence of pertactin, the immunodominant sequence in the Bordetella pertussis bacteria (whooping cough).  Pertactin is considered a highly immunogenic virulence factor, and is used in vaccines to amplify the adaptive immune response.  It is possible the immune system may confuse this 33-mer with a pathogen resulting in either or both a cell-mediated and adaptive immune response against Self.
• Wheat Contains High Levels Of Excito-Toxins
  John B. Symes, D.V.M. is responsible for drawing attention to the potential excitotoxicity of wheat, dairy, and soy, due to their exceptionally high levels of the non-essential amino acids glutamic and aspartic acid.  Excitotoxicity is a pathological process where glutamic and aspartic acid cause an over-activation of the nerve cell receptors (e.g. NMDA and AMPA receptor) leading to calcium induced nerve and brain injury.   Of all cereal grasses commonly consumed wheat contains the highest levels of glutamic acid and aspartic acid.  Glutamic acid is largely responsible for wheat’s exceptional taste. The Japanese coined the word umami to describe the extraordinary “yummy” effect that glutamic acid exerts on the tongue and palate, and invented monosodium glutamate (MSG) to amplify this sensation.  Though the Japanese first synthesized MSG from kelp, wheat can also be used due to its high glutamic acid content.   It is likely that wheat’s popularity, alongside its opiate-like activity, has everything to do with the natural flavor-enhancers already contained within it.  These amino acids may contribute to neurodegenerative conditions such as Multiple sclerosis, Alzhemier’s, Huntington’s disease, and other nervous disorders such as Epilepsy, Attention Deficit Disorder and Migraines.

Conclusion

In this article I have proposed that celiac disease be viewed not as a rare “genetically-determined” disorder, but as an extreme example of our body communicating to us a once universal, species-specific affliction: severe intolerance to wheat.  Celiac disease reflects back to us how profoundly our diet has diverged from what was, until only recently a grain free diet, and even more recently, a wheat free one.  We are so profoundly distanced from that dramatic Neolithic transition in cultural time that “missing is any sense that anything is missing.” The body, on the other hand, cannot help but remember a time when cereal grains were alien to the diet, because in biological time it was only moments ago. 

Eliminating wheat, if not all of the members of the cereal grass family, and returning to dicotyledons or pseudo-grains like quinoa, buckwheat and amaranth, may help us roll back the hands of biological and cultural time, to a time of clarity, health and vitality that many of us have never known before.  When one eliminates wheat and fills the void left by its absence with fruits, vegetables, high quality meats and foods consistent with our biological needs we may begin to feel a sense of vitality that many would find hard to imagine. If wheat really is more like a drug than a food, anesthetizing us to its ill effects on our body, it will be difficult for us to understand its grasp upon us unless and until we eliminate it from our diet.  I encourage everyone to see celiac disease not as a condition alien to our own. Rather, the celiac gives us a glimpse of how profoundly wheat may distort and disfigure our health if we continue to expose ourselves to its ill effects.  I hope this article will provide inspiration for non-celiacs to try a wheat free diet and judge for themselves if it is really worth eliminating.