Celiac.com 12/01/2015 - Lectins are carbohydrate binding proteins which promote inflammatory responses like Crohn's disease, systemic lupus, asthma, and rheumatoid arthritis. They were discovered over 100 years ago and cause leaky gut and gastrointestinal dysbiosis yet the push for a plant-based diet focusing on legumes as meat alternatives has overlooked the damage lectins cause to the gut. Legumes offer inferior nutrition compared to animal proteins so toxicity needs to be considered when recommending food choices.

As carbohydrate binding proteins, lectins are difficult to digest and irritate the brush border of the small intestine. Consequently, the tight junctions of the microvilli are damaged by prolamin and agglutinins which can lead to numerous disorders of the gastrointestinal tract and autoimmune diseases. Lectins are also a major contributor to leptin resistance which contributes to obesity.

As described in The Handbook of Plant Lectins: Properties and Biomedical Applications (John Wiley, 1998), foods that contain these toxic lectins are members of the pea family and include peanuts, pigeon peas, soybeans, kidney beans, mung beans, lima beans, lentils, fava beans, chickpeas, carob, green and yellow peas. Green beans, snow peas and snap peas are usually well tolerated once the gut has been healed since they are immature protein sources with minor amounts of lectins.

Lectins are found in other foods including grains and pseudo-grains. Grains are seeds from grasses—barley, oats, rice, rye, millet, wheat, teff, corn, kamut, spelt and possibly wild rice. Many gastroenterologists believe that the detrimental affects of lectins in grains are a factor in the development of celiac disease. Genetics and frequent consumption possibly play a critical role in the severity of sensitivities to these foods.

Pseudo-grains are seeds from broadleafed plants—amaranth, buckwheat, chia, and quinoa. These seed products were geographically limited to specific populations and only available on a limited basis seasonally. But modern agriculture has greatly increased the consumption of these pseudo-grains because they can be labeled “gluten-free” because US standards allow any grain with less than 20 ppm gluten to be called gluten-free.

Omitting toxic lectins—prolamins and agglutinins—from the diet is critical for gut health. Prolamins are predominately found in the seeds of plants. Gluten is the most widely known source of prolamins. They get their name from the high content of the amino acid proline. Research studies have shown that the prolamins in quinoa, corn and oats can cause damage to the digestive tract in people with celiac disease, yet these grains are frequently included in a gluten-free diet.

Aggltinins are named for their ability to cause clumping of red blood cells. The most recent example of how this toxic lectin works is the bioterrorism threat caused from ricin. Ricin is the compound in castor beans that is so toxic that only tiny amounts are needed to cause death. Agglutinins are found on the seed coatings of grains and pseudo-grains and serve to protect the seed from fungus growth. Genetically modified crops—wheat, corn, soybeans—have higher amounts of agglutinins to insure higher yields.

A leaky gut is harmful to the innate and adaptive immune systems. Toxic lectins cause inflammation and induce cytokine production. As few as five soaked, uncooked kidney beans can lead to gut distress for the raw foodies while 1 tablespoon of peanut butter leads to peanut agglutinins entering the bloodstream soon after consumption.

Paolo Zatto and Pamela Zambenedetti from Padova, Italy studied lectins, microglia and Alzheimer's Disease (AD) as reported in Lectins and Pathology, 2000. The microglia of 10 AD brains stained intensely for agglutinins. Their research concluded that the glycation reaction seen in AD from lectins may serve as a significant factor in amyloid plaque development and disease progression.

Bacteria overgrowth in the gut is associated with a wide variety of diseases- septicemia, pulmonary infections, enteropathies. Adhesion of pathogenic bacteria to epithelial cells in the gut can be a critical first stage in the infectious disease process. Michele Mouricout and Bruno Vedrine of Limoges, France described how lectins cause adhesion of numerous bacterial strains to intestines, brain tissues, urinary tract, lung and corneal cells. Their research is reported in Lectins and Pathology, 2000 illustrates the mosiac effect of how agglutinins cause tissue damage.

Even though lectins have been identified for decades, little interest has been shown by biological and medical science. Since they are so widely distributed in foods consumed daily, lectins may finally become recognized as partners in the pathogenesis of diseases like cancer. Galectin-3 (gal 3) galactoside-binding lectin is found on the surface of most cancer cells and has been reported to promote angiogenesis. Lectins are not oncogenes but they help in cancer progression once initiated. Some are implicated in adhesion while others cause metatasis.

Isn't it about time that nutrition science took a closer look at the lectin levels in foods consumed daily and customize the diet for lectin sensitivity to better manage inflammation and auto immune diseases? The higher intact of GMO food in the diet, the more lectins are consumed. Without food labeling of GMOs, consumers will continue to be misled and many will remain sick.

Celiac.com 11/24/2015 - Polyphenols are a group of compounds produced by plants, highly variable in strucure, physical, chemical and biological properties. Currently science knows of several thousand natural phenolic compounds. A common feature of polyphenols is their ability to enable redox reactions. With their ability to transport protons and electrons, phenolic compounds not only readily get oxidized, but also, through the compounds called quinones that result from their oxidation, may mediate oxidation of other compounds that do not directly react with oxygen.

Anthocyanins
Anthocyanins are a large group of plant dyes that are soluble in water and are found in flowers, fruits, leaves and stems. In the cell they are located in the vacuoles, in the form of granules of various sizes, however, the cell walls of the pulp and tissues do not contain anthocyanins. Anthocyanins give fruits and vegetables different colors like orange, red, pink, purple and dark blue.

Anthocyanins belong to the polyphenol organic compounds. The name “anthocyanin” was first used in 1835 by Marquart to refer to the blue dye of the cornflower. The structure of anthocyanins can be very complex and diverse. Acid hydrolysis of anthocyanins leads to decay into sugars and anthocyanidins, called aglycones. The anthocyanins are natural products usually in the form of mono-, di- or tri-glycosides.

Hundreds of natural anthocyanins are known, and over 100 could be produced synthetically. These dyes can be extracted from plants and are used as food additives to impart or reinforce the color of drinks, juices, candies and jellies.

Anthocyanins determine the hue and color stability, for example, in strawberries the dominant dye is pelargonidin 3-glucoside. Anthocyanin synthesis is a photochemical process because the fruit which is directly irradiated by solar radiation has a more full coloration compared to fruit picked early and ripened in storage.

Health Aspects
The healing properties of anthocyanins have long been known in folk medicine, and now they are increasingly being used in the pharmaceutical and cosmetic industries. Anthocyanin’s name was derived from the Latin name of the plant from which the particular compound was extracted: cyanine flowers or cornflower (Centaurea cyanus L.). Anthocyanins are unstable compounds and reside in an aqueous environment and depend on pH levels that trigger changes in the color of products from which they were isolated. In acidic conditions they have a red color, in nutral conditions violet, and in alkaline they are blue.

The structure of anthocyanin molecules has a significant impact on the hue, intensity and color stability. Irreversible changes of anthocyanin pigments are mainly due to oxidative polymerization processes and cause changes in natural red color of fruits to red-brown which is characteristic of long storage. The rate of these changes depends mainly on the presence of factors in the raw material, temperature and time.

Chokeberry - Aronia
The addition of these compounds to food does not raise concerns of consumers, and they are accepted. An example of a source of anthocyanins is the chokeberry, which contains a lot of polyphenol (above 20 mg/g), including anthocyanins. With a considerable amount of polyphenols, the chokeberry has a significant level of antioxidant activity. Its distinctive tart flavor comes from the high content of tannins which reduces the possibility of direct consumption of the fruit and its products. Generally it is used in combination with other fruits, or in a diluted form.

Chokeberry fruit is used for the manufacture of nectars, drinks, wines, jams, as well as food dyes and bioactive compounds. Anthocyanins isolated from chokeberry have antimutagenic and anticarcinogenic activity, and chokeberry juice has antioxidant properties. Chokeberry juice is more and more relevant in the food industry as a source of natural red color for products that are poor in stable color.

Products made from chokeberries are mainly aronia juice that is mixed with other fruit juices. Other applications include food coloring additives teas and syrups. In Russia, aronia and apple juices are combined and fermented to produce red wine. In Lithuania, dessert wines are produced with the use of chokeberry or chokeberry juice, which is mixed with other fruit juices. Commercial juices are produced by pressing ripe berries, then fining and filtering the juice. To reduce the tannin content gelatin may be added prior to filtration.

Tannins sometimes form complexes, which cause clouding of clear juice. Reducing the level of tannins also makes juice have a less tart taste. Clear juice can then be bottled and pasteurized or concentrated and used as a food ingredient. The whole fruit can be used for the production of a puree that is a highly colored product of uniform consistency once the seeds and skins are removed. The product can be frozen and used as a food ingredient in sauces.

Antioxidant Effect
In the scientific literature, we can find a number of studies on the antioxidant properties of chokeberry, chokeberry extracts or phenolic components. Fresh chokeberry fruits have the highest antioxidant capacity of the fruit measured by ORAC method. Literature reports that chokeberry juice has the highest antioxidant capacity of beverages rich in polyphenols—four times higher than other berry juice, cranberry juice, or red wine. Anthocyanidins and procyanidins containing o-dihydroxyphenyl group are excellent metal chelators and form complexes with, for example iron (III) and copper (II). The presence of free iron and copper in biological systems catalyzed free radical reactions, such as the Fenton reaction. The ability of the phenolic components to bind divalent metal effectively reduces the concentration of these cations, and therefore their oxidative properties.

It should be noted that the in vitro data does not say a lot about the role they can play in in vivo systems for prevention of oxidative stress. The literature also describes the antioxidant effects in animals, where chokeberry anthocyanins reduce lipid peroxidation and increase the activity of enzymes that are involved in the antioxidant defense system. It was also observed that the fraction of the red dye from chokeberry, both in vitro and in vivo. is able to prevent damage to the gastric mucosa. Antioxidant effects observed in humans, with chokeberry juice supplementation reduces oxidative damage to red blood cells produced during exercise.

Celiac.com 11/17/2015 - For most people, when they think of gluten, the first thing that comes to mind is bread. And for most people with celiac or a gluten sensitivity, that is what we miss most.

While people with celiac or gluten sensitivity may never be able to experience the wide selection or soft texture that "glutenous" bread offers, there are still some tasty gluten-free bread options available at most grocery stores. In order to find the best gluten-free bread options, I went to my local Giant Eagle and tried all of the gluten-free bread available and explored four main aspects: taste, texture, price, and variety.

The three brands of gluten-free bread offered at Giant Eagle were Schar, Udi's, and Goodbye Gluten.

In the variety category, Udi's offered the largest selection of bread with the choice of white bread, multigrain bread, cinnamon raisin bread, and millet-chia bread and omega flax and fiber bread. Udi's also offers a large variety of other products ranging from muffins and cookies, to pizza crusts and tortillas.

While Udi's may have the largest variety of the three brands, Schar offered a few different kinds of bread as well, with a cinnamon raisin and multigrain option along with an assortment of rolls.

In the category of price, Goodbye Gluten came in as the most inexpensive per ounce at $0.27 per ounce. Udi's was in the middle $0.37 per oz. and Schar was the most expensive of the three, coming in at $0.40 per oz.

Now let's get down to business. Taste and texture—the two aspects that are hardest to get right when making gluten-free bread. In my opinion, Udi's won both categories with the tastiness, most normal textured bread. My only critique was the slices of bread weren't big enough! All three brands seemed to have their slices of bread on the smaller side, but Udi's bread seemed to be especially small.

Although Udi's took the first prize in three of the four categories, that is not to say the other two brands were not good. I was impressed with all three brands, but my main critique covers the texture category.

The Goodbye Gluten bread seemed to be very dense, and while most gluten-free bread crumbles more than normal, I felt that the Goodbye Gluten loaf broke easier than the other two. However, it was very moist, something that is hard to come by in gluten-free bread.

With the Schar bread, I felt that it was a little dry and grainy rather than moist and chewy like normal gluten filled bread. However, I found that when I toasted the bread, it had a texture more consistent with normal toast.

Overall, I was satisfied with all three brands, but Udi's was the favorite. With the texture and taste being spot on, I did not need much else to convince me, but the added bonus of the reasonable price and large variety made it the most desirable gluten-free bread available.

Celiac.com 11/10/2015 - I can only imagine the gut wrenching betrayal Caesar must have considered in the final moments of his life. Brutus, a trusted friend, took it upon himself to rid Rome of his long time ally for the betterment of society, wielding the dagger that (for better or worse) ultimately changed the Roman Empire and altered history.

Most of us will go our whole lives blissfully unaware of how deep that dagger cuts; but not so for the staff of P.F. Changs. After years of being leading pioneers in the gluten-free restaurant business they were served with a discriminatory lawsuit. Anna Marie Phillips decided to file the suit against the gluten-free restaurant claiming the extra dollar surcharge is both discriminatory and unfair for those who are required to maintain a gluten-free diet. Suing for potentially millions, her class action law suit could be the legal dagger that changes the celiac landscape for years to come.

The legal basis for this law suit is most likely buried in the Americans with Disabilities Act (ADA), which expanded its legal guidelines in the ADA Amendments Act (ADAAA) of 2008. Mark Heller, Ms. Phillips attorney, was quoted from Yahoo Health "To have to pay a premium price is discriminatory, and there is legal basis for a case. It would be like installing a handicapped ramp and then charging people a dollar to use it." While I do not doubt either of their noble intentions, I would argue that a business does not incur an additional cost or delay each and every time someone utilizes their wheel chair ramp.

The greater issue is what is at risk for the entire gluten-free community. Living most of my life on the diet (since the 1990's) I have witnessed the remarkable achievements celiacs have made over the years. While costs are still higher for gluten-free food, our capitalist society allows for the market to react to supply and demand. The more profitable the industry the more options become available to consumers. The more options there are, the lower the price goes in the marketplace. This is the American way of life.

Now, imagine for a moment that the gluten-free restaurant industry was no longer as profitable. gluten-free restaurants could not legally charge a premium for their products; but, were still required to go through the extra steps of preparing them correctly. Would their willingness to create a gluten-free menu fade? Would a gluten-free meal prepared by someone with a legal dagger to their back taste as delectable? Will there be anyone left to make it?

"Render unto Caesar the things that are Caesar's."

Celiac.com 11/03/2015 - Many people today are dealing with the need to be gluten-free, whether from allergies, intolerance or celiac disease. Being gluten-free can be the difference between being healthy and having chronic, potentially debilitating, symptoms.

However, sometimes being gluten-free is not enough.

The challenge with a gluten-free diet is that many of the most popular gluten-free flours are actually high in oxalate! Oxalate is a toxin that occurs naturally in most plant foods, but at very different levels, some relatively safe, and some not. Oxalate can even kill at high enough doses. The scientific challenges in the oxalate field, as well as oxalate's potential relationship to celiac sprue, were discussed in the feature article by Susan Costen Owens which appeared in the Spring issue of this journal. In this follow up article, you'll find the practical advice on how you can reduce the level of oxalate in your gluten-free diet.

A great example of a popular high oxalate gluten-free flour is almond flour. Almonds are one of the very highest oxalate foods, with about 300 mg of oxalate for one half cup of whole nuts. Given that you will actually have more nuts in a half cup of flour than you will in a half cup of whole nuts, you could have 400 or more milligrams of oxalate in that single half cup of flour.

So, your daily morning muffin made with almond flour could be 200-250 mg of oxalate. This means that you may not feel as good on your gluten-free diet as you might expect because your digestive tract can be suffering with ongoing inflammation from a new source – oxalate.

Now 250 mg of oxalate might not seem so bad – unless you consider that a low oxalate diet is defined as 40-60 mg of oxalate per day! That makes your morning muffin the equivalent of 4-5 days worth of oxalate, for someone who is eating a typical low-oxalate eating plan.

If you've been eating a lot of nut flours, you might be wondering what you can substitute instead? The one nut flour that is low oxalate is coconut flour. This can be a great option, if you like the density of nut flours, and want a flour with higher nutrition. All other nut flours are high; most seed flours are high too. Nuts themselves are some of the highest oxalate foods in nature. Baked products made with nut flours will be particularly high in oxalate – and if you add chocolate, you compound the problem.

Unfortunately, this is more bad news for lovers of chocolate baked goods. Chocolate is another extremely high oxalate ingredient: cocoa has more than 35 mg of oxalate per tablespoon and the substitute carob, is no better! Given that many baked goods could easily have 1-2 tablespoons of chocolate or carob per serving, you can see how your oxalate intake could really add up. Of course, this doesn't include the fact that many baked goods – like brownies – will combine both cocoa and nuts, for a double hit of oxalate.

The same problem arises with many of our common gluten-free baking flours and spices. They can often add an overload of oxalate to each serving, with the potential for problems later as oxalate accumulates in the body. So, how can you avoid gluten, and not introduce more of a known toxin into your body?

The trick is knowing enough about oxalate to avoid it effectively.

The first thing to learn is how to get flavor in your food without the oxalate. Oils and extracts are typically much lower in oxalate than the whole herb or spice, and yet retain the flavor for baking and cooking purposes. The process by which oils are pressed and extracts are made appears to leave the oxalate behind.

This rule of thumb gives us a way to get the taste we want, and avoid oxalate. For instance, to get a chocolate taste without too much cocoa, you can carefully craft a recipe that balances the use of cocoa with chocolate extract, chocolate flavoring and even a bit of coffee. Using food grade cocoa butter, which has zero oxalate, in place of butter or oil, is another way to boost that chocolate flavor. If you use the lowest oxalate flours as well, you leave some room for a bit more cocoa because you are not adding a lot of oxalate in the flour. By doing this, you can get the flavor you want while avoiding the oxalate.

Another example of baking smart is an almond flavored cookie. You can actually make a cookie with almond oil as well as almond extract for extra taste – while almonds themselves are extremely high, both the oil and the extract have almost no oxalate at all!

This concept of using oils and extracts is particularly important if you like the sweet taste of cinnamon. Cinnamon is a very high oxalate spice with over 38 mg of oxalate for just one teaspoon! Choose instead cinnamon oil or cinnamon extract. Cinnamon oil is available from various outlets that sell culinary oils. You can get cinnamon extract in the supplement section of your grocery or health food store – generally, it is sold in capsules. When cooking with it, you simply open the capsules and put the powdered extract into your dish. Substitute about the equivalent amount of dry extract for ground cinnamon.

The second thing to learn is how to pick low oxalate flours. While many of the gluten-free flours are high in oxalate, the process of picking appropriate flours may not be as hard as it first appears.

Oxalate is often present in the "bran" of a grain. As a result, most whole grain flours are actually high in oxalate. This seems strange to us because we are told to get more fiber and eat whole grain. But the truth is that not all whole grains are good for us and we can get our fiber in other ways not so tied to oxalate.

Interestingly, most starches are low oxalate (even if they come from high oxalate whole foods), in the same way that oils are low oxalate. This means that starches are our friends when we want to cook! Most starches (including potato, corn, green bean and sweet potato) are low in oxalate, and can be used as part of the flour combination in a baked good to get a lighter, fluffier result.

Again, the explanation is similar to the explanation regarding oils and extracts: when we remove the starch from even a high oxalate food, we appear to leave the majority of the oxalate behind. But be careful to get starches and not flours when you are dealing with high oxalate whole foods – items like potato flour or sweet potato flour are extremely high in oxalate, and should be avoided. Only the starches are safe on a low-oxalate eating plan.

You can consume some medium oxalate foods, and still remain low oxalate overall. This expands the possible flours that you can use. Good options include white masa (which is a corn flour), green pea, lupin, sorghum, and sweet rice flours. While buckwheat and quinoa are also common in gluten-free foods, these grains are very high in oxalate. You should ideally avoid them.

So what do you do if you are used to baking with nut flours? If you want high nutrition flours that are much lower in oxalate than nut flours, look to legume flours. Consider black-eyed pea flour (also called cowpea bean flour), garbanzo bean flour, or yellow pea flour. All of these legume flours are low in oxalate. However, because legume flours can be heavy, combine them with low oxalate starches, like corn, rice, green bean, potato or sweet potato starch to get the right texture in your baked goods.

When we combine the lowest oxalate flours with others that are medium (and sometimes small amounts of higher oxalate flours), we can get the right kind of flavor and texture, yet remain low in oxalate per serving. A great example is a flour mix that contains a variety of flours. One easy combination of flours is ½ cup of sweet rice flour (medium oxalate), with ½ cup of coconut flour (medium oxalate), ½ cup of potato starch (low oxalate) and ½ cup of cornstarch (low oxalate). This particular flour combination can be used in crepes, and results in a crepe that has the same kind of stretch that you have with gluten flours, because of the properties of the various flours used in the combination.

While some of us will be experimental and will like the idea of playing with flours and starches to develop our own recipes, others will not. If you are looking for a good quality gluten-free flour mix that you can use at home, consider Orgran. Another great option for baking (as well as pancakes) is gluten-free Bisquick.

So far we've presumed that you are baking or making your own gluten-free items. But what if you are buying packaged gluten-free foods?

When looking at baked goods, look for starches in the first five ingredients. So, you should see low oxalate flours early in the ingredients, because these will be the largest components of your baked good. Avoid items with buckwheat flour, hemp, quinoa, sesame seeds, and teff in general. All of these ingredients are so high in oxalate, that even small amounts would be a problem. While tapioca starch and white rice flour are high in oxalate, in smaller amounts, they should be fine.

If you are considering reducing oxalate in your diet, the best way to do that is slowly! When you reduce oxalate too quickly, you can experience stressful symptoms as the oxalate that is stored in your body leaves too quickly. The process of oxalate moving out of your tissues and into your blood, seeking then a site of secretion, is called "dumping" by our project since it is a very common experience. This can be the culprit behind digestive symptoms, fatigue, brain fog, rashes and other symptoms.

Ideally, you would slowly phase high oxalate foods out of your diet. So rather than completely abandoning your morning muffin made with almond flour, you would slowly reduce your portion by ¼ of a muffin per week, until you were no longer eating an almond flour muffin after 4 weeks. During those 4 weeks, you slowly introduce your new morning muffin, ¼ at a time, which is now made with coconut flour.

You would also want to remove only one food at a time in this way – so that oxalate is very slowly phased out, and you can also use up some of the high oxalate foods that you have in your home. It's not only easier on your body to do this change slowly, but it's also easier on your pocket book!

Oxalate is not just an issue with grains and flours – it can also be an issue with other foods. So while this article has focused more on the specific issues with gluten-free baking and cooking, there are other high oxalate foods that you need to be aware of if you want to reduce oxalate in your overall diet.

You may have heard or seen information that points at leafy greens as high oxalate foods. While such common staples as spinach, beets and Swiss chard are extremely high in oxalate, you can enjoy other greens in a healthy diet. Consider other leafy greens like arugula, turnip greens, mustard greens or certain varieties of kale, like dino / lacinto or purple, to get leafy veggies in your diet. Most lettuces are low in oxalate and high in nutrition, including romaine and leaf lettuce. Eating low oxalate does not have to mean removing whole food groups from your diet, nor losing all your high nutrition options!

Many of the common fruits are lower in oxalate and can be incorporated in your diet – including berries. Many people have mistakenly heard that all berries are high oxalate. Testing done by Dr. Michael Liebman of the University of Wyoming shows this is not true! According to test results from his lab, both blueberries and strawberries are low oxalate, and raspberries are medium oxalate. So while you might want to avoid blackberries (which are very high in oxalate), you can safely eat other healthy berries.

However, other fruit can be extremely high in oxalate. Citrus can be tricky because it's important to know not just which fruit you are eating, but which parts. Many citrus juices, like grapefruit, orange, lemon and lime, are low oxalate per serving, so you can still get the taste of these items when cooking with the juice. But don't eat a lot of grapefruit – the whole fruit is high oxalate. Similarly, if you use citrus zest for extra flavor, you'll find that it's a problem: the oxalate levels are too high.

Sometimes you need to know the variety of a food, or need to watch your serving size. Pears are a great example. Some varieties of pears have tested low; others have tested high. When choosing pears, go for Bartlett (also called Williams pear).

Many exotic and tropical fruits are high, including kiwi, figs, papaya, gauva, and pomegranate. Some are so high that they could be dangerous to consume in a single serving! Star fruit has this dubious distinction: it is so high that people have had seizures and even died from eating star fruit when their kidneys were in trouble.

It is important to recognize that many of the foods that we think of as being the healthiest may also contain a lot of oxalate. Vegans can be particularly susceptible to eating a very high oxalate diet, as they may be getting their protein primarily from high oxalate legumes, including soybeans. If you want to include legumes in your diet for the fiber and nutritional benefits, focus on the low and medium oxalate legumes. That list includes red, green, brown and yellow lentils, green peas, red kidney beans, tofu, garbanzo beans, yellow and green split peas, lima beans and black-eyed peas.

Note that tofu is okay – but whole soybeans are not. This is one of the most challenging aspects of the diet. Some foods are okay in the right form, or with the proper processing. So much as extracts, oils and starches are lower in oxalate than the whole foods they come from, some processed forms of foods are lower than the whole, unprocessed food. So you can eat tofu – but don't eat edamame.

A last point that can help you to reduce oxalate in your diet is to consider how a food is cooked. When a food is boiled, you may actually reduce the amount of oxalate in the food. Oxalate can be soluble, and so it will leach into the cooking water, and can then be thrown away. There is no other cooking method that can reliably reduce oxalate, other than cooking or soaking in water. However, this flies in the face of current nutritional advice, which focuses on eating as many foods as possible raw. While you don't have to boil everything you eat – there are a number of very low oxalate veggies and fruits that can be eaten and enjoyed raw – boiling can be a valuable strategy to reduce this known toxin, and leave you with a more nutritious end result.

If you have more questions about oxalate and your diet, please see the website Open Original Shared Link. There is also an associated support group, which is currently at Yahoo, called Trying_Low_Oxalates. In addition, we have a Facebook group with the same name. On Facebook, we also have two additional recipe groups, one of which is focused specifically on vegan eating. These support groups can help you to make lower oxalate choices part of your diet and can also help you gain a perspective on how oxalate may have been affecting other issues in your health.

Lower Oxalate Flours, Starches and Products

• Potato starch
• Cornstarch
• Green Bean starch
• Sweet Potato starch
• Flax meal / seed
• White masa corn flour
• Green pea flour
• Lupin flour
• White rice flour
• Sweet rice flour
• Coconut flour
• Black-eyed pea (cowpea) flour
• Garbanzo bean (chickpea) flour
• Water chestnut flour
• Yellow pea flour

Low Oxalate per serving

• General Mills Corn Chex (1/2 cup)
• General Mills Rice Chex (1/2 cup)
• Arrowhead Mills gluten-free Popcorn (1 cup)
• Eden Kuzu Pasta (1/2 cup)
• Thai Kitchen Rice Noodles (1/2 cup)
• Annie's Homegrown Macaroni and Cheese, gluten-free (1/2 cup)
• Tinkyada White Rice Spaghetti (1/2 cup)
• Lotus Foods Bhutan Red Rice (1/2 cup cooked)

Higher Oxalate Gluten-free Products

• Medium oxalate per serving
• Udi's White Sandwich Bread (1 slice)
• Nabisco Cream of Rice (1/4 cup dry)
• Envirokids Gorilla Munch (1 cup)
• Orville Redenbacher's Popcorn (1 cup)
• Mission Yellow Corn Tortillas (1)
• Tinkyada Brown Rice Spaghetti (1/2 cup cooked)
• Tolerant Foods Red Lentil Rotini (1/2 cup cooked)
• Lundberg Brown Jasmine Rice, boiled (1/2 cup)

Extremely High Oxalate foods

• Beans (Anasazi, Black/Turtle, Cannellini, Great Northern, Navy, Pink, Pinto, Red, Soy, White)
• Cactus/Nopal
• Carob
• Cocoa Powder/dark and milk chocolate
• Fruits (Apricot, Blackberries, Figs, Guava, Kiwi, Pomegranate, Rhubarb, Star Fruit/Carambola)
• Grains (Amaranth, Buckwheat, Quinoa, Teff)
• Nuts (Almonds, Cashew, Brazil, Hazelnut/filberts, Macadamia, Peanuts/Spanish Peanuts, Pine)
• Seeds (Caraway, Chia, Hemp, Poppy, Sesame)
• Herbs/Spices (Allspice, Cinnamon, Clove, Cumin, Curry Powder, Ginger, Onion Powder, Turmeric)
• Potatoes (Russet, Burbank, Idaho, Fingerling)
• Vegetables (Artichoke, Beets, Eggplant, Hearts of Palm, Jerusalem Artichokes, Okra, Plantain, Swiss chard,
• Spinach, Sweet Potato/Yam)

Guide to Lower Oxalate Substitutions 

(chart on substitutions is used by permission from: Open Original Shared Link)

From the author:

If you have ever been diagnosed with an autoimmune disease and have been trying to lower oxalate, will you participate in the development of this science by filling out a survey?

We would also like to find out whether reducing oxalate has affected your autoimmune condition.

The link to our survey is here: Open Original Shared Link

Celiac.com 10/27/2015 - In 2006, I presented a research paper called "Open Original Shared Link". At that time I was thinking about the sick children who were coming through my clinic with skin, gut and brain symptoms: that is they had eczema and itchy skin; sore tummies and constipation; and behaviour disturbances. It turned out that most of this group of children had high levels of Anti-Gliadin-Antibodies (AGA), of whom 80% got completely better when they went on a gluten-free diet. This was a landmark paper for me, and it led me to describe "Open Original Shared Link".

However, that was nearly 10 years ago! and a lot has happened since then. Perhaps most notable the publication of the consensus paper on the Open Original Shared Link. The algorithm developed to diagnose gluten sensitivity/ intolerance relies on the elimination and challenge of gluten, rather than immunologic blood tests. I have been using the AGA test in my clinic since 1989 (that is for 25 years!) and I have found it extremely useful as a diagnostic test, when it is positive. But, many people react to gluten and have negative AGA results. So I agree with the authors of the "Spectrum" paper. The basis of a gluten-sensitivity/intolerance diagnosis should be based on elimination and challenge. Importantly, prior to removing gluten from your diet, please ensure that you get the appropriate tests for celiac disease (Open Original Shared Link).

So who in the year 2015 should be suspected of having a gluten-related-illness? Well anyone who has chronic symptoms. Even if they have a diagnostic label - because they might have the wrong diagnosis. so here are the 3 steps in my gluten-free logic:

Step ONE - the premise IF:

• a) Gluten sensitivity is common: estimates show it affects over 10% of the population;
• Gluten-related illnesses are varied and have multiple symptoms: a quote from the consensus paper on the Spectrum of Gluten-Related-Disorders emphasizes this. The symptoms in gluten sensitivity may resemble those associated with celiac disease but with a prevalence of extra-intestinal symptoms, such as behavioral changes, bone or joint pain, muscle cramps, leg numbness, weight loss and chronic fatigue. Their symptoms include abdominal pain (68%); eczema and/or rash (40%); headache (35%); "foggy mind" (34%); fatigue (33%); diarrhea (33%); depression (22%); anemia (20%); numbness in the legs, arms or fingers 20%; and joint pain (11%);
• c) There is no definitive diagnostic test for gluten sensitivity: the Consensus paper goes on to say "However, currently there are no laboratory biomarkers specific for gluten sensitivity. Usually the diagnosis is based on exclusion criteria; an elimination diet of gluten-containing foods followed by an open challenge is most often used to evaluate whether health improves with the elimination or reduction of gluten from the patient’s diet";
• d) There is no harm from going on a gluten-free diet; in other words a gluten-free is healthy.

Step TWO - The logical THEN:
Then the logical conclusion is that "anyone", with "any symptoms" that are "chronic and unexplained" (that is they do not have a definite diagnosis) and "at any time" (people can develop gluten-illness at any time in their life) should be put onto a gluten-free diet for a clinical trial for three months or more.

Step THREE - The CONCLUSION:
The logical conclusion is that whatever the blood-test results, and whatever the endoscopy results, and whatever the symptoms, a beneficial response to a gluten-free diet suggests that their illness is gluten-related (some people might demand a double blind food challenge).

Comment
Up until now, most gluten/celiac doctors have dismissed the idea that their patients might be suffering from "non-celiac gluten-sensitivity" (NCGS). They have attributed their patients beneficial response to a gluten-free diet as a placebo response (all in their head!). This is clearly not the case. There is mounting evidence for this: see this research paper - Open Original Shared Link. In this paper the authors conclude: "In a cross-over trial of subjects with suspected NCGS, the severity of overall symptoms increased significantly during 1 week of intake of small amounts of gluten, compared with placebo".

The above logic means that ALL people, with ANY undiagnosed illnesses, at any TIME in their life, should be given a gluten-free trial. This is likely to have huge health benefits and wide ramifications on the management and burden of ill health on the community. Already 10% of Australians and Canadian are adopting a gluten-free diet, and 30% percent of adults in the USA are interested in avoiding or cutting down on gluten in their diets, says a survey from the NPD Group, a consumer research firm. NDP has been following gluten-free issues since 2009 and its January 2013 survey revealed the highest interest in gluten-free diets yet (reported in HuffPost - 26 Feb 2015).

It is my prediction that in another generation most people who wish to stay healthy, will choose to adopt a gluten-free diet, before they get harmed by gluten.

Celiac.com 10/16/2015 - Y Net News, under their "Health & Science" banner, published an article titled "Open Original Shared Link", on April 17, 2015 (1). ALS refers to amyotrophic lateral sclerosis, or Lou Gehrig's disease, also known as motor neuron disease. Authorship of this article is attributed to the news agency, Reuters. The article refers to a study in which the investigators identify an autoimmune dynamic in the brain (2). The Y Net News article quotes one of these investigators as warning ALS patients against experimenting with a gluten-free diet: "Patients should not be tempted to use a gluten-free diet without clear evidence for antibodies, because an unbalanced diet might harm"(1). This is the kind of advice that frequently appears in the popular media. There can be little doubt that a gluten-free can be unhealthy, just as gluten containing diets can be unhealthy. When contacted on this issue, Dr. Drory said that "Patients with ALS tend to lose weight due to symptoms of their disease and it is well known that weight loss has a negative influence on disease progression and survival. Therefore it is very important for these patients not to lose weight" (3). Although Dr. Drory did not mean to impugn the gluten-free diet for the general population, she is legitimately concerned about the longevity and health of ALS patients, so she believes that only those with positive antibody tests should try the diet, and then only under the supervision of a dietitian. Reuters, on the other hand, have not responded to my request, through Y Net News, to contact the author of this article.

While Dr. Drory's concerns are reasonable, I think that she has missed an important feature of the gluten-free diet and she puts too much faith in the connection between TG6 and ALS [an abbreviation for a recently discovered enzyme named tissue transglutaminase six] apparently believing that it will identify all ALS patients who might benefit from avoiding gluten. However, if we can judge based on those who have celiac disease, it is a diet that is more likely to increase the body mass of someone who is underweight. Dr. Drory also seems to have missed the sentiment expressed in the abstract of her own report. It says: "The data from this study indicate that, in certain cases, an ALS syndrome might be associated with autoimmunity and gluten sensitivity. Although the data are preliminary and need replication, gluten sensitivity is potentially treatable; therefore, this diagnostic challenge should not be overlooked" (1). Thus, when dealing with an otherwise irreversible and unstoppable disease, patients are cautioned not to try the diet without these marker antibodies which the authors identify as "preliminary" findings.

Dr. Drory's caution also assumes that dietitians will generally be competent to guide the ALS patient in their gluten-free diet. However, it is important to recognize that the neurological patient needs to be even more strict with the diet than a person with celiac disease, and there are many uncertainties and debates around this diet. The average dietitian may not be up to date with the application of the gluten-free diet for such conditions, or the relevant controversies, or their application. Also, the beneficial results of a gluten-free diet are widespread across so many ailments and much medical research currently lags well behind patients' positive experiences. This is what has led to the continuing debate about the frequency and importance of non-celiac gluten sensitivity. Until very recently, it was usually given no attention at all. Further, since "gluten sensitivity is potentially treatable," and the current life expectancy for an ALS patient is about 2 years, it seems irresponsible to warn patients to wait for further research results before trying a gluten-free diet.

This latter sentiment captures the essence of my current view of the gluten-free diet. Until I was diagnosed with celiac disease, more than twenty years ago, I would have ignored Dr. Drory, and subscribed to the bias inherent in the Y Net News article. Sadly, I used to dismiss people who talked about diet in the same way that I responded to those who talked about "astro travel" and Astrology. I viewed them as foolish concepts that were popular fads among drug-crazed hippies of the 1960s and 1970s, and other similarly deranged individuals. I still question many other diets, astro travel, and Astrology, but hope I do not do so with the same arrogant certitude of my youth.

You see, I experienced a startling change of perspective shortly after I was diagnosed with celiac disease. Just three days after beginning the gluten-free diet, I awoke to an altered state of consciousness. The closest I can get to describing it is that I felt somewhat like I remember feeling as a kid when I awoke on Christmas morning. I felt optimistic, hopeful, and I looked forward to the day ahead. That was a big change. I was used to waking up feeling tired, depressed, and usually with a sense of foreboding about the coming day. I also found, after about the first six months or so of avoiding gluten, that my mind was becoming sharper, I was more aware of my surroundings, and my memory seemed to improve. My reflexes also seemed quicker. My sense of balance got better and my reaction time was faster. When I looked at others, I saw that many people were similarly challenged and didn't seem to be aware of their limitations—or perhaps they had just become used to them. Thus, I now believe that many people unknowingly suffer from the myriad harms induced or facilitated by gluten consumption. I also see, given the many venues in which the diet made a difference for me, why others might be skeptical.

But how did Dr. Drory get from the notion that since gluten sensitivity is treatable, and should therefore be investigated as a potential factor in some cases of ALS, to the notion that ALS patients should be cautioned against experimenting with a gluten-free diet because it can cause weight loss? The gluten-free diet can be an effective weight loss strategy for some people. As I have mentioned in previous columns, the gluten-free diet seems to reduce the appetites of overweight individuals with celiac disease by about 400 calories per day. Equally, underweight celiac patients usually gain weight. Dr. Drory's concern about weight loss for those with ALS might be well founded if it was a universally good weight loss strategy. But it isn't. The data regarding weight loss on a gluten-free diet are only available, to my knowledge, with regard to celiac patients, where underweight patients almost always gain weight and about half of overweight patients lose weight. She also thinks that experimentation without a positive antibody test and the oversight of a dietitian might be risky. So her concerns may not be as valid as they first appear. If those ALS patients are gluten sensitive, then they might behave similarly to those with celiac disease, at least with regard to weight gain and loss. Further, how can anyone say, without trying it, that a gluten-free diet would not benefit those ALS patients who do not show TG6 antibodies?

The Reuters article goes on from there to state: "It’s also worth remembering that an association is not the same as a cause. At least one earlier study concluded that there was no association between TG6 antibodies and either neurological disease or gluten itself" (1). The preceding comment refers to a retrospective research report in which the records of patients, on a Swedish data-base, who had been diagnosed with celiac disease, were further examined for an additional diagnosis of ALS (4). This is more than a little strange, since the very study the Reuters journalist used to distinguish between associations and causality, seeks only evidence of an association between the ALS and celiac disease. The notion that correlation is not causation is valid. However, using a study that looks for a correlation between celiac disease and ALS is not a reasonable basis for differentiating between correlation and causation. Neither is it a valid example of a causal relationship.

Further, it is difficult to imagine a study design that would be less likely to reveal an association between transglutaminase TG6 and any other ailment, than one based on recorded data from a large number of patients who were diagnosed with celiac disease between 1969 and 2008. All, or almost all of these patients were diagnosed prior to the first published report of the discovery and diagnostic utility of transglutaminase 6 (5). So if one looks through records that predate the discovery of TG6 to find evidence of a connection between TG6 and any other disease, one is highly unlikely to find it.

The abstract of the study that asserts there is no association between these ailments is based on a very weak design. It also ends with the statement: "Earlier reports of a positive association may be due to surveillance bias just after celiac disease diagnosis or expedited diagnostic work-up of ALS" (4). They are so confident of their own findings that they suggest that contrary findings are either due to bias or fast, careless work. I will leave it to the reader to infer whether there is bias among the authors of this report. Additionally, the Y Net News article, by one or more journalists at the Reuters News Agency, reports that this study found no association between TG6 antibodies and ALS, even though the study in question examines data that predates the use of TG6 antibody testing. While the study in question does appear to claim that there is no connection between celiac disease and ALS, the mention of TG6 and whether there is a connection between these antibodies and ALS appears to be information added by Reuters.

Regardless of this possibly 'added' information, it really is quite a stretch to warn the public or ALS patients of the dangers of a gluten-free diet in reporting about research that has found evidence of a possible connection between ALS and gluten consumption. In a balanced report, the Reuters journalist would have mentioned the seven other research publications that have reported associations, and/or cause to suspect such associations, between gluten and ALS (5-11). It really isn't rocket science. It is just ethical, balanced reporting, which should serve as a minimum standard for an organization that is engaged in reporting the news. Since there are always at least two sides to almost any argument, both sides should at least have been acknowledged. Thus, in addition to the weak study reporting that they didn't find an association, the seven other reports of possible associations really should have been mentioned.

It would also have been informative to their readers to mention Stephen Hawking, the longest living patient who was diagnosed with ALS. Dr. Hawking is still alive and has been on a gluten-free diet for the last 40+ years (12). He had already lived well beyond the two year life expectancy predicted by his doctors when, in 1963, Hawking's ALS had progressed to the point where he had begun to choke on his food. That is when he eliminated gluten, sugar, and plant oils from his diet. He has continued to avoid gluten for all these years and has also added several vitamins and supplements to his diet. Whether any or all of these measures have made "the" life extending difference, or if it is all of these measures combined that have allowed him to continue for so long, we can't know. Nonetheless, it may be that the gluten-free diet has been a determining factor in Dr. Hawking's longevity in the context of ALS. We also don't know if he would have tested positive for TG6 back when he was first diagnosed. However, he might not still be with us if he had opted to wait for this research to emerge and be confirmed.

Since Hawking began his self-directed dietary experiment, researchers at the Royal Hallamshire Hospital in Sheffield, UK, have shown that the TG6 antibodies, while present in some celiac patients, are also found in some patients with non celiac gluten sensitivity and either neurological disease or an increased risk of developing one (5).

Others, reporting a case study, had diagnosed ALS, then identified, diagnosed, and treated co-existing celiac disease with a gluten-free diet. They then retracted their ALS diagnosis saying: "Ultimately, improvement in the patient’s symptoms following treatment for celiac disease rendered the diagnosis of ALS untenable" (6). It would appear that any improvement in ALS symptoms obviates a diagnosis of ALS. It also raises the possibility that some cases of ALS can be effectively treated with a gluten-free diet.

Similarly, in another case study report, the authors state: "ALS is a condition with relentless progression; for this reason, the simple observation of an improvement in symptoms is most pertinent in rendering the diagnosis of ALS untenable" (7). Again, the patient's ALS symptoms regressed following institution of a gluten-free diet.

Yet another report that connects ALS with autoimmunity in general states: "The significance of increased premorbid celiac disease in those with ALS, and in family members of patients with MMN [multifocal motor neuropathy] remains unclear at present."(9). Still others have offered genetic evidence of connections between gluten sensitivity and ALS (10).

Thus, the Reuters article raises an important question. Why are we seeing so many media attacks on those who are taking responsibility for their own health and experimenting with a gluten-free diet? It might come as a surprise to the Reuters journalist to learn that we humans had evolved and spread into most habitable areas of the world long before a few farmers began cultivating grains in regions of what are now known as Iraq and Iran. She/he might also be surprised to learn that we have known, for decades, that variants of wheat, rye, and barley have a deleterious impact on human neurological tissues (13, 14, 15) and that a variety of neurological ailments arise both in the context of celiac disease and non-celiac gluten sensitivity (14).

The conclusion in the abstract of the 'no relationship' study dismisses reports of opposing findings as either due to "surveillance bias" or "expedited diagnostic work-up" (4). (This latter is a euphemistic statement suggesting that the work that led to these other reports was conducted too quickly and errors resulted.) Whatever your personal view of the attitude expressed there, the greater concern may be that the media continue to identify the gluten-free diet as potentially harmful (1) while researchers and individuals experimenting with a gluten-free diet have found evidence connecting gluten sensitivity with, at least, some cases of ALS (2).

Over the years, I have heard many reasons for resisting this diet, but the one that is probably the least defensible is the assertion that it is potentially harmful. Almost any dietary regimen can be hazardous, of course, but the assertion that it might cause a harmful dietary imbalance fails to recognize that gluten has only been part of the Human experience for a very short time, in evolutionary terms. The simple fact is that we humans have spent far more of our evolutionary past eating a gluten-free diet than we have spent eating gluten. Some populations have only been eating these grains since European incursions over the last several hundred years. Some of these populations have only been eating it for less than one hundred years. Still others have been eating gluten for a few thousand years. In Israel, where Dr. Drory's study originated, grains were probably incorporated into the diet much earlier than in most of the rest of Europe, probably sometime between 15,000 and 10,000 years ago. It is difficult to imagine that after hundreds of thousands of years of eating a gluten-free diet, that avoiding gluten can pose a health hazard. The Reuters journalist appears to have another axe to grind, but I continue to wonder why we are seeing so many journalists on the attack against the gluten-free lifestyle?

The driving force behind these journalists' attacks may well be similar to the perspective that I experienced before my diagnosis with celiac disease. Perhaps they suspect, whatever their reasons, that the gluten-free diet has little or no merit, and their only concession is to grudgingly allow that it may be helpful to those with celiac disease. My suspicion is that this attitude is driven by an insecurity. We want to believe conventional wisdom that gluten grains are healthy and that our medical professionals, and the institutions in which they serve, are above reproach. Nobel Laureate, Kary Mullis, is one highly vaunted physician's voice, among many, who dismiss most diets as fads, arguing that we are omnivores whose secret of successful adaptation to a wide variety of environments is the result of our flexibility in sources of nourishment (18). Many of us want to be able to rely on our physicians. We don't want the insecurity of knowing that our medical establishment is a flawed, human institution. The self-directed experimentation with a gluten-free diet poses a threat to that credibility, and hence, our sense of security, especially when it results in improved health. We don't want to feel the resulting uncertainty that comes from doubting the medical cornerstone of our civilization.

It is not long ago that Don Wiss, myself, and others, argued extensively with physicians and researchers who insisted that the rate of celiac disease in the USA was variously one in 12,000 persons or one in 25,000 people. Sometimes these discussions became quite heated. Some of the people posting to these newsgroups were asking for suggestions for how they might proceed with various health complaints. When Don or I saw a post asking about symptoms that had been reported in the peer reviewed literature, in association with untreated celiac disease, we suggested a trial of a gluten-free diet. Some of the physicians and researchers contacted these individuals privately, saying things to discredit us. It seems doubtful that they would not have said such things where they were likely to be held accountable for what they said. Their reactions, I suspect, were driven by a sense of feeling threatened. As soon as controlled testing was done, it became clear that the rate of celiac disease, among Americans, is at least 1 in 133 Americans, and many of those individuals we advised to try a gluten-free diet might well have had celiac disease. Yet many journalists, physicians, and researchers have a great deal invested in the current status quo. Any threat to the established order is likely to incite the ire of many members of these groups.

Thus, while others may consider it prudent to await the end of the current debate about ALS and a gluten-free diet, the ALS patient might be better advised to take dietary steps to ensure against weight loss, while trying a strict gluten-free diet. I know what I would do if were diagnosed with ALS...on second thought, since I've been gluten-free for more than twenty years, maybe I won't ever be diagnosed with ALS. I will continue to hope. In the meantime, Thomas Kuhn clearly outlined this stage of acceptance of new ideas in science (19). We appear to be in the "denial" stage, which is the last one before we can expect the emergence of widespread claims that 'we knew it all along'. If so, then broad acceptance is in the offing, and these nay-saying journalists will move on to some other controversial new discovery, and we can be spared the condescending remarks suggesting that the gluten-free diet is a mere placebo and a 'fad diet' for most of those who follow it.

Sources:

1. Open Original Shared Link
2. Gadoth A, Nefussy B, Bleiberg M, Klein T, Artman I, Drory VE. Transglutaminase 6 Antibodies in the Serum of Patients With Amyotrophic Lateral Sclerosis. JAMA Neurol. 2015 Apr 13.
3. Drory V. Personal communication via email
4. Ludvigsson JF, Mariosa D, Lebwohl B, Fang F. No association between biopsy-verified celiac disease and subsequent amyotrophic lateral sclerosis--a population-based cohort study. Eur J Neurol. 2014 Jul;21(7):976-82.
5. Hadjivassiliou M, Aeschlimann P, Strigun A, Sanders D, Woodroofe N, Aeschlimann D. Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Ann Neurol 2008;64:332-343
6. Brown KJ, Jewells V, Herfarth H, Castillo M. White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. AJNR Am J Neuroradiol. 2010 May;31(5):880-1.
7. Turner MR, Chohan G, Quaghebeur G, Greenhall RC, Hadjivassiliou M, Talbot K. A case of celiac disease mimicking amyotrophic lateral sclerosis. Nat Clin Pract Neurol. 2007 Oct;3(10):581-4.
8. Ihara M, Makino F, Sawada H, Mezaki T, Mizutani K, Nakase H, Matsui M, Tomimoto H, Shimohama S. Gluten sensitivity in Japanese patients with adult-onset cerebellar ataxia. Intern Med. 2006;45(3):135-40.
9. Turner MR, Goldacre R, Ramagopalan S, Talbot K, Goldacre MJ. Autoimmune
10. disease preceding amyotrophic lateral sclerosis: an epidemiologic study. Neurology. 2013 Oct 1;81(14):1222-5.
11. Auburger G, Gispert S, Lahut S, Omür O, Damrath E, Heck M, BaÅŸak N. 12q24
12. locus association with type 1 diabetes: SH2B3 or ATXN2? World J Diabetes. 2014
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15. R, Mazzini L. Coeliac disease mimicking Amyotrophic Lateral Sclerosis. Amyotroph
16. Lateral Scler Frontotemporal Degener. 2015 Feb 3:1-3.
17. Hawking J. Travelling to Infinity: My Life with Stephen. Alma Books, Richmond, UK. 2014.