One cardiologist thinks so, but scientists don't agree
Wikimedia Commons/ Bluemoose
No one is certain why there's been a rise in celiac disease.
If you’ve heard of author William Davis, a cardiologist from Milwaukee, it’s probably because of his popular book Wheat Belly, which extols the virtues of a wheat-free diet. After Davis stopped eating wheat, he claims that a host of ailments including diabetes, mood swings, joint pain, and acid reflux subsided. Davis has claimed that the rise in celiac disease, an aversion to wheat gluten, in the past 20 years is largely due to the fact that new varieties of wheat were introduced, intended to increase grain yields. But this week a research chemist with the U.S. Department of Agriculture released findings of a study refuting this claim.
According to NPR, the chemist, Donald Kasarda, gluten levels in wheat have remained the same over time, and celiac expert Daniel Leffler agrees that the cause of the disease is largely due to a series of factors.
"I don't think there's one evil food causing the problem in our society," Leffler told NPR. "There's good evidence that the vast majority of people actually do just fine with wheat."
So while celiac disease is up, to about 1 percent of the population, there’s no consensus as to why this is the case. Whether it’s because of antibiotic use early in life, the so-called "hygiene hypothesis," which claims that our surroundings are so clean that our bodies find non-toxic things, like peanuts, to become allergic to, or whether it’s a different protein in wheat entirely that makes people ill, it’ll most likely be a long time before we get to the bottom of gluten intolerance.
The Horrors of Gluten-Free Food
It continues to happen: I run into people who say to me “I follow the Wheat Belly lifestyle. I eat gluten-free!” When I ask them what that means, they tell me that they only eat gluten-free bread, pasta, pizza, cookies, etc.
I’m not entirely sure why this misinterpretation of the Wheat Belly message is so common. Let’s talk about this important distinction, as being gluten-free can be an absolute health and weight disaster, unlike the magnificent health and weight loss we enjoy on the Wheat Belly lifestyle when done right.
It’s perfectly fine to be gluten-free, i.e., avoiding wheat, rye, and barley that contains the gliadin protein within gluten responsible for celiac disease and other gliadin-induced reactions. People with celiac disease often argue “But I have to be gluten-free!” But the problem comes when food manufacturers try to get a slice of the action and recreate gluten-free breads, rolls, pizza crust etc. using one or more of four ingredients:
Wheat and related grains raise blood sugar to high levels, higher than table sugar, due to the unique digestibility of amylopectin A. Very few foods raise blood sugar higher than wheat. So what foods raise blood sugar even higher than sugar, higher than wheat? Yup: cornstarch, rice flour, tapioca starch, and potato flour. Eat any gluten-free foods made of these ingredients and you will experience sky-high blood sugars. Do this repeatedly and you develop insulin resistance, pre-diabetes, and type 2 diabetes. But it doesn’t end there.
What else do gluten-free replacement ingredients do to the hapless consumer who eats them thinking they are healthy and safe? Plenty. Among the effects of gluten-free foods are:
- Glycation reactions—High blood glucose alters the proteins of the body via a process called glycation, an irreversible reaction that essentially generates cellular debris. While you can detect glycation via the common HbA1c test (glycated hemoglobin), you won’t detect glycation of the proteins in the lenses of your eyes until they accumulate as cataracts, or in the kidneys until you develop kidney failure, or the heart as small glycated LDL particles accumulate as atherosclerotic plaque and heart attack, or in the brain that contributes to Alzheimer’s dementia.
- Zein corn protein mimics gliadin—The zein protein residues in cornstarch, while present in only small quantities, can act like gliadin in people with celiac disease and gliadin sensitivities (e.g., cerebellar ataxia, peripheral neuropathy, Hashimoto’s thyroiditis, gastric autoimmune parietal cell loss). In other words, gluten-free foods can reactivate celiac disease and other conditions.
- Wheat germ agglutinin in rice—Although it’s in rice, it’s still called “wheat” germ agglutinin because the structure is identical to that in wheat. While also present in small quantities, there is enough to disrupt the intestinal lining in celiac-like ways (direct toxicity, rather than then indirect immune-mediated path of celiac).
- Weight gain—The sky-high blood sugars generated by gluten-free ingredients also provoke sky-high insulin that, in turn, leads to insulin resistance that, in turn, causes visceral inflammatory fat to accumulate. This is why people who consume gluten-free foods grow a “spare tire” around their waist that reflects accumulation of fat around abdominal organs and heart.
- Ignite inflammation—High insulin levels and visceral fat accumulation cause inflammation to increase, trackable as increased C-reactive protein, Il-2, TNF-alpha and other measures. Inflammation underlies numerous health conditions such as heart disease, cancer, and dementia.
- Disrupt hormonal status—As visceral fat accumulates, a variety of hormonal disruptions develop that cause, for instance, men’s breasts to enlarge and their testosterone to drop. It causes women to develop higher estrogen levels that correlate with increased risk for breast cancer. In women with PCOS, testosterone rises, blood sugar and blood pressure rise, and infertility develops.
- Dysbiosis and small intestinal bacterial overgrowth(SIBO)—Highly-refined carbohydrate-rich flours like gluten-free flours are like putting a trail of breadcrumbs out for ducks: they will follow the path of crumbs. Consuming the highly-digestible carbs of gluten-free foods is a setup for inviting colonic microbes up into the small intestine, the situation that defines SIBO. It also changes the composition of bowel flora species in unhealthy ways.
- Tooth decay—The amylopectin A carbohydrates of some gluten-free flours such as cornstarch hugely amplify potential for tooth decay, just as wheat does.
You get the idea? Gluten-free foods made with common gluten-free flours shouldn’t even be sold. Or at least should be recognized as no better than eating sugar out of a bowl. Nobody on the Wheat Belly lifestyle should be eating such foods with their disastrous consequences.
Really: Get the Wheat Belly lifestyle right and you will be rewarded with astounding health, weight loss, and youthfulness.
There’s more to wheat than celiac disease
I want to take this issue head on, since popular “wisdom” is that problems with consumption of wheat and related grains begins and ends with celiac disease. The Wheat Lobby, for instance, frequently argues that, if you do not have celiac disease, you have no business avoiding wheat and related grains.
Defenders of wheat, such as those cited in this New York Times article, argue that celiac disease affects 1% of the human population, but that the other 99% of people not only can consume wheat with impunity, but can actually do so and obtain health benefits due to fiber and B vitamin content. They say that eliminating wheat and grains is therefore unnecessary, unhealthy, even dangerous.
Let’s therefore examine what health conditions can develop in the 99% of people who do not have celiac disease:
- Cerebellar ataxia–This is a condition in which antibodies to gliadin (though different than those occurring in celiac disease) damage the cerebellum, the part of the brain responsible for coordination, bladder control, and other bodily functions. People with this condition develop progressive incoordination, begin to stumble, lose control over their bladder, then end up in a wheelchair and experience premature death. Stop eating wheat and related grains and progression of the disease stops, and can partially reverse (only partially, since brain and nervous system tissue are poor at healing).
- Peripheral neuropathy–While most cases of peripheral neuropathy, or damage to the nerves to the legs and organs (e.g., stomach, resulting in a non-functional stomach or gastroparesis) are due to longstanding diabetes, of the remaining cases in people without diabetes, 50% of cases of non-diabetic peripheral neuropathy are caused by an autoimmune reaction triggered by gliadin with high levels anti-gliadin antibody. As with cerebellar ataxia, the incoordination, leg pain, even gastroparesis reverse, sometimes entirely, with wheat/grain elimination.
- Iron deficiency anemia–The phytates of wheat and grains reduce iron absorption by up to 90%, making wheat/grain consumption the second most common cause of iron deficiency anemia in the world after blood loss. Get rid of the wheat/grains, iron deficiency reverses.
- Gynecomastia–This is the “man boob” issue–enlarged breasts in males, embarrassing, disfiguring, and now responsible for male breast reduction surgery being among the most common elective surgeries in men. Recall that the A5 pentapeptide from partial digestion of the gliadin protein is a powerful stimulant of pituitary prolactin release (pro- + lactin = increases lactation) remove wheat and grains, removing all sources of gliadin, and prolactin levels drop and breast size recedes. Even better, lose the wheat and grains, lose the amylopectin A responsible for high blood sugars and insulin, inflammatory belly fat recedes, the activity of the enzyme aromatase in belly fat drops, and testosterone levels increase, estrogen levels drop in males (since overactive aromatase in belly fat converts male testosterone to estrogen).
- Vitamin B12 deficiency–Absorption of vitamin B12, vital for numerous body processes, such as production of blood cells and nervous system function, is impaired because wheat and grains trigger an autoimmune response against the parietal cells of the stomach that produce a protein (“intrinsic factor”) required for B12 absorption. Damage to parietal cells impairs intrinsic factor production, and B12 is not absorbed. This reverses with wheat/grain elimination and is accompanied by a rise in B12 levels and reversal of pernicious or macrocytic anemia.
- Hashimoto’s thyroiditis–Up to 50% of people with this autoimmune thyroid condition have high antibody levels against the gliadin protein of wheat and related grains. Remove wheat/grains and autoimmune thyroid inflammation subsides (particularly when combined with vitamin D and cultivation of healthy bowel flora) but, unfortunately, is usually not accompanied by full restoration of thyroid hormone production, meaning thyroid hormones, T4 and T3, may still need to be taken to obtain normal thyroid status.
- Type 1 diabetes–The evidence is quite clear: many, if not most, cases of autoimmune destruction of pancreatic beta cells that produce insulin are initiated by the gliadin protein of wheat and related grains (as well as the zein protein of corn and the casein beta A1 protein of dairy, though less commonly), borne out by both the human as well as the experience in two experimental models. As with Hashimoto’s destruction of the thyroid, pancreatic beta cells are very poor at recovering and the great majority of type 1 diabetics are insulin-dependent diabetics for life.
- Rheumatoid arthritis–Rheumatoid arthritis serves as the prototypical autoimmune disease, in this case an autoimmune attack against the joints of the body. The autoimmune process is initiated by intact forms of gliadin protein, the pathway elegantly worked out by Dr. Alessio Fasano and colleagues while at the University of Maryland.
- Hyperglycemia/type 2 diabetes–The formula to make a person diabetic is simple: eat foods that raise blood sugar and insulin, resistance to insulin develops, visceral fat grows that adds to inflammation that further blocks insulin, fatty liver develops (due to liver de novo lipogenesis) that also further blocks insulin, and blood sugars rise to the diabetic range. The process is therefore started by foods that raise blood sugar the highest. What foods have the highest glycemic index (and glycemic loads) of all foods? Grains–even more so than white table sugar. Follow a diet dominated or rich in grains, white or whole, and blood sugars go up many times per day (since there is virtually no difference from a blood sugar perspective): a perfect setup for type 2 diabetes. Get rid of all wheat and grains and the entire cycle unwinds.
- Eczema, psoriasis, seborrhea, rosacea–These common autoimmune skin conditions that affect millions of people occur in people without celiac disease, and recede or disappear in the majority with wheat/grain elimination.
- Paranoia of schizophrenia, mania of bipolar illness, depression–A substantial subset of people with each of these conditions experience a reduction in symptoms with wheat/grain elimination. Schizophrenics will not be cured, but have reduced paranoia, reduced auditory hallucinations (hearing voices), and improved capacity for social engagement. The people most likely to respond to wheat/grain elimination tend to be the people with high antibodies to gliadin, but there are many who do not have such antibodies who also improve, likely due to the mind- and behavior-altering effects of removing gliadin-derived opioid peptides.
I could go on, as there are literally hundreds of other conditions caused by consumption of wheat and grains in people without celiac disease, all documented in the scientific literature (many references listed in the Wheat Belly Total Health book)—it is not a short list. You can begin to appreciate how patently absurd this “gluten-free is only for people with celiac disease” argument truly is. Wheat and related grains (especially rye, barley, and corn) have far-ranging effects on the brain, thyroid, skin, airways and sinuses, joints, pancreas, breasts, stomach, etc. not just the small intestine. Understand this basic principle, recognize that the Wheat Lobby is defending a flawed collection of food products with misleading smokescreens—reminiscent of the tactics used by Big Tobacco a few years back to defend cigarettes—and you have found the key to an astoundingly powerful return to health: eat no wheat or grains.
Debunking 4 Big Myths About Celiac Disease
For so many of us, the internet is our lifeline, giving us access to gluten-free recipes, and connecting us with others who share our experiences. Alongside this wealth of information, however, comes a wealth of misinformation.
It’s no surprise that myths about celiac disease circulate on the web. These myths, however, leave people to make their own best guesses at how this information applies to their lives.
The Beyond Celiac team works with researchers from around the world and to keep on top of the latest celiac research to hit medical journals. Here, we identify four common research myths that are currently circulating.
1. Myth: Wheat breeding has increased the prevalence of celiac disease.
Researchers don’t know why celiac disease is on the rise. What they do know is that wheat breeding is most likely not responsible for it. In 2013, celiac disease expert Donald Kasarda, PhD, released study results that showed that wheat breeding does not result in additional gluten protein in the finished product.
To determine this, Kasarda studied data on wheat from the 20th and 21st centuries. He found that wheat breeding did not increase the content of gluten in wheat. What he did find, however, is that there has been an increased use of “vital gluten” in foods. This is a concentrated gluten protein that can be added to make products fluffier and give them more elasticity.
While this is not a result of wheat breeding, the rise in celiac disease coincided with the rise in the use of additional vital gluten. Kasarda emphasizes that more research is needed, and while vital gluten is found in more products, it still is not a major part of the average total gluten intake resulting from intake of wheat flour-based products. Ultimately, researchers are still looking for answers to the question of why celiac disease is more common today.
2. Myth: Delaying gluten introduction in a child’s diet can prevent celiac disease.
In 2015, a team of researchers examined 15 studies conducted on this topic. What they found was that children who were given gluten for the first time after six months of age had a 25 percent higher chance of developing celiac disease. Currently, pediatric recommendations say that gluten introduction should occur between four and six months of age.
In a Beyond Celiac interview with expert Dr. Stefano Guandalini, he suggested that the best window may be between five and six months of age, and that there’s no scientific evidence that early gluten introduction (adding gluten to the diet at or before three months of age) increases the chances of preventing celiac disease.
3. Myth: Breastfeeding can prevent celiac disease.
Breastfeeding is recommended by doctors over formula-feeding infants for a variety of health reasons. Preventing celiac disease, however, is not one of them.
In that 2015 study review, researchers found that breastfeeding vs. not breastfeeding played no role in the development of celiac disease. While it may not prevent celiac disease, breastfeeding is still recommended by doctors for the host of benefits it provides to mothers and their babies.
4. Myth: Clinical trials to study new celiac disease treatments are unnecessary because the gluten-free diet is the cure.
The gluten-free diet is quite literally a life-saver for people with celiac disease, but it is by no means a cure. According to Dr. Joseph Murray of the Mayo Clinic, up to 70 percent of people with celiac disease continue to be exposed to gluten, despite their best attempts to remain strictly gluten-free. The evidence in the research is clear: the gluten-free diet alone is not enough.
There are several clinical trials in progress that are seeking to either supplement or replace the gluten-free diet. While these advances are extremely exciting, it’s important to know that other research is just as important. While the involvement of people with celiac disease is critical for drug trials, participation is still needed in other areas of research such as: developing new blood tests or other diagnostic tools, or learning more about symptoms and associated conditions.
Opportunities to participate may include surveys, focus groups and other information-sharing to help researchers better understand a variety of areas associated with living with celiac disease.
Sorting through the myths and facts can feel daunting, especially when you are newly diagnosed with celiac disease. Beyond Celiac shares credible, evidence-based information regularly. Don’t miss any of the research news by signing up for the Beyond Celiac research newsletter.
Alice Bast is the CEO of Beyond Celiac, the national organization working on behalf of the celiac patient community. Visit Beyond Celiac to learn more.
There are more than 300 reported symptoms of celiac disease, according to Beyond Celiac that vary from person to person. The most common include:
- Abdominal bleeding
- Chronic diarrhea
- Stomach pain
- Lactose intolerance
In young children and infants, additional symptoms can include:
- Failure to thrive
- Unexplained weight loss
- Slowed growth/delayed puberty
- Irritability or change in mood
- Stained teeth
Staying Healthy in the New Year with Celiac Disease
Every New Year begins with the best of intentions. Read on for specialized info for those on the gluten-free diet to take your health to the next level in 2015 (plus tips to help these changes stick!)
Maximize Your Health with Naturally Gluten-Free Foods
There’s no need for expensive gluten-free health products that boast claims that seem too good to be true. Take advantage of the positives of the celiac way of life by utilizing naturally gluten-free foods to maximize your health:
Rotate your whole grains: the vitamin and mineral content of each grain varies. If your diet is mostly full of the common rice, corn, and potato-based gluten-free products, your body keeps getting the same nutrients over and over (and is missing out on some amazing super-grains!). Also be sure to choose grain-based products that are LABELED gluten-free to avoid naturally GF foods that are potentially cross-contaminated with wheat, barley or rye (read more about this). A sample day maximizing GF grains might look like this:
- Breakfast: buckwheat (kasha) and oats hot cereal served with nuts, berries, and a dollop of yogurt
- Lunch: mixed greens salad with white beans, cooked quinoa and millet
- Dinner: broiled salmon and sauteed kale served with amaranth and corn flatbread
- Find more easy nutritious recipes HERE!
Institute Meatless Mondays and Fatty Fish Fridays:The American diet often relies too heavily on animal fats and proteins, which means that in the process we are missing out on the heart-healthy benefits of plant proteins and fats. Plant-based proteins (i.e. beans and legumes, including soy) deliver great omega-3 and omega-6 fatty acids, are low in saturated fat, naturally contain NO cholesterol, and may prevent many chronic illnesses. To further boost health, studies show that just two servings of fatty fish per week deliver essential fatty acids that calm inflammation in the body, something that those with celiac disease greatly need.
Get at least one leafy green per day: Dark leafy greens are a beautiful gift from nature. Underneath the green color is actually a plethora of other phytochemicals like those found in orange, red, and purple vegetables. One serving per day of kale, chard, spinach, or mustard greens will give you a boost of vitamins A, C, K, and folate to help combat the oxidative stress of daily life, plus many essential minerals. Maximize vitamin and mineral absorption by lightly cooking greens and serving with a fat source, such as sauteed in olive oil. You can also enjoy them in a salad for great texture or add them to a smoothie without any change in flavor (even your kids won’t notice!).
Vary your cooking oils and salad dressings: Similar to the different nutrient contents in grains, the properties and benefits of different fats have richly diverse benefits for the body. Did you know that every cell in our body is composed of fatty acids? To help improve the health of your skin, intestines, and cardiovascular system, keep several different oils on-hand for both hot and cold dishes. Flaxseed, hemp, pumpkin seed, and walnut oils are too delicate for heat but add wonderful flavors to salads and other cold dishes. Olive, grapeseed and sesame oil are appropriate for quick sauteeing, and coconut, avocado, safflower, and canola oils are stable for longer frying and baking. When varying your sources of fat from the typical vegetable oil and butter, you are certain to receive a wonderful balance of monounsaturated, polyunsaturated, and saturated fats in the best proportions.
Weight Management after Diagnosis
If your New Year’s Resolution includes a weight goal, keep the following information in mind to make a realistic and healthy plan:
- Weight gain is typical after diagnosis of celiac disease, even if you were already considered normal or overweight. The food you were eating was only partially absorbed prior to diagnosis, and it may continue to be for several months on the gluten-free diet until intestinal villi fully heal. In this sense, weight gain is a sign that the body is healing well and you’re succeeding at the gluten-free diet.
- Portion sizes and overall intake may need to be reduced because of the above appetite before diagnosis may have been higher than normal since nutritional needs were not being met. This can be an unpleasant adjustment that needs to be made (in addition to the huge life change of eliminating gluten!). Focus on the above health-maximizing tips and do not rely heavily on packaged gluten-free products to simultaneously prevent weight gain and improve your health.
- If you were underweight at diagnosis and weight gain does not begin after a couple months, or it starts but then stalls before returning to normal, consult your gastroenterologist for more workup and a registered dietitian for diet counseling. The most common cause of continued malabsorption is gluten exposure. Other common causes of malabsorption on the GF diet include: small-intestinal bacterial overgrowth (SIBO), chronic diarrhea, and colitis (read more about poorly responsive celiac disease)
- While weight should return to normal as the intestines heal, some may benefit from weight-gain techniques to speed up the healing process if they are grossly underweight at the time of diagnosis. This can be especially true for children whose growth and development has been stunted, or who are averse to eating from chronically negative symptoms after eating.
- Typically, it is not advised to limit a child’s diet calorically until they return to their usual growth curve, even if growth or intake seem to be extreme. Consult a pediatrician and/or a registered dietitian specialized in pediatrics to help ensure that your celiac child’s growth is headed on the right track after diagnosis.
Weight Management in Absence of Celiac Disease
- The gluten-free diet is not a good weight-loss diet, despite what you’re hearing from celebrities.
- Nothing about gluten itself is “fattening” or “high in calories”. No credible research exists that proves gluten or wheat are responsible for overweight or obesity in America.
- Substituting common grain-based foods (bread, pasta, baked goods) with gluten-free processed foods typically leads to weight gain. This is because gluten-free substitutes are frequently higher in sugar, fat, and calories in order to mimic the texture of gluten, and less filling because they are often lower in fiber than their gluten-containing counterparts.
- There is not enough scientific research regarding non-celiac gluten sensitivity (NCGS) to know how a gluten-free diet effects weight in NCGS.
Conquer the “New Years Resolution” Phenomenon
Make positive goals rather than negative ones. Behavior is most successfully changed when, instead of just eliminating something, an old behavior is substituted with a new one:
Start small and realistic drastic changes rarely stick!
Get back on the wagon no matter what month of the year the calendar says. Behaviors change with practice and with time don’t expect yourself to change overnight, and don’t see yourself as a failure if there are ups and downs in the process.
Enlist the help of others changes stick best when not done alone. For individualized and expert help, find a registered dietitian in the CDF Healthcare Practitioner Directory!
Can a Gluten-Free Diet Help With Vitiligo?
Celiac disease and vitiligo, a skin disorder, are both linked to autoimmune diseases and a gluten-free diet could be beneficial in helping treat both.
Vitiligo is a skin condition that causes skin to lose its natural color, causing patches of lighter skin to appear. The condition impacts about 1 percent of the world’s population, and 2 to 5 million people in the United States.
According to the American Academy of Dermatology, vitiligo develops when melanocytes, the cells that give the skin and hair color, die. It is not fully known why the cells die, though non-segmental vitiligo is believed to be an autoimmune disease. Though vitiligo occasionally causes pain or itchiness on the skin, it typically does not have other symptoms. Several treatment options are available, including light therapy, topical medicine and sometimes surgery.
“We know that patients with autoimmune conditions are generally at higher risk of developing certain other autoimmune conditions, and a few small studies have found vitiligo patients to have a slightly higher risk of developing celiac disease compared to the normal population,” said Dr. Kristina Liu, director of the Vitiligo Clinic at Brigham and Women’s Hospital.
According to Mercola , a gluten-free diet could cause vitiligo to improve.
“Wheat is one of the grains in many of the processed foods at your grocery store that interferes with a healthy complexion and contributes to psoriasis and eczema outbreaks. Proteins in wheat are responsible for inflammation and changes to your gastrointestinal tract, nervous system and cardiovascular system.”
Acne, atopic dermatitis, psoriasis, eczema and vitiligo may be exacerbated by gluten in the diet, particularly to those who are gluten intolerant. According to Mercola, in a case report, a 22-year-old patient was placed on a gluten-free diet after undergoing medical therapy for vitiligo without success. “Partial, but rapid repigmentation occurred in the first month and stabilized after four months of remaining gluten-free.”
Dr. Alessio Fasano, a world-renowned expert on celiac disease and gluten sensitivity at Mass General Hospital for Children and director of the Center for Celiac Research, said it is not common to see patients with celiac disease also affected by vitiligo. “However, as with other chronic inflammatory diseases, there have been descriptions of this co-morbidity of vitiligo with celiac disease,” Fasano said.
The component found in wheat has been linked to inflammation, which can trigger the immune system to become active and start attacking your melanocytes, this Mercola article explains.
Since vitiligo and celiac disease come from the same family of autoimmune disorders (there are 14 known genes associated with vitiligo, and 13 of them have been found to be a component in celiac disease too), avoiding gluten may be beneficial to treating both.
Fasano said medical experts don’t know for sure if consuming gluten exacerbates vitiligo symptoms. “There have been several anecdotal reports suggesting that cross-contamination with gluten can ignite both gastrointestinal symptoms and make vitiligo worse in people affected by both diseases,” he said.
Liu said a gluten-free diet is a “reasonable” option for those struggling with autoimmune conditions. “There has a few case reports of patients with vitiligo and celiac disease improving when they adhered to a strict gluten-free diet,” she said. “I think it’s reasonable for patients who have celiac disease, which was diagnosed by a physician, to adhere to a gluten-free diet, since this would be very beneficial for their celiac disease, and may be helpful with vitiligo if they also have this condition.”
Most medical experts agree that there has not been enough research done to determine whether a gluten-free diet can help with vitiligo. However, some small studies and anecdotal reports imply that it can help. Overall, in a patient with celiac, vitiligo or both, a healthy and balanced diet is essential.
“Just as in many other autoimmune diseases, it is intuitive that a nutritious, balanced diet that maintains the gut microbiome as a healthy ecosystem may mitigate the inflammatory process that characterizes this autoimmune process in vitiligo,” Fasano said.
Learn more about the health and medical experts who who provide you with the cutting-edge resources, tools, news, and more on Gluten-Free Living.
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Are Changes in Wheat Responsible for the Rise in Celiac Disease? - Recipes
Here, I present my assessment of celiac disease in relation to cereal grains. What I have to say is based on many years of research in the area of gluten proteins as they relate to celiac disease, but because of the complexity of the subject, I do not claim definitive knowledge. My conclusions do not necessarily represent those of the Agricultural Research Service, United States Department of Agriculture (USDA), and are not intended to define USDA policy. There is much to be learned about celiac disease and some of my conclusions based on current knowledge may be modified as new information develops. In other words, some things I say here might turn out to be incorrect. Finally, I am a research chemist, not a physician, and do not intend this essay to be taken as medical advice in any legal sense.
Celiac disease (coeliac is the usual spelling in Europe and Australia) is a condition that may develop in certain genetically susceptible individuals. People with celiac disease cannot eat wheat, rye, or barley. Proteins in these grains (and peptides derived from the proteins during digestion) initiate pathophysiological processes that may eventually lead to severe damage to the absorptive epithelium lining the small intestine. It appears likely that celiac disease is initiated by a mechanism involving immune response, but this has not been proved beyond any question. Certainly, immune reactions become involved after initiation.
Because almost all nutrients, vitamins, minerals, amino acids, carbohydrates, and so on are absorbed by way of the small intestine, malabsorption resulting from damage to the absorptive lining of the small intestine can have wide ranging consequences weight loss, osteoporosis, neuropathy, and so on. There is a wide range in response among those with celiac disease-some may have only minimal changes in the intestinal epithelium and no obvious symptoms, others may have severe damage to the lining of the intestine and severe symptoms. Although poor digestion of food usually leads to diarrhea, one of the most common symptoms in celiac disease, patients presenting with constipation have been reported.
Although there is a definite genetic component, celiac disease is apparently a multigene disease, and its inheritance is not completely understood. It has been strongly associated with European populations and may be rare in African blacks or Asians of Chinese or Japanese descent. There is a strong correlation with certain histocompatibility antigens, but some people with the suspect antigens show no evidence of celiac disease.
Although some people manifest evidence of celiac disease in the first year of life shortly after the introduction of gluten into the diet, others experience the onset of disease manifestations later in life-even very late in life. Consequently, it has been hypothesized that some environmental factor is likely to be involved in triggering the disease. Candidates for this environmental factor are viral infection, parasite infection (Giardia?, Cryptosporidium? Eimeria?), surgery, childbirth, even the stress of giving up smoking-these suggestions are highly speculative.
The manifestations of celiac disease are initiated (and re-initiated) in susceptible individuals upon eating wheat, rye, or barley, or any products from these grains that contain the main storage proteins of these grains. Both the proteins themselves and relatively small peptides derived from the proteins by enzymatic digestion are active in celiac disease. Accordingly, testing for intact proteins rather than peptides derived from then will often be ineffective. Celiac disease may be signalled by the presence of antibodies to gliadins or to endomysium in the blood serum and there are a number of commercial testing centers that provide testing for these antibodies. These tests are valuable, but do not provide complete certainty-either in indicating celiac disease or in indicating its absence.
The presence of antigliadin or anti-endomysium antibodies will frequently result in a recommendation by the diagnosing physician to proceed to the most generally accepted test, intestinal biopsy. In severe cases, the biopsy will show mucosal damage, indicated especially by a flattening of the surface and loss of villous structure. Even this latter test is not entirely specific. A flattened mucosa may be the consequence of a few other diseases and damage may be patchy. The tiny tissue sample excised from the intestine in the biopsy procedure might by chance be taken from a relatively normal patch. To eliminate false negative histological results, the latest recommendation is to obtain 4-5 biopsies from different spots in the small intestine. The earliest stages of the disease may be subtle, perhaps indicated only by lymphocyte infiltration of the epithelium.
Nevertheless, the finding of a flattened mucosa by way of the biopsy, followed by a marked improvement in symptoms and healing of the intestine upon initiation of a wheat, rye, and barley free diet are a pretty good indication of celiac disease. Because antibody levels decline and the intestinal mucosa recovers on such a diet, it is best for tests to be carried out before the potential celiac patient initiates the appropriate diet, thereby making testing impossible or difficult without a new challenge. This is especially so because the time for a challenge to take effect may vary considerably from person-to-person and too short a challenge might fail to bring about changes sufficient for diagnosis.
The only plants demonstrated to have proteins that damage the small intestines of people with celiac disease are those from wheat, rye, and barley, (and the man-made wheat-rye cross called triticale). Until recently, oats have been considered harmful on the basis of early studies. Several recent studies of very high quality involving testing approaches that were not available to earlier workers, indicate that oats are not harmful to celiac patients or to those with dermatitis herpetiformis, but these findings have not been accepted by all physicians. There is also a practical problem with oats in that they tend to be grown in rotation with wheat or in nearby fields, the same machinery and storage bins might be used for both. Consequently, oats can be contaminated with small amounts of wheat.
Wheat, rye, and barley are members of the grass family and are quite closely related to one another according to various schemes of plant classification (taxonomy). However, not all members of the grass family have proteins capable of damaging the intestines of celiac patients. Rice and corn, for example, are apparently harmless.
Many other grains have not been subjected to controlled testing or to the same scrutiny as wheat, rye, barley, oats, rice, and corn in relation to celiac disease. If we accept corn and rice as safe, then members of the grass family that are more closely related to these species (on the basis of taxonomy) than to wheat are likely to be safe. Such grasses include sorghum, millet, teff, ragi, and Job's tears, which appear to be reasonably closely related to corn, and wild rice, which is closely related to cultivated rice. In some cases, there are protein structure studies that support of this conclusion, although the studies are not sufficiently complete to provide more than guidance. Scientifically controlled feeding studies with celiac patients would provide a better answer. However, such studies are not likely to be carried out in the forseeable future because of high costs and the difficulty of obtaining patient participation (such studies would be very likely to involve intestinal biopsy and patients are reluctant to undergo challenge once they are well).
The scientific name for bread wheat is Triticum aestivum--the first part of the name defines the genus (Triticum) and the second part, the species (aestivum). Species falling in the genus Triticum are almost certain to be harmful to celiac patients. Grain proteins of these species include the various types characteristic of the gluten proteins found in bread wheats (including the alpha-gliadins) that cause damage to the small intestine in celiac disease. Some Triticum species of current concern include Triticum spelta (common names include spelt or spelta), Triticum polonicum (common names include Polish wheat, and, recently, Kamut), and Triticum monococcum (common names include einkorn and small spelt). I recommend that celiac patients avoid grain from these species.
Rye (Secale cereale) and barley (Hordeum vulgare) are also toxic in celiac disease even though these two species are less closely related to bread wheat than spelta and Kamut. They belong to different genera, Secale and Hordeum, respectively, and lack alpha-gliadins, which may be an especially toxic fraction. There have been anecdotal reports suggesting a lack of toxicity in celiac disease for spelta and Kamut. Controlled tests would be necessary to draw a firm conclusion, but I don't consider anecdotal reports as reliable for the following reasons.
The diagnosis, sometimes self-diagnosis, of celiac disease is occasionally made without benefit of reasonably rigorous medical or clinical tests, especially intestinal biopsy. Individuals who are "diagnosed" in this way without rigorous testing may not actually have celiac disease. Claims that particular foods cause this latter group no problems in relation to their celiac disease could cause confusion.
Furthermore, celiac patients who report no problems in the short run with spelta or Kamut will very likely relapse later. There is now adequate evidence that when celiac patients on a "gluten-free" diet (that is, a diet free of any proteins or peptides from wheat, rye, barley, and oats) have wheat reintroduced to their diets, times-to-relapse vary enormously among individuals, ranging from hours to months, or even years. And this is for wheat, presumably the most toxic of all cereal grains to celiac patients.
Additionally, the relapse may not be accompanied by obvious symptoms, but could be recognized only by physicians through observation of characteristic changes in the small intestinal tissues obtained by biopsy. The reasons for the enormous variability of response times are not known. It may be speculated that they have something to do with the degree of recovery of the lining of the small intestine on a gluten-free diet, the degree of stress that the patient had been experiencing (including infections), and individual genetic differences.
As I have indicated, all known grain species that cause problems for celiac patients are members of the grass family. In plant taxonomy, the grass family belongs to the Plant Kingdom Subclass known as monocotyledonous plants (monocots). The only other grouping at the Subclass level is that of dicotyledonous plants (dicots). Some other species about which celiac patients have questions actually are dicots, which places them in very distant relationship to the grass family. Such species include buckwheat, amaranth, quinoa, and rape. The seed of the last plant listed, rape, is not eaten, but an oil is pressed from the seeds that is becoming commonly used in cooking. This oil is being marketed as canola oil.
Because of their very distant relationship to the grass family and to wheat, it is highly unlikely that dicots will contain the same type of protein sequence found in wheat proteins that causes problems for celiac patients. Of course, some quirk of evolution could have given rise in these dicot plants to proteins with the harmful amino acid sequence found in wheat proteins. But if such concerns were carried to a logical conclusion, celiac patients would have to exclude all plant foods from their diets.
It may be in order to caution celiac patients that they may have undesirable reactions to any of these foods--reactions that are not related to celiac disease. Allergic reactions may occur to almost any protein, but there is a great deal of individual variation in allergic reactions, and there are possibly non-allergic food reactions, such as to the sulfites used to preserve certain foods, which further complicates the situation. Also, buckwheat, for example, has been claimed to contain a photosensitizing agent that will cause some people who have just eaten it to develop a skin rash when they are exposed to sunlight. Such reactions, apparently rare, should be looked for, but for most people, buckwheat eaten in moderation apparently does not cause a problem. (Buckwheat is sometimes found in mixture with wheat, which of course would cause a problem for celiac patients.) It seems no more necessary for all people with celiac disease to exclude buckwheat from their diets because some celiac patients react to it than it would be for all celiac patients to exclude milk from their diets because some celiac patients have a problem with digestion of milk sugar (lactose) or are allergic to milk proteins, such as lactalbumin. Buckwheat, quinoa, and amaranth have been reported to have relatively high levels of oxalic acid, almost as much as in spinach, and may not be suitable for very young children because the oxalic acid may cause gatrointestinal problems.
Some celiac patients may exhibit allergic reactions to gluten proteins or non-gluten proteins of wheat (and rye and barley), the alpha-amylase inhibitors being an example of the non-gluten proteins that can cause allergic reactions. Related inhibitor proteins can be found in rice as well. Alpha-amylase inhibitors might also interfere with starch digestion, causing symptoms similar to lactose intolerance in people with a weakened digestive capability. Celiac disease is thought to involve delayed immunoreaction and patients would not generally be expected to have an immediate and violent reaction to eating wheat whereas allergic reactions of the immediate hypersensitivity type might be both immediate and violent. It is also possible that both immediate hypersensitivity and delayed reactions might be present in the same person. There is a considerable potential then for confusion between allergy and celiac disease. It may be difficult to distinguish immediate hypersensitivity reactions or allergies from celiac disease as traditionally defined, but more research on this problem is needed.
In conclusion, scientific knowledge of celiac disease, including knowledge of the proteins that cause the problem, and the grains that contain these proteins, is in a continuing state of development. There is much that remains to be done. Nevertheless, steady progress has been made over the years. As far as I know, the following statements regarding various grains are a valid discrimination of the state of our knowledge:
- Spelt or Spelta and Kamut are wheats. They have proteins toxic to celiac patients and should be avoided just as bread wheat, durum wheat, rye, barley, and triticale should be avoided.
- Rice and corn (maize) are not toxic to celiac patients.
- Certain cereal grains, such as various millets, sorghum, teff, ragi, and Job's tears are close enough in their genetic relationship to corn to make it likely that these grains are safe for celiac patients to eat. American wild rice is sufficiently closely related to normal rice that it is likely also to be safe. Significant scientific studies with celiac patients have not been carried out, however, for these grains.
- There is no reason for celiac patients to avoid plant foods that are very distantly related to wheat. These include buckwheat, quinoa, amaranth, and rapeseed oil (canola). Some celiac patients might suffer allergies or other adverse reactions to these grains or foodstuffs made from them, but there is currently no scientific basis for saying that these allergies or adverse reactions have anything to do with celiac disease. A celiac patient may be lactose intolerant or have an allergy to milk proteins, but that does not mean that all celiac patients will have an adverse reaction to milk.
A list of my publications with pertinence to celiac disease follows. Cross-references to the literature for most of the points discussed above can be found in these publications.
Who Has the Guts for Gluten?
WE know that the proteins called gluten, found in wheat and other grains, provoke celiac disease. And we know how to treat the illness: a gluten-free diet. But the rapidly increasing prevalence of celiac disease, which has quadrupled in the United States in just 50 years, is still mystifying.
Scientists are pursuing some intriguing possibilities. One is that breast-feeding may protect against the disease. Another is that we have neglected the teeming ecosystem of microbes in the gut — bacteria that may determine whether the immune system treats gluten as food or as a deadly invader.
Celiac disease is generally considered an autoimmune disorder. The name celiac derives from the Greek word for “hollow,” as in bowels. Gluten proteins in wheat, barley and rye prompt the body to turn on itself and attack the small intestine. Complications range from diarrhea and anemia to osteoporosis and, in extreme cases, lymphoma. Some important exceptions notwithstanding, the prevalence of celiac disease is estimated to range between 0.6 and 1 percent of the world’s population.
Nearly everyone with celiac disease has one of two versions of a cellular receptor called the human leukocyte antigen, or H.L.A. These receptors, the thinking goes, naturally increase carriers’ immune response to gluten.
This detailed understanding makes celiac disease unique among autoimmune disorders. Two factors — one a protein, another genetic — are clearly defined and in most cases, eliminating gluten from the patient’s diet turns off the disease.
Yet the more scientists study celiac disease, the more some crucial component appears in need of identification. Roughly 30 percent of people with European ancestry carry predisposing genes, for example. Yet more than 95 percent of the carriers tolerate gluten just fine. So while these genes (plus gluten) are necessary to produce the disease, they’re evidently insufficient to cause it.
Animal studies have reinforced that impression. In mice engineered to express those H.L.A.’s, tolerance to gluten must be deliberately “broken.” Without an immunological trigger of some kind, the rodents happily tolerate the protein.
A recent study, which analyzed blood serum from more than 3,500 Americans who were followed since 1974, suggested that such a trigger could strike adults at any time. By 1989, the prevalence of celiac disease in this cohort had doubled.
“You’re talking about an autoimmune disease in which we thought we had all the dots connected,” says Alessio Fasano, head of the Center for Celiac Research and Treatment at the Massachusetts General Hospital for Children in Boston, and the senior author of the study. “Then we start to accumulate evidence that there was something else.”
Identifying that “something else” has gained some urgency. In the United States, improved diagnosis doesn’t seem to explain the rising prevalence. Scientists use the presence of certain self-directed antibodies to predict celiac disease. They have analyzed serum stored since the mid-20th century and compared it to serum from Americans today. Today’s serum is more than four times as likely to carry those antibodies.
BLAME for the increase of celiac disease sometimes falls on gluten-rich, modern wheat varietals increased consumption of wheat, and the ubiquity of gluten in processed foods.
Yet the epidemiology of celiac disease doesn’t always support this idea. One comparative study involving some 5,500 subjects yielded a prevalence of roughly one in 100 among Finnish children, but using the same diagnostic methods, just one in 500 among their Russian counterparts.Image
Differing wheat consumption patterns can’t explain this disparity. If anything, Russians consume more wheat than Finns, and of similar varieties.
Neither can genetics. Although now bisected by the Finno-Russian border, Karelia, as the study region is known, was historically a single province. The two study populations are culturally, linguistically and genetically related. The predisposing gene variants are similarly prevalent in both groups.
Maybe more telling, this disparity holds for other autoimmune and allergic diseases. Finland ranks first in the world for Type 1 autoimmune diabetes. But among Russian Karelians, the disease is nearly six times less frequent. Antibodies indicative of autoimmune thyroiditis are also less prevalent, and the risk of developing allergies, as gauged by skin-prick tests, is one-fourth as common.
What’s the Russians’ secret?
“It’s a remote territory of Russia,” says Heikki Hyoty, a scientist at the University of Tampere in Finland. “They live like Finns 50 years ago.”
At the time of this research, roughly a decade ago, Russia’s per-capita income was one-fifteenth of Finland’s. Analysis of house dust and potable water suggests that the Russian Karelians encountered a greater variety and quantity of microbes, including many that were absent in Finland.
Not surprisingly, they also suffered from more fecal-oral infections. For example, three of four Russian Karelian children harbored Helicobacter pylori, a corkscrew-shaped bacterium, while just one in 20 Finnish children did. The bacterium can cause ulcers and stomach cancer, but mounting evidence suggests that it may also protect against asthma.
Professor Hyoty suspects that Russian Karelians’ microbial wealth protects them from autoimmune and allergic diseases by, essentially, strengthening the arm of the immune system that guards against such illnesses.
Meanwhile, Yolanda Sanz, a researcher at the Institute of Agrochemistry and Food Technology in Valencia, Spain, makes a compelling case for the importance of intestinal microbes.
Years ago, Dr. Sanz noted that a group of bacteria native to the intestine known as bifidobacteria were relatively depleted in children with celiac disease compared with healthy controls. Other microbes, including native E. coli strains, were overly abundant and oddly virulent.
How to determine cause or consequence?
In a test tube, she found that those E. coli amplified the inflammatory response of human intestinal cells to gluten. But bifidobacteria switched the response from inflammation to tolerance.
In rats, the E. coli again intensified inflammation to gluten, prompting what’s sometimes called a “leaky gut” — the milieu suspected of contributing to celiac disease. Conversely, bifidobacteria protected the intestinal barrier. Microbes, it seemed, could influence the immune response to gluten.
Bifidobacteria occur naturally in breast milk, which, along with protective antibodies and immune-signaling proteins, conveys hundreds of prebiotic sugars. These sugars selectively feed certain microbes in the infant gut, particularly bifidobacteria. Breast-fed infants tend to harbor more bifidobacteria than formula-fed ones.
All of which may explain a curious historical phenomenon — an “epidemic” of celiac disease that struck Sweden some 30 years ago. Anneli Ivarsson, a pediatrician at Umea University, recalled a sudden wave of “terribly sick” infants.
Sleuthing revealed that, just before the spike, official guidelines on infant feeding had changed. In an effort to prevent celiac disease, paradoxically, parents were instructed to delay the introduction of gluten until their babies were six months old. That also happened to be when many Swedish mothers weaned their children. Coincidentally, companies had increased the amount of gluten in baby food.
This confluence produced an unwitting “experiment with a whole population,” says Dr. Ivarsson — a large quantity of gluten introduced suddenly after weaning. Among Swedes born between 1984 and 1996, the prevalence of celiac disease tripled to 3 percent. The epidemic ebbed only when authorities again revised infant-feeding guidelines: keep breast-feeding, they urged, while simultaneously introducing small amounts of gluten. Food manufacturers also reduced the gluten content of infant foodstuffs. Dr. Ivarsson found that, during the epidemic, the longer children breast-fed after their first exposure to gluten, the more protected they were.
Not all subsequent studies have found nursing protective, but partly as a result of Sweden’s experience, the American Academy of Pediatrics now recommends that infants start consuming gluten while still breast-feeding.
Research by Dr. Sanz of Spain again illuminates how this may work. Some years back, she began following a cohort of 164 newborns with celiac disease in the immediate family. By four months, children with celiac-associated genotypes — 117 of them — had accrued a microbial community with fewer bifidobacteria compared to those without. If bifidobacteria help us tolerate gluten, these children appeared to be edging toward intolerance.
There was one notable exception: Breast-feeding “normalized” the microbes of at-risk children somewhat, boosting bifidobacterial counts.
Dr. Fasano of Boston has made another potentially important find. He followed 47 at-risk newborns, regularly collecting microbes from 16 of them, which he analyzed after two years. Like Dr. Sanz, he found these genetically at-risk children to accumulate a relatively impoverished, unstable microbial community.
But it’s a secondary observation that has Dr. Fasano particularly excited. Two of these children developed autoimmune disease: one celiac disease, another Type 1 diabetes, which shares genetic susceptibility with celiac disease. In both cases, a decline of lactobacilli preceded disease onset.
Assuming that the pattern holds in larger studies, “imagine what would be the unbelievable consequences of this finding,” he says. “Keep the lactobacilli high enough in the guts of these kids, and you prevent autoimmunity.”
The caveats here are numerous: the tiny sample size in Dr. Fasano’s study Dr. Sanz hasn’t yet revealed who actually developed celiac disease in her cohort and even if these microbial shifts reliably precede disease onset — as they do in larger studies on allergic disease — they’re still bedeviled by the old “chicken or the egg” question: Which comes first, the aberrant microbial community, or the aberrant immune response?
Bana Jabri, director of research at the University of Chicago Celiac Disease Center, notes that immune disturbances change the microbial ecosystem. But here’s the catch: Even if the chicken comes first, she says, the egg can contribute. Rodent experiments show that intestinal inflammation can select for unfriendly bacteria that further inflame. “You can have a positive feedback loop,” she says.
SO your microbes change you, but your genes also shape your microbes — as do environment, breast milk, diet and antibiotics, among many other factors.
Such complexity both confounds notions of one-way causality and suggests different paths to the same disease. “You have the same endpoint,” Dr. Jabri says, “but how you get there may be variable.”
The intricacies don’t stop there.
Not all breast milk is the same. It varies according to diet and other factors. One study found that milk from overweight mothers had fewer of those bifidobacteria than milk from thinner mothers. Another observed that breast milk from farming mothers, who inhabit a microbially enriched environment, carried more anti-inflammatory proteins compared with urban mothers’ milk. “All these things are going to matter,” Dr. Jabri says. And they’re all potential nudge points in the quest to prevent disease.
The tangled web of possibilities should not, however, distract us from the facts on the ground. In a far-flung corner of Europe, people develop celiac disease and other autoimmune diseases as infrequently as Americans and Finns did a half-century ago. The same genes exposed to the same quantity of gluten do not, in that environment, produce the same frequency of disease.
“We could probably prevent celiac disease if we just give the same environment to the Finnish children as they have in Karelia,” says Dr. Hyoty. “But there’s no way to do it now, except to move the babies there.”
Should you go gluten-free?
If you feel you might be suffering from some of the above mentioned symptoms of gluten intolerance, it might help to take a break from gluten for a little while. At Parsley Health, to assess your tolerance to gluten we recommend a four to six week elimination of gluten and other commonly inflammatory foods from the diet to be followed by a reintroduction to “challenge” how you react.
To eliminate gluten, remove all refined grains and processed foods from the diet including bread, baked goods and pastas along with processed foods that sneakily contain gluten such as salad dressings, cheese, soy sauce and most beer. It’s important to remember that new fad foods labelled ‘gluten-free’ tend to be processed and usually incredibly high in sugar and carbs, which could make inflammation worse so it’s best to stick to naturally gluten-free foods such as fresh fruit, vegetables, beans, legumes, nuts, seeds, fish, seafood, meat and poultry. After the elimination period, talk to your doctor and a health coach about reintroduction and the right balance of gluten in your diet for overall health.
Even if you do not think you have an intolerance, there is some evidence to suggest that the gluten component gliadin increases inflammation in the digestive tract that can contribute to intestinal permeability or “leaky gut.” This can cause bacteria and other toxins to seep through the intestine into the rest of the body. If the tight junctions that seal the intestine are chronically opened, it can contribute to long-term issues like brain fog, bloating, and joint pain.
Test tube studies have shown that when intestinal cells are exposed to gluten, intestinal permeability occurs in all samples — not just those with a known sensitivity. This study suggests that gluten may promote inflammation and leaky gut in everyone. In clinical studies, gluten was shown to increase leaky gut in patients with irritable bowel syndrome (IBS) while other research found that intestinal permeability only occurred in those with CD, NCGS or IBS but not others.
While individuals with Celiac disease, non-Celiac gluten sensitivity and irritable bowel syndrome clearly have a greater extent of intestinal permeability that occurs when consuming gluten, because there is some evidence to suggest gluten is generally inflammatory it’s worth considering how much, how often and what types of gluten you’re consuming to ensure optimal gut and overall health. The truth is that everyone’s body is different and that’s exactly why we practice personalized medicine and do high-tech speciality testing here at Parsley Health to figure out what works best for you.
Credentials: Internal Medicine Physician • Institute for Functional Medicine Practitioner Training Institutions: Summa Cum Laude Graduate of the University of Pennsylvania • Columbia University’s College of Physicians and Surgeons • Internal Medicine Residency at Mount Sinai Hospital in New York City • Institute for Functional Medicine Clinical Interests: Thyroid & Adrenal Health • Autoimmune Disorders • Gastrointestinal Health • Biology of Stress • Cancer Prevention • Fertility Optimization Previous and Additional Positions: Founder and CEO of Parsley Health. Co-founded the&hellip
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