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Celiac.com 04/29/2024 - Getting enough calcium in the diet is essential for people of all ages, as this mineral performs many important functions in the body. In addition to bone health, calcium is required for muscle contractions, nerve impulses, normal blood clotting and regulating blood pressure. It may also offer protection from colon cancer. Children and adults with celiac disease need to pay particular attention to calcium and other nutrients as many already have or will develop early bone disease such as osteopenia or osteoporosis. Osteopenia is low bone mineral density and osteoporosis is characterized by a significant decrease in bone mass resulting in brittle, easily broken bones. The hip, spine and wrist are most susceptible to fracture. Early diagnosis and treatment of celiac disease is critical for the prevention of bone disease. To maintain good bone health it is important that all people with celiac disease have routine bone density tests done to assess their overall bone health, and to follow the tips outlined below. Follow a strict gluten-free diet Healthy villi will result in normal absorption of nutrients. Meet your daily calcium requirements Table 1: Dietary Reference Intake for Calcium /* DivTable.com */ .divTable{ display: table; width: 100%; } .divTableRow { display: table-row; } .divTableHeading { background-color: #EEE; display: table-header-group; } .divTableCell, .divTableHead { border: 1px solid #999999; display: table-cell; padding: 3px 10px; } .divTableHeading { background-color: #EEE; display: table-header-group; font-weight: bold; } .divTableFoot { background-color: #EEE; display: table-footer-group; font-weight: bold; } .divTableBody { display: table-row-group; } Age Calcium (mg/day) Infants 0- 6 months 7-12 months 210 270 Children 1-3 years 4-8 years 500 800 Females and Males 9-13 14-18 19-30 31-50 51-70 71 + 1300 1300 1000 1000 1200 1200 Choose calcium-rich foods See Table 2 for a list of gluten-free foods. Remember that not all calcium sources are created equal. Milk (fl uid, powdered or evaporated) and milk products such as cheese and yogurt contain the most readily available source of calcium. Other foods such as salmon and sardines with the bones, calcium-fortifi ed beverages (soy, rice and orange juice), tofu made with calcium sulfate and vegetables (broccoli, collards, kale, mustard greens, turnip greens and bok choy) also contain calcium that is easily absorbed by the body. However, the calcium found in almonds, sesame seeds, dried beans and spinach are absorbed less effi ciently because these foods contain calcium-binding substances called oxalates. Although the calcium content of these foods should not be counted as part of your daily calcium intake; they do provide many other nutrients important for good health. Table 2 Calcium Content of Gluten-Free Dairy Foods /* DivTable.com */ .divTable{ display: table; width: 100%; } .divTableRow { display: table-row; } .divTableHeading { background-color: #EEE; display: table-header-group; } .divTableCell, .divTableHead { border: 1px solid #999999; display: table-cell; padding: 3px 10px; } .divTableHeading { background-color: #EEE; display: table-header-group; font-weight: bold; } .divTableFoot { background-color: #EEE; display: table-footer-group; font-weight: bold; } .divTableBody { display: table-row-group; } Food Serving Calcium (mg) Buttermilk 1 cup (250 ml) 303 Cheddar cheese 2 oz. (50 g) 350 Cottage cheese, creamed ½ cup (125 ml) 76 Feta cheese 2 oz (50 g) 255 Ice cream ½ cup (125 ml) 90 Milk (whole, 2%, 1%, skim) 1 cup (250 ml) 315 Milk (chocolate) 1 cup (250 ml) 301 Milk, powder, dry 3 Tbsp. (45 ml) 308 Mozzarella cheese 2 oz (50 g) 287 Parmesan cheese, grated 3 Tbsp. (45 ml) 261 Processed cheese slices 2 regular (62 g) 384 Swiss cheese 2 oz (50 g) 480 Yogurt, fruit-flavored ¾ cup (175 g) 240 Yogurt, plain ¾ cup (175 g) 296 Table 2: Calcium Content of Other Gluten-Free Foods /* DivTable.com */ .divTable{ display: table; width: 100%; } .divTableRow { display: table-row; } .divTableHeading { background-color: #EEE; display: table-header-group; } .divTableCell, .divTableHead { border: 1px solid #999999; display: table-cell; padding: 3px 10px; } .divTableHeading { background-color: #EEE; display: table-header-group; font-weight: bold; } .divTableFoot { background-color: #EEE; display: table-footer-group; font-weight: bold; } .divTableBody { display: table-row-group; } Food Serving Calcium (mg) Almonds ½ cup (125 ml) 200* Baked beans 1 cup (250 ml) 163* Bok choy, cooked ½ cup (125 ml) 84 Broccoli, cooked ½ cup (125 ml) 38 Collards, cooked ½ cup (125 ml) 81 Orange juice, calcium fortified 1 cup (250 ml) 300-350 Salmon, sockeye, canned with bones Half a 7.5 oz (213 g) can 243 Sardines, canned with bones 6 medium (72 g) 275 Sesame seeds ½ cup (125 ml) 89* Soybeans, cooked ½ cup(125 ml) 93 Soy beverage, fortified 1 cup (250 ml) 312 Tofu, regular, processed with calcium sulfate** 1/3 cup (100 g) 150 * The calcium from these sources is absorbed less efficiently by the body. ** The calcium content of tofu is an approximation based on products available on the market. Calcium content can vary greatly from one brand to another and can be low. Tofu processed with magnesium chloride also contains less calcium. Consider calcium supplementation If you are unable to consume enough dietary calcium you many to need a gluten-free calcium supplement. Look for the amount of “elemental calcium” on the label. Your body can only absorb 500 mg at one time therefore it is best to divide your dose throughout the day. Calcium carbonate is more slowly absorbed and should be consumed with meals. Calcium citrate is well absorbed with meals or an empty stomach. Bone meal or dolomite calcium supplements are not recommended as some products have been found to contain lead and mercury. Limit caffeine intake Studies have shown that caffeine increases calcium loss through the urine. Most experts agree that 2-3 cups of coffee/day is probably not harmful provided that calcium intake is adequate, so limit your coffee and cola intake. Limit sodium intake Sodium also has been shown to increase the loss of calcium through the urine. Therefore it is advisable to limit your intake of processed foods, table salt and salt in cooking. Get enough Vitamin D Vitamin D helps the body use the calcium in food. It can increase calcium absorption by as much as 30-80 %. See Table 3 for the Dietary Reference Intake for vitamin D. The easiest way to get vitamin D is from exposure to sunlight, which causes the body to make its own vitamin D. All you need is 15 minutes per day; however, aging significantly decreases 1) the ability of the skin to produce vitamin D and 2) kidney function that is involved in converting the inactive to active form of vitamin D. Also, sunscreen blocks the production of vitamin D in the skin. Another concern is that between the months of October and March in Canada and the northern USA, vitamin D synthesis in the skin is very limited. To make up for the lack of sunlight look for other sources of vitamin D listed in Table 4, and remember the points below. Table 3: Dietary Reference Intake for Vitamin D /* DivTable.com */ .divTable{ display: table; width: 100%; } .divTableRow { display: table-row; } .divTableHeading { background-color: #EEE; display: table-header-group; } .divTableCell, .divTableHead { border: 1px solid #999999; display: table-cell; padding: 3px 10px; } .divTableHeading { background-color: #EEE; display: table-header-group; font-weight: bold; } .divTableFoot { background-color: #EEE; display: table-footer-group; font-weight: bold; } .divTableBody { display: table-row-group; } Age Vitamin D (IU) Birth – 50 years 200 51- 70 years 400 Over 70 years 600 Milk is fortified with vitamin D but most other dairy products such as cheese, yogurt and ice cream are not fortified. Recently some companies have been adding vitamin D to other dairy products so be sure to read the ingredient label and nutrition panel. Fatty fish (sardines, salmon and herring) and cod liver oil and halibut liver oil are high in vitamin D. Many soy and rice beverages are fortified with vitamin D. Check the ingredient list carefully as some products may contain barley malt extract/flavoring and must be avoided. Nut beverages (e.g. Blue Diamond Almond Breeze) and potato beverages (e.g. Vances DariFree) are fortified with vitamin D. Multivitamin supplements usually contain 200-400 IU of vitamin D. Some calcium supplements may contain vitamin D. Amounts vary so check the label. Table 4: Sources of Vitamin D /* DivTable.com */ .divTable{ display: table; width: 100%; } .divTableRow { display: table-row; } .divTableHeading { background-color: #EEE; display: table-header-group; } .divTableCell, .divTableHead { border: 1px solid #999999; display: table-cell; padding: 3px 10px; } .divTableHeading { background-color: #EEE; display: table-header-group; font-weight: bold; } .divTableFoot { background-color: #EEE; display: table-footer-group; font-weight: bold; } .divTableBody { display: table-row-group; } Food Serving Size Vitamin D (IU) Cod liver oil Cod liver oil capsule 1 tsp. (5 ml) 1 capsule 450 100 Halibut liver oil capsule 1 capsule 400 Sardines, canned 3.5 oz (100 g.) 300 Salmon, canned, with bones 3.5 oz (100 g.) 500 Egg 1 medium 25 Milk 1 cup (250 ml) 90 Soy Beverage (fortified) 1 cup (250 ml) 90 Don’t just sit there…get moving! Regular weight bearing exercises such as walking, stair climbing, dancing and tennis and muscle-strengthening exercises can reduce the risks of falls and fractures. Consult your doctor before beginning a vigorous exercise program. So remember the ABC’s…All Bones Need Calcium, Vitamin D and Exercise!

Celiac.com 08/16/2019 - A recent study looked at nine possible factors in children that might contribute to the development of celiac disease later in life. The study found a connection between skim milk consumption, and vitamin D drop use for more than 3 months, and later development of celiac disease. It also found evidence to support earlier data that early life exposure to antibiotics and early life infection, especially ear infection, are also associated with the development of celiac disease in children. Read more in Clinical and Experimental Gastroenterology This study and several others point to the importance of the following risk factors in the development of celiac disease. Other studies have found factors that may contribute to celiac disease. The Ten Risk Factors Most Associated with Celiac Disease Include: Genetic Factors Genetic factors play a role in celiac disease. Having a family member with celiac disease or dermatitis herpetiformis increases the chances of developing celiac disease. The risk of developing celiac disease is also increased by certain variants of the HLA-DQA1 and HLA-DQB1 genes. These genes provide instructions for making proteins that play a critical role in the immune system. A recent study shows high celiac disease rates among first-degree family relatives. Associated Diseases Having associated autoimmune or other diseases increases the likelihood of developing celiac disease. Associated diseases include: Autoimmune thyroid disease Dermatitis herpetiformis Lupus erythematosus Microscopic colitis (lymphocytic or collagenous colitis) Rheumatoid arthritis Type 1 diabetes Down syndrome or Turner syndrome Addison's disease Being Female Being female is a risk factor for celiac disease? It's true. Women get celiac disease at rates up to twice as high as men. The exact reasons for this are unknown, but many researchers are focused on the role of female immune response, and how it differs from that of men. Antibiotics Courses of antibiotics before 2 years old are associated with higher celiac disease rates. Ear Infection Incidence of ear infection before 2 years old are associated with higher celiac disease rates. The ORs for the raw categorical variables on ear infection increase with the number of such infections. In addition, the scaled ear infection exposure variable is associated with a subsequent diagnosis of celiac disease. Other studies have also shown a connection between ear infections and later celiac disease. Viral Infection Several studies have shown that exposure to certain viruses is associated with higher rates of celiac disease later on. Implicated viruses include enterovirus and reovirus. Vitamin D Drop Exposure in Infancy Some recent evidence points to the role of oral vitamin D exposure in later celiac development. While the OR on only one of the vitamin D drop categorical variables is statistically significant (Table 2), these variables do suggest a pattern. Specifically, the data suggests that infants who receive oral vitamin D drops for longer than 3 months are at increased risk of subsequently developing celiac disease. Skim Milk Recent data suggests that consumption of skim milk as the primary form of liquid cow’s milk between 2-3 years old is associated with a subsequent diagnosis of celiac disease. In general, kids who drank skim or low-fat milk had more celiac disease, and more diarrhea. Age at First Gluten Consumption A 2015 study by Carin Andren Aronsson, from the department of clinical sciences at Lund University in Sweden, and colleagues, shows that children who eat more foods with gluten before they're 2 years old have a greater risk of developing celiac disease if they carry a genetic risk factor for the condition. It's important to note, however, that while the study found an association between eating more gluten early in life and celiac disease, it wasn't designed to prove a cause-and-effect relationship. Amount of Gluten Consumed The results of a recent study showed that every daily gram increase in gluten intake in 1-year olds increases the risk of developing celiac disease autoimmunity by 5%.

Celiac.com 01/19/2022 - A number of researchers have encouraged screening children with celiac disease for vitamin D status, but, so far, studies to support these recommendations have not been definitive. A team of researchers recently set out to assess the vitamin D status in newly diagnosed children with celiac disease and in a non-celiac disease control population and relate them to vitamin D intake. The research team included Rajni Ahlawat; Toba Weinstein; James Markowitz; Nina Kohn; and Michael J. Pettei. They are variously affiliated with the Division of Pediatric Gastroenterology, Hepatology & Nutrition, Steven and Alexandra Cohen Children's Medical Center; and the Department of Biostatistics, Feinstein Institute for Medical Research, NY. For their study, they team assessed levels of serum 25-hydroxyvitamin D (25-OHD) in children with newly diagnosed celiac disease, and compared them against non-celiac children seen for functional abdominal complaints. The team calculated vitamin D intake based on milk and multivitamin ingestion. The researchers studied nearly forty newly diagnosed celiac disease patients ranging from about eight to thirteen years old, and evenly divided between girls and boys, along with just over eighty control subjects. Except for average daily D intake and BMI, both groups were similar. There was no meaningful difference in average 25-OHD levels between celiac disease patients and control subjects. Nearly seventy percent of celiacs and eighty percent of control subjects showed high percentages of suboptimal D status. 25-OHD levels reflected patient age, and estimated vitamin D intake. The data showed no significant difference in 25-OHD levels between newly diagnosed celiac disease and control subjects, with both groups showing inadequate 25-OHD levels. Patient 25-OHD levels correlated strongly with vitamin D intake, indicating similar vitamin D absorption between patients and control subjects. Because celiac disease is associated with low vitamin D levels and with bone disease, the researchers suggest that doctors should work with patients to maintain optimal levels of vitamin D, including screening vitamin D levels upon diagnosis for celiac disease. Read more in the Journal of Pediatric Gastroenterology and Nutrition, October 2019, Volume 69 - Issue 4 - p 449-454

Celiac.com 07/29/2020 - Vitamin and micronutrient deficiencies are common in people with both treated and untreated celiac disease. Fortifying processed foods with vitamins and micronutrients is common method for enhancing public health. In the latest iteration of that practice, researchers Dr David Aldridge and PhD student David Willer, from Cambridge University and UK company BioBullets, have figured out a way to deliver fortified levels of vitamins in bivalve shellfish such as oysters, clams and mussels by using new micro-encapsulation technology. The resulting shellfish offer a way to get high levels of vitamins into people with vitamin deficiencies. The results offer promise for people with chronic vitamin deficiencies, including those with celiac and other diseases. The team is now working with major seafood manufacturers to further test and optimize the efficacy of their "Bio Bullets" micro-encapsulation process. Shellfish fed Vitamin A and D fortified microcapsules for eight hours while being held in cleansing tanks after harvest, showed the most promise. Aldrige and Willer found that fortified oysters provide about 100 times more Vitamin A, and over 150 times more Vitamin D, than natural oysters, and far more than Salmon, a good natural source for these nutrients. In fact, a serving of just two supercharged shellfish a day met the U.S. recommended daily allowance for both vitamins A and D. The shellfish are also environmentally friendly, and highly sustainable, with a lower energy demand than animal meat, fish, or many plant crops such as wheat, soya, and rice. Fortifying shellfish with vitamins offers a "cheap and effective way to get micronutrients into a sustainable and delicious source of protein. Targeted use of this technology in regions worst affected by nutrient deficiencies...could help improve the health of millions," says Willer. Obviously, some people cannot eat shellfish, but the vast majority of people can, including people with celiac disease. For people with celiac disease who face challenges with vitamin and micronutrient deficiency, fortified shellfish could offer a tasty, easy way to load up on essential vitamins, which will likely improve overall health and wellbeing. This technology could be a gamer changer for both celiacs, and for other people across the globe who are suffering from vitamin and micronutrient deficiencies. Read more in Newfoodmagazine.com

Celiac.com 06/28/2019 (originally published 07/12/2010) - The report by R.H. Wasserman titled “Vitamin D and the Dual Processes of Intestinal Calcium Absorption“ is very important. I have some writing to do (and corrections to make) as a result of reading this. It helps to explain why dogs don’t suffer from clinical osteoporosis. It’s obvious that there are processes taking place in the ileum of humans that do not take place in the dog. This came up as I was counseling an Internet acquaintance concerning his osteoporosis. He was not improving with conventional therapy and was also suffering from chronic lymphocytic colitis. I knew that the ileum actively absorbs calcium but the numbers in the study above were news to me. I’ve been telling people for years that one of the biggest difference between a person doing well after gastric bypass vs. crashing and burning had to be the health of their ileum and now I understand a little more as to why this is the case, especially when it comes to bone density. So, I’ve turned my attention to the health and wellbeing of the ileum. I have assumed for years that one of the biggest factors in humans is dairy products. So much points to that. But…is it the casein and other dietary glycoproteins causing villous atrophy that does it OR is there something IN the milk that is doing it? We know that Mycobacterium paratuberculosis can be involved in Crohn’s and that it can come from milk, even when pasteurized. Are there other pleomorphs that are doing this? I like to point out that, of the “big 4” foods, only dairy is of animal origin and that it is “public enemy number one” for a reason: It not only contains damaging lectins, loads of estrogen, and casomorphins (BCM7) but is a veritable petri dish of microorganisms. In fact, they now know that the bovine leukemia virus can cause leukemia in primates. What about mycoplasma, mycobacteria, and the myriad of pleomorphic bacteria is contains, some of which could take up to a year to culture out (e.g. mycoplasma). I’m working on a paper that deals with the zoonoses associated with cow’s milk. So…I still contend that dairy is one of the biggest culprits in Crohn’s and other chronic diseases of the lower intestine but these are likely to be more examples of “syndromes”, in which resident viruses and bacteria (including those viruses in the DNA) react to chronic insults like gluten, dairy, etc. and other man-made components of food along with newly acquired viruses and bacteria, some of which are coming from vaccines. (Gotta wonder about those weaponized versions of mycoplasma floating around.) Also, there is no place like the gut for secondary infections. Here is the application I am wondering about: Could antibiotics help a person with osteoporosis, knowing that pleomorphic bacterial infections are showing up in other areas of “autoimmune” disease, such as rheumatoid arthritis, scleroderma, and sarcoidosis? The process appears to be the same in all cases: The residential viruses and bacteria are all involved in adaptive processes throughout the body. They are reason for inflammation, as they react to immune challenges being brought against the cell. Once this process escalates and the immune system crashes, the bacteria become a significant secondary problem requiring specific treatment (see www.bacteriality.com and the “miracles” that are occurring using long-term doxycycline, etc.). As long as the immune system remains competent, these individuals can still be rescued by employing nutritional therapy, holistic approaches and avoidance of the obvious insults (food lectins, preservatives, pollutants, cigarettes, etc.). Vitamin D3 therapy would be crucial here for both calcium absorption and immune competence. But the dog, once again, may give us a clue as to which aspect of D3 is the most important in the pathogenesis of osteoporosis. I believe that the average dog is woefully deficient in D3, with their dismally high incidence of cancer being a leading indicator. Why wouldn’t they be low? They convert sunlight to D3 much less efficiently than humans, are covered with fur, and spend most of their time indoors. If and when we start measuring their D3 levels, we will likely be stunned at their low levels. And yet…they don’t suffer from clinical osteoporosis. Is it because they don’t live long enough? Hey, they get everything else. So again, I am wondering more and more about the immune aspects of osteoporosis in humans. Once the patient crosses the line and their immune system becomes incompetent (which is when many present initially), bad things happen. They go from subclinical to clinical, from bad to much worse, or from “stage two” (“autoimmune” diseases) to “stage three” (cancer). We know now that pleomorphic bacteria are involved in cancer, which makes perfect sense. They were involved in the adaptive processes from the start (through their influence on the cell’s mitochondria) and play a vital role in determining when the cell (and the viruses it contains) finally decides to form a tumor to escape further insults. This process is taking place all over the body in every tissue we have. So…this must be happening in the ileum, where they now say 70-80% of the calcium is absorbed. Could antibiotics of the right type be of help when these immune incompetent individuals need rescuing, even in cases of refractory osteoporosis? Certainly, we should try to avoid their use for as long as possible but we have to be realistic sometimes in what the patient or the owner of a pet is willing to do. Those who are into holistic medicine can avoid this last ditch effort for the longest time, even indefinitely. But if the last ten years have done anything for me, they’ve made me a realist. Sadly, most people want a quick fix. Source: Wasserman RH, Vitamin D and the Dual Processes of Intestinal Calcium Absorption, J. Nutr. 134:3137-3139, November 2004 Article Corrected 07/01/2019 - The original article was corrected as it referenced a study linking the measles portion of the MMR vaccine with ileum damage in humans, however, this study was retracted.

Celiac.com 07/06/2020 - Although researchers are just beginning to learn about the role of vitamin D on the immune system and on infection, recent studies point to vitamin D as an immune system regulator and signaling component. Over 900 genes are reportedly regulated by vitamin D. Researchers are investigating numerous potential influences of Vitamin D on chronic diseases such as diabetes, celiac disease and cardiovascular, neurological, and autoimmune diseases. A team of researchers recently set out to define the possible role of vitamin D in celiac disease development, taking into account potential links among vitamin D, the immune system and celiac disease. The research team included Giorgia Vici, Dalia Camilletti, and Valeria Polzonetti. They are variously affiliated with the School of Biosciences and Veterinary Medicine, University of Camerino in Camerino, Italy. Beside supporting and protecting the skeletal system by assisting in calcium production, researchers have described additional potential roles for vitamin D. Studies have shown that vitamin D may be a key player in inflammation and immunity, and in controlling the intestinal mucosa barrier. Researchers suspect that vitamin D influences numerous conditions, such as immune-mediated diseases, and due to its involvement in immune modulation it could be a major factor in the onset of celiac disease. Celiac disease is a chronic auto-immune condition that often results in damage to the small intestine when those with it consume gluten proteins. Researchers have begun to understand that other factors also play a role in the development of celiac disease, and recent vitamin D research has shown that tissues and cells that have nothing to do with mineral and bone metabolism present a vitamin D receptor (VDR) and vitamin D-activating enzymes. Researchers have noted that the VDR expresses itself as antigen-presenting cells and lymphocytes, which indicates that vitamin D is a key modulator of immune and inflammation mechanisms, and suggests that VDR gene polymorphisms function as markers of either resistance or susceptibility to autoimmune diseases. For these reasons, the researchers call for clarifying the role of vitamin D in the onset of celiac disease. They are calling for international studies to assess the variables that can influence celiac onset, such as vitamin D levels of pregnant women, vitamin D supplementation and/or UV exposure. Better understanding of the role played by vitamin D in celiac disease could lead the way to new strategies for preventing celiac disease. Stay tuned for more on the role of vitamin D in celiac disease onset, treatment, and prevention. Read more in Nutrients. 2020 Apr; 12(4): 1051.doi: 10.3390/nu12041051

Celiac.com 05/16/2020 - Yes, I’m “just a vet,” but I have realized something very important. If MDs studied veterinary medicine like I have studied human medicine, we would be a lot further down the road toward solving many medical puzzles. For instance, dogs get multiple sclerosis (MS). We call it degenerative myelopathy. It occurs primarily in large breed dogs, with German Shepherds being the number one victim. In fact, the condition in the dog is so similar to that in people that it was once thought that humans may have contracted it from dogs. (As canine distemper virus is a paramyxovirus, and with measles and mumps being paramyxoviruses, such transmission may be possible, especially when we see that many viruses that afflict humans are harbored in animals). If the distemper virus is causing it, why do such a small, select number of dogs get it? Why don’t we see it across the board in all breeds? If it were a parasite (which is highly unlikely), then the same would be true... it should not select the specific breeds. Thus, since genetic traits are specific to breeds, we have to look at “genetics”. But what are “genetics”? They are basically two things- Gene sequences that determine traits and body functions and sequences derived from viruses. Yes, approximately 45% of the genetic information in our DNA is from viruses. This is a very important “fun fact”. The DNA IS “command central.” It contains both the information for normal development and the potential for things to go wrong. Researchers have tried to nail down the “genetics” of MS for a long time but it just doesn’t seem to be working out for them. That’s because MS is complicated and multiple factors have to come together to make it happen. What do we know, other than it happens in select breeds of dogs and that MDs think there is a hereditary link but can’t seem to prove it? M.S. occurs most prevalently in northern climates, above the 33rd parallel. Why? Relative lack of vitamin D, with the consequent lack of sunlight exposure being the main culprit, is the accepted theory. I think they are right. Vitamin D is crucial for the immune system to function properly. A recent medical study boldly proclaimed that if all Americans took an effective vitamin D supplement, we would cut the cancer risks by over a 1/3. Air pollution, which is horribly neurotoxic and immune suppressive, also has a major detrimental effect on MS patients. It does sound like an immune system problem (weakness) doesn’t it? So, what is being unleashed by this weakened immune system? A parasite? (Not likely...we would have SEEN that microscopically long ago. Also, parasites would not be nearly so selective.). A bacteria? ( For the same reasons, this isn’t likely either. A virus? Ahhh...maybe. But why haven’t researchers been able to culture it or at least identify it yet? Perhaps because it is already in the DNA, as is suggested by the limited number of breeds of dogs that are afflicted? We know this happens in the case of retroviruses and cancer. What we also know is that there are some viruses that require “helper” viruses that provide essential amino acid sequences that are missing in the genetic make-up of the primary virus or segment already in place in the DNA. This is well established. Imagine someone who has that incomplete sequence in their DNA then contracts a virus that supplies the missing information. It is like someone putting the right code into a stalled computer....suddenly it starts running. This would help explain the relatively uncommon incidence of MS in both species as well as the “genetic” tendency that investigators just can’t seem to find. It would also explain the demise of the immune system, nutrition, the northern climate prevalence (the vitamin D connection), and just about every other loose end that we have before us right now. With this kind of “idiopathic condition” (MS, epilepsy, Alzheimer’s, Parkinson’s, etc.) we should be looking for a “syndrome”...a number of factors that come together that produce a particular range of results. The really cool thing to see is the role that the big “4” foods play in all of this. Just add the potentially cataclysmic effects of the malabsorption syndrome that goes along with the intolerance (to gluten, casein, soy, corn, which dominate our diet) the direct effect of lectins on cellular function, and the role of viruses, both overt and those whose information is already embedded in our very genome. We need to study all we can about these three things: food intolerance; lectins, and; viruses. If we do, the world of medicine will open up before us. It becomes readily apparent that bacteria, parasites, and fungi/yeast are secondary players. They are opportunists that arise and cause problems as this process unfolds. In fact, I look at them as the clues that can help us understand what is missing - our immune system and microscopic damage done to our tissues. Once we examine them in this way, then we can see them as warning signs to go along with the other signs that preceded their arrival, such as heartburn, IBS, allergies, asthma, chronic fatigue, insomnia, etc. etc.

Celiac.com 02/07/2020 - Over the last couple of decades, celiac disease has increased significantly in some developed countries in recent decades. Possible risk factors listed in medical literature don't seem to offer a convincing reason for the rise in rates. This has led some researchers to hypothesize that there is a “missing environmental factor” that increases the risk of developing the disease. We've written previously about the possible link between vitamin D and celiac disease over the years, including the fact that vitamin D is one of the top ten risk factors for celiac disease. There's also some interesting evidence that people with celiac disease can recover normal vitamin D levels through a gluten-free diet, without requiring any supplementation. Based on evidence from medical literature, researcher Seth Scott Bittker of the Ronin Institute proposes that elevated plasma levels of 1,25-dihydroxyvitamin D [1,25(OH)2D] might be an overlooked risk factor for celiac disease. Bittker also proposes that significant oral vitamin D exposure is a “missing environmental factor” for celiac disease. Bittker notes that celiac patients often have elevated plasma levels of 1,25(OH)2D, especially when first diagnosed. He also notes that nine separate celiac-associated conditions raise plasma levels of 1,25(OH)2D. He cites a retrospective study showing that regular dose of oral vitamin D in infants are tied to a higher celiac disease risk later on, along with other studies that support the connection. It turns out that high doses of oral vitamin D increase activity in cytokines, chemokines, and toll-like receptors that are also active in celiac disease. Lastly, Bittker points to epidemiological connections, like the start of a celiac disease “epidemic” in Sweden, the increased prevalence of celiac disease in Finland and the U.S. in recent decades, oddly low rates of celiac disease in Germany, and differences in celiac rates between Finnish Karelians and Russian Karelians, may all be explained by oral vitamin D exposure increasing celiac disease risk. The same is true of some seemingly contradictory results in the literature on the effects of breastfeeding on celiac disease risk. If future research validates this hypothesis, reducing intake of oral vitamin D among those with genetic susceptibility may lower celiac risk for these people. Read more at DovePress.com

Celiac.com 10/28/2019 - Among other things, a recent study on nutrition and bone health in adults with probable undiagnosed, untreated celiac disease drives home the importance of early diagnosis and quick adoption of a gluten-free diet. The importance can be seen in the findings of a research team that recently looked at variations in nutritional intake of calcium, vitamin D, and phosphorus; their levels in the blood; and bone health in adults with and without likely, undiagnosed celiac disease. The research team included Lara H. Sattgast, Sina Gallo, Cara L. Frankenfeld, Alanna J. Moshfegh, and Margaret Slavin. They are variously affiliated with the Department of Nutrition & Food Studies, George Mason University, Fairfax, Virginia, USA; the Department of Global & Community Health, George Mason University, Fairfax, Virginia, USA; and the Food Survey celiac diseases Research Group, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, Maryland, USA. The team analyzed data from 48 adults with likely undiagnosed celiac disease and positive immunoglobulin A endomysial antibody tests, and 13,634 controls. The data came from What We Eat in America and the National Health and Nutrition Examination Survey 2009–2014, and included self-reported information on dietary and supplement intake from a single day of 24-hour recalls, serologic indicators, and dual x-ray absorptiometry images. The team's statistical analysis included multiple linear regression modeling controlled for age, sex, race/ethnicity, energy intake, and poverty income ratio. Rates of likely undiagnosed celiac disease were 1 in 285. Patients with likely celiac disease showed an average 251.6 mg higher daily total calcium intake, higher dairy consumption by 0.7 cups per day, and higher serum phosphorus levels. Probable celiac patients showed a substantially higher total dietary and supplement intake measured in calcium density and phosphorus density. The researchers saw no differences in serum calcium, vitamin D, or alkaline phosphatase levels between the groups. Patients with likely celiac disease were associated with lower femur bone mineral density (BMD) and a lower femoral neck BMD, but showed no difference in total spine BMD. This is one of the first studies to examine variations in nutritional intake of calcium, vitamin D, and phosphorus; their levels in the blood; and bone health in adults with and without likely, undiagnosed celiac disease. Adults with probable undiagnosed celiac disease had lower bone density than those without celiac disease, even though they reported higher calcium intake and nutritional density of calcium and phosphorus. Among other things, the variations in BMD in this study demonstrate the importance of early diagnosis and the rapid adoption of a gluten-free diet for patients with undiagnosed celiac disease. Read more in the J Am Coll Nutr. 2019 Jul 19:1-10.

Celiac.com 05/04/2018 - It has been recognized for several decades that both children and adults with celiac disease have a significantly increased frequency of osteoporosis and increased risk of fractures as compared to the age-matched non-celiac healthy individuals. Based on published data the prevalence of osteoporosis among celiac patients varies from as low as 4% to as high as 70%. The data from our clinic indicate that prevalence of osteoporosis among adults with gluten intolerance and celiac disease is in the vicinity of 30-40%. Characteristics and causes of osteoporosis Osteoporosis is a bone disease characterized by the reduced bone mineral density and impaired bone architecture that leads to an increased risk of fracture. The three main mechanisms by which osteoporosis develop include an inadequate peak bone mass, excessive bone resorption and inadequate formation of new bone during remodeling. At a given age, bone mass results from the amount of bone acquired during growth (the peak bone mass) minus the acquired bone loss due to variety of reasons including age-related processes, malabsorption syndromes, chronic steroid use etc. The rate and magnitude of bone mass gain during the pubertal years may markedly differ from one individual to another. It has been demonstrated that pediatric onset of celiac disease and poor compliance with gluten-free diet during childhood do significantly reduce peak bone mass. One of the main causes of osteoporosis is an alteration in bone remodeling due to imbalance between bone formation and resorption, with a predominance of resorption resulting in a reduction in bone mass and increased risk of fractures. Formation of the new bone is facilitated by specialized cells, osteoblasts, which actively synthesize bone matrix. Bone resorption is mediated by other specialized cells, osteoclasts. One of the main regulators of bone remodeling is the RANK/RANKL/OPG system. During bone remodeling, bone marrow cells and osteoblasts produce RANKL(receptor activator for nuclear factor kB ligand), which bonds with a transmembrane receptor of the osteoclast precursor, RANK(receptor activator of nuclear factor kB), causing their differentiation and activation. Osteoprotegerin (OPG) binds to RANKL before it has an opportunity to bind to RANK, and hence suppresses its ability to increase bone resorption. Normal bone remodeling is based on the permanent renovation of the skeleton and consists of an initial phase of bone resorption followed by a phase of formation, both of which are regulated by general (endocrine) factors and local (paracrine) factors. The main endocrine factors include parathyroid hormone [PTH] and vitamin D as well as estrogens and, to a lesser extent, testosterone, thyroid hormones, growth hormone and leptin. Local factors include various cytokines (IL-1, IL-6 and TNF-a playing a role) key growth factors that regulate the process. There are several well-characterized risk factors which contribute to the development of osteoporosis in celiac patients. These include: 1. Malabsorption of vitamin D and secondary hyperparathyroidism Villous atrophy in celiac patients reduces the active absorption surface and induces steatorrhea (exces fat in feces), which has a chelating effect on calcium and vitamin D, making their absorption difficult. This reduces levels of the vitamin D transporting protein (calbindin and calciumbinding protein) and increases PTH synthesis which, in turn, lead to increased bone resorption causing osteoporosis. 2. Malabsorption of vitamin K Malabsorption of fat soluble vitamins including vitamin K is a common finding in celiac patients. Three vitamin-K dependent proteins have been isolated in the bone: osteocalcin, matrix Gla protein (MGP), and protein S. Osteocalcin is a protein synthesized by osteoblasts. The synthesis of osteocalcin by osteoblasts is regulated by the active form of vitamin D—1,25-dihydroxy-cholecalciferol. The mineral-binding capacity of osteocalcin requires vitamin K-dependent gamma-carboxylation of three glutamic acid residues. MGP has been found in bone, cartilage, and soft tissue, including blood vessels. The results of animal studies suggest MGP facilitates normal bone growth and development. The vitamin K-dependent anticoagulant protein S is also synthesized by osteoblasts, but its role in bone metabolism is unclear. Children with inherited protein S deficiency suffer complications related to increased blood clotting as well as decreased bone density. The data on the role of vitamin K in osteoporosis came from the clinical observations indicating that a chronic use of vitamin K antagonists such as warfarin increases risk of vertebral and rib fractures. Accordingly, vitamin K supplementation significantly lowers risk of vertebral and hip fractures. 3. Magnesium deficiency Magnesium deficiency may be an additional risk factor for celiac-associated osteoporosis. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium. Several human studies have suggested that magnesium supplementation may improve bone mineral density. Magnesium deficiency is easily detected with laboratory tests (eg, low serum magnesium, low serum calcium, resistance to vitamin D) or clinical symptoms (eg, muscle twitching, muscle cramps, high blood pressure, irregular heartbeat). Screening for magnesium deficiency should be routinely included in the screening of celiac patients with osteoporosis. 4. Chronic diarrhea and metabolic acidosis Chronic diarrhea in patients with celiac disease results in significant bicarbonate losses and development of metabolic acidosis. Bone is a major site for the extracellular buffering of the retained acid. Therefore, one of the main compensatory mechanisms maintaining a stable serum bicarbonate level in the face of an uncorrected metabolic acidosis is the dissolution of bone buffers and net efflux of calcium from bone. Bicarbonate supplementation in patients with metabolic acidosis decreases urinary calcium, phosphorus and hydroxyproline wasting supporting the concept of negative effects of acidosis on bone health. 5. Hypogonadism Decline of estrogen production and activity is one of the main events in the development of age-related osteoporosis. It is well known that estrogen deficiency is important in the pathogenesis of osteoporosis not only in women but also in men. Increase in bone mineral density in young men and declines in older men are related to circulating free estrogen, not testosterone. In general, patients with celiac disease are characterized by low levels of circulating estrogens which contributes to the development of premature osteoporosis. 6. Chronic use of Proton Pump Inhibitors Proton pump inhibitors (PPIs) are one of the most widely used classes of drugs. The commonly used PPIs include such drugs as Omeprazole (brand name: Prilosec), Lansoprazole (brand name: Prevacid), Dexlansoprazole (brand names: Kapidex, Dexilant), Esomeprazole (brand name: Nexium), Pantoprazole (brand name: Protonix) and Rabeprazole (brand name: AcipHex). Chronic use of PPIs for gastroesophageal reflux disease and other related conditions has been associated with impaired calcium and magnesium absorption and increased risk of vertebral and nonvertebral fractures. 7. Chronic use of Selective Serotonin Reuptake Inhibitors Selective Serotonin Reuptake Inhibitors (SSRIs) are frequently used in celiac patients for treatment of depressive disorders. The commonly used SSRIs include such drugs as Citalopram (brand name: Celexa), Escitalopram (brand name: Lexapro), fluoxetine (brand name: Prozac), fluvoxamine (brand name: Luvox), Paroxetine (brand name: Paxil) and Sertraline (brand name: Zoloft). It has been demonstrated that SSRIs increase extracellular 5-HT (5-Hydroxytryptophan) levels that have deleterious skeletal effects. The skeletal serotonergic system consists of 5-HT receptors and the 5-HT transporter (5-HTT) in osteoblasts and osteocytes. 5-HTT is a transmembrane protein targeted by SSRIs. 5-HT restrains osteoblastic activity, thus leading to bone loss. 8. Autoimmune mechanisms Autoimmune mechanisms have been long suspected as risk factors contributing to development of osteoporosis in celiac patients. Near a decade ago, it was demonstrated that sera from celiac patients with osteoporosis contains significantly high titers of antibodies against bones as compared to non-celiac osteoporotic patients. The immunostaining was localized in areas where an active mineralization process occurred and was similar to the distribution of the native bone tissue transglutaminase. Recently, it has been described that a subset of patients with celiac disease has autoantibodies to osteoprotegerin, which block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-kappaB (RANK), and are associated with severe osteoporosis and high bone turnover. 9. Chronic inflammation Chronic inflammatory diseases, including celiac disease, are associated with overproduction of proinflammatory cytokines such as TNF-a, interleukin(IL)-1, IL-6, IL-11, IL-15 and IL-17 among others which activate osteoclasts and accelerate bone resorption leading to osteoporosis. In conclusion, osteoporosis associated with celiac disease is not a coincidental problem. It is a consequence of disease-specific (autoantibodies to osteoprotegerin), disease-nonspecific (malabsorption of vitamin D, K and magnesium, hypogonadism, chronic inflammation, chronic diarrhea and metabolic acidosis) and jatrogenic (overuse of PPIs and SSRIs) events accelerating resorptive processes in the skeleton. Correction of the aforementioned risk factors in celiac patients can reverse the development of osteoporosis and reduce the risk of osteoporosis-associated fractures. Bibliography: Bab I, Yirmiya R. Depression, selective serotonin reuptake inhibitors, and osteoporosis. Curr Osteoporos Rep. 2010 Dec;8(4):185-91. Bianchi ML. Inflammatory bowel diseases, celiac disease, and bone. Arch Biochem Biophys. 2010 Nov 1;503(1):54-65. Ito T, Jensen RT. Association of long-term proton pump inhibitor therapy with bone fractures and effects on absorption of calcium, vitamin B12, iron, and magnesium. Curr Gastroenterol Rep. 2010 Dec;12(6):448-57. Katz S, Weinerman S. Osteoporosis and gastrointestinal disease. Gastroenterol Hepatol (N Y). 2010 Aug;6(8):506-17. Riches PL, McRorie E, Fraser WD, Determann C, van't Hof R, Ralston SH. Osteoporosis associated with neutralizing autoantibodies against osteoprotegerin. N Engl J Med. 2009 Oct 8;361(15):1459-65. Stazi AV, Trecca A, Trinti B. Osteoporosis in celiac disease and in endocrine and reproductive disorders. World J Gastroenterol. 2008 Jan 28;14(4):498-505. Sugai E, Cherñavsky A, Pedreira S, Smecuol E, Vazquez H, Niveloni S, Mazure R, Mauriro E, Rabinovich GA, Bai JC. Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis. J Clin Immunol. 2002 Nov;22(6):353-62. Turner J, Pellerin G, Mager D. Prevalence of metabolic bone disease in children with celiac disease is independent of symptoms at diagnosis. J Pediatr Gastroenterol Nutr. 2009 Nov;49(5):589-93. Vasquez H, Mazure R, Gonzalez D, Flores D, Pedreira S, Niveloni S, Smecuol E, Mauriño E, Bai JC. Risk of fractures in celiac disease patients: a cross-sectional, case-control study. Am J Gastroenterol. 2000 Jan;95(1):183-9.

Celiac.com 08/01/2019 - Rates of celiac disease have climbed steeply in recent decades in some developed countries. However, there really isn't much in the current medical literature to clearly explain the increase. Researchers Seth Scott Bittker and Kathleen Roberta Bell recently set out to determine whether nine variables are associated with the development of celiac disease in children. They are variously affiliated with the Interdisciplinary Center for Innovative Theory and Empirics (INCITE), Columbia University, New York, New York, US; and the Ontario College of Teachers, Toronto, Ontario, Canada. The team looked at the following variables: "incidence of ear infection before 2 years old, courses of antibiotics before 2 years old, duration of breastfeeding, vitamin D drop exposure in infancy, vitamin D supplement exposure between 2–3 years old, age at gluten introduction into the diet, fat content of cow’s milk consumed between 2–3 years old, quantity of cow’s milk consumed between 2–3 years old, and type of water consumed at 2 years old." To gather their data, the team used an internet survey to quiz parents living in the US with at least one biological child between 3 and 12 years old. To recruit participants, the team used social media, websites, electronic newsletters, and advertisements. The team ended up with a total of 332 responses for children with celiac disease, and 241 responses from the non-celiac control group. The team's data showed that skim liquid cow’s milk consumed between 2–3 years old, vitamin D drops used for longer than 3 months, early doses of antibiotics, and early ear infection are all associated with later development of celiac disease in children. This study found a connection between skim milk consumption, and vitamin D drop use for more than 3 months, and later development of celiac disease. It also found evidence to support earlier data that early life exposure to antibiotics and early life infection, especially ear infection, are also associated with the development of celiac disease in children. Read more in Clinical and Experimental Gastroenterology

Celiac.com 08/16/2018 - What is the significance of vitamin D serum levels in adult celiac patients? A pair of researchers recently set out to assess the value and significance of 25(OH) and 1,25(OH) vitamin D serum levels in adult celiac patients through a comprehensive review of medical literature. Researchers included F Zingone and C Ciacci are affiliated with the Gastroenterology Unit, Department of Surgery, Oncology and Gastroenterology, University of Padua, Padua, Italy; and the Celiac Center, AOU San Giovanni di Dio e Ruggi di Aragona, University of Salerno, Department of Medicine and Surgery, Salerno, Italy. Within the wide spectrum of symptoms and alteration of systems that characterizes celiac disease, several studies indicate a low-level of vitamin D, therefore recent guidelines suggest its evaluation at the time of diagnosis. This review examines the data from existing studies in which vitamin D has been assessed in celiac patients. Our review indicates that most of the studies on vitamin D in adult celiac disease report a 25 (OH) vitamin D deficiency at diagnosis that disappears when the patient goes on a gluten-free diet, independently of any supplementation. Instead, the researchers found that levels of calcitriol, the active 1,25 (OH) form of vitamin D, fell within the normal range at the time of celiac diagnosis. Basically, their study strongly suggests that people with celiac disease can recover normal vitamin D levels through a gluten-free diet, without requiring any supplementation. Source: Dig Liver Dis. 2018 Aug;50(8):757-760. doi: 10.1016/j.dld.2018.04.005. Epub 2018 Apr 13.

Celiac.com 07/17/2018 - What can fat soluble vitamin levels in newly diagnosed children tell us about celiac disease? A team of researchers recently assessed fat soluble vitamin levels in children diagnosed with newly celiac disease to determine whether vitamin levels needed to be assessed routinely in these patients during diagnosis. The researchers evaluated the symptoms of celiac patients in a newly diagnosed pediatric group and evaluated their fat soluble vitamin levels and intestinal biopsies, and then compared their vitamin levels with those of a healthy control group. The research team included Yavuz Tokgöz, Semiha Terlemez and Aslıhan Karul. They are variously affiliated with the Department of Pediatric Gastroenterology, Hepatology and Nutrition, the Department of Pediatrics, and the Department of Biochemistry at Adnan Menderes University Medical Faculty in Aydın, Turkey. The team evaluated 27 female, 25 male celiac patients, and an evenly divided group of 50 healthy control subjects. Patients averaged 9 years, and weighed 16.2 kg. The most common symptom in celiac patients was growth retardation, which was seen in 61.5%, with abdominal pain next at 51.9%, and diarrhea, seen in 11.5%. Histological examination showed nearly half of the patients at grade Marsh 3B. Vitamin A and vitamin D levels for celiac patients were significantly lower than the control group. Vitamin A and vitamin D deficiencies were significantly more common compared to healthy subjects. Nearly all of the celiac patients showed vitamin D insufficiency, while nearly 62% showed vitamin D deficiency. Nearly 33% of celiac patients showed vitamin A deficiency. The team saw no deficiencies in vitamin E or vitamin K1 among celiac patients. In the healthy control group, vitamin D deficiency was seen in 2 (4%) patients, vitamin D insufficiency was determined in 9 (18%) patients. The team found normal levels of all other vitamins in the healthy group. Children with newly diagnosed celiac disease showed significantly reduced levels of vitamin D and A. The team recommends screening of vitamin A and D levels during diagnosis of these patients. Source: BMC Pediatrics

Celiac.com 05/10/2018 - Most people who suffer from inflammatory bowel diseases (IBD) have either Crohn’s disease or ulcerative colitis. Some research has suggested that patients with Crohn's disease have an altered response to vitamin D, among other issues. The exact mechanism behind this is not well understood. To get a better picture of the problem, a team of researchers recently set out to investigate disease-specific gene expression profiles of peripheral blood mononuclear cells (PBMCs) from Crohn’s disease patients in clinical remission. The research team included Holger Schäffler, Maria Rohde, Sarah Rohde, Astrid Huth, Nicole Gittel, Hannes Hollborn, Dirk Koczan, Änne Glass, Georg Lamprecht, and Robert Jaster, with the Department of Medicine II, Division of Gastroenterology, Rostock University Medical Center in Rostock, Germany. The team began by genotyping patients with Crohn's disease in clinical remission or with very low disease activity according to nucleotide-binding oligomerization domain 2 (NOD2), and PBMCs from wild-type (WT)-NOD2 patients, and patients with homozygous or heterozygous NOD2 mutations. Meanwhile the team isolated healthy donors for further analysis. The team then cultured the cells with vitamin D, peptidoglycan (PGN) and lipopolysaccharide (LPS) for defined periods of time before RNA was isolated and subjected to microarray analysis using Clariom S assays and quantitative real-time PCR. They assessed the NOD2- and disease-specific gene expression profiles with repeated measure ANOVA using a general linear model. The team used microarray assays to find 267 genes that were significantly up- or downregulated in PBMCs of WT-NOD2 patients, compared to healthy donors after challenge with vitamin D and/or a combination of LPS and PGN (P < 0.05; threshold: ≥ 2-fold change). For further analysis by real-time PCR, the team selected genes with known impact on inflammation and immunity that fulfilled predefined expression criteria. In a larger group of patients and controls, the team found a disease-associated expression pattern, with higher transcript levels in vitamin D-treated PBMCs from patients, in three of these genes, CLEC5A (P < 0.030), lysozyme (LYZ; P < 0.047) and TREM1 (P < 0.023). The team found six genes that were expressed in a NOD2-dependent manner (Crohn's disease101, P < 0.002; CLEC5A, P < 0.020; CXCL5, P < 0.009; IL-24, P < 0.044; ITGB2, P < 0.041; LYZ, P < 0.042). Interestingly, the team saw the highest transcript levels in patients with heterozygous NOD2 mutations. This study identifies CLEC5A and LYZ as Crohn's disease- and NOD2-associated genes of PBMCs and supports the need for further studies on their pathomechanistic roles. The team found that PBMCs of patients with Crohn's disease display alterations in their response to vitamin D and PAMPs. Disease-associated and NOD2-dependent gene expression profiles are preserved even during clinical remission. The team’s data identifies CLEC5A, LYZ and TREM1 as good candidates for follow-up study. The researchers propose that these genes may act in a common network relevant to celiac disease development. The research team remains committed to the longterm goal of biomarkers to that will accurately predict the clinical course of celiac disease. Source: World J Gastroenterol. 2018 Mar 21; 24(11): 1196–1205. doi: 10.3748/wjg.v24.i11.1196