Celiac diease, gluten and the brain-gut connection supported by finding of intestinal and brain antibody deposits.

Antibodies for tissue transglutaminase found in intestine of blood test negative celiac disease are also found in intestine and brain in people with brain disease due to gluten. Gluten ataxia is a brain disorder characterized by balance disturbance not explained by any other cause but due to ingestion of gluten. The disorder responds to a gluten free diet if irreversible brain damage has not already occurred. Calcifications can be seen in the brain on magnetic resonance imaging (MRI).

Deposits of gluten related antibodies have been found in brain tissue obtained on biopsy and autopsy specimens. Mario Hadjivassiliou, M.D. from Sheffield England recommends gluten ataxia be added to a list of gluten related diseases that includes peripheral neuropathy and the skin disorder dermatitis herpetiformis. He has called for a new paradigm to be accepted where celiac disease is not considered primarily as an intestinal disease.

Dr. Hadjivassiliou and colleagues recently published a report of nine patients with gluten ataxia compared with seven patients with ataxia due to other causes. They found tissue transglutaminase IgA deposition on jejunum intestinal tissue on all nine patients with gluten ataxia but none of the control patients. Brain tissue from an autopsy of one patient with gluten ataxia was also found to have IgA tTG deposits in the cerebellum, pons and medulla of the brain but not in a control brain.

Previous studies have found negative blood celiac blood tests in patients with gluten ataxia suggesting that they may not have celiac though they had gluten related disease. In light of a new report that blood test negative celiac disease can have intestinal tTG and advanced intestinal damage it is curious to wonder if the gluten ataxia patients with blood tests negative are seronegative celiac disease. It is increasingly appearing that there is a very broad spectrum of gluten related disease and there are non-celiac gluten related symptoms that include the brain, skin, musculoskeletal system as well as the gut.

Many patients I have seen with gluten sensitivity describe symptoms of balance difficulty, concentration problems or “brain fog”, headaches, and neuropathy and a few report symptoms such as “bug crawling” sensations and strange muscle twitches. These symptoms commonly improve with gluten-free diet and return with intentional or accidental gluten exposure. In some intestinal symptoms or skin rashes occur, often at the same time as the onset of the brain symptoms but some don't have any gut symptoms. The concept of gluten as a cause of brain symptoms is still not one widely known or accepted by many doctors, especially in the United States. However in Europe, especially England, Germany and Scandinavian countries, as well as Australia and New Zealand the gluten brain-gut connection is more accepted.

The concept that casein, the major milk protein, causes brain symptoms that imrove on a dairy-free diet, casein-free diet, is also not commonly accepted by doctors in the U.S. though many lay public organizations and support groups have found casein-free diet to be associated with improvement of brain function as well as helping autism.

What is needed is more openness of U.S. doctors to role of diet and foods in such symptoms and diseases and much more scientific research. I ask you to join me on the journey of the food, bacteria, gut-brain-joint-skin connection to disease and health. You may help spread the word through e-mailing this post to others by clicking on the letter icon below. You may subscribe to the Food Doc blog by clicking on subscribe to this post atom on the right side of this post so that you will be automatically alerted to my new posts.

Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia. Hadjivassiliou M. et. al. Neurology 2006; 66:373-377.

Endomysial antibody-negative coeliac disease: clinical characteristics and intestinal autoantibody deposits. Gut 2006; 55:1746-1753.


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Ostoporosis risk increased by celiac and heartburn medications: Is there a collision of increase risk?

Osteoporosis is increased by long-term use of acid blocker medications called proton pump inhibitors for chronic heartburn, a symptom commonly missed as a sign of celiac disease. So, not only doctors frequently unaware that osteoporosis is a common complication of undiagnosed and untreated celiac disease but are also likely aggravated the problem in many of these people by prescribing acid blocking medications for heartburn symptoms that are due to gluten.

Osteoporosis risk goes up with age. The prevalence is less than 15% at age 50 but increases to almost 30% at age 60, 50% at age 70 and 70% at age 80. I have however, noted increasing number of below 60 year old women and more men diagnosed with osteoporosis, almost none of whom have been screened for celiac disease or inflammatory bowel disease.

At least one study has documented that less than half of doctors are aware that osteoporosis is a manifestation of celiac disease. Heartburn is a common symptom also not commonly recognized by doctors as a manifestation of celiac disease. Gluten ingestion can impair gastric emptying resulting in more gastro-esophageal reflux. Initiation of gluten-free diet has been shown to diminish reflux symptoms and result in healing of esophagitis.

Several patients I have evaluated for reflux symptoms, particularly when these symptoms were poorly controlled or the patient was considering surgery rather than take daily medications, were found to have celiac disease or non-celiac gluten sensitivity. In my experience, reflux symptoms frequently dramatically improve on a gluten free diet.

This effect I have observed not only in celiac disease patients but also in those not meeting strict diagnostic criteria for CD. Prior to starting a gluten-free diet I took a daily proton pump inhibitor myself. After a GFD, I occasionally experience heartburn when I drink too much coffee or combine coffee, alcohol and chocolate in the same meal. In my opinion, everyone with significant heartburn or a diagnosis of reflux disease should be screened for gluten sensitivity and/or consider a trial of GFD.

Celiac increases the risk of osteoporosis. How much celiac disease increases osteoporosis is debated. Studies have shown from small increases (1.5-1.8 times) to much larger (3-5 times) increases osteoporosis in CD. Such increased risk has prompted for calls for screening all people with celiac disease for osteoporosis and all people with osteoporosis for celiac disease.

With this new study raising the concern about long-term use of acid blocking medications, especially the so-called proton pump inhibitors like nexium and prilosec, causing an increase risk of osteoporosis and the frequently unrecognized association of heartburn with undiagnosed celiac disease that also increases the risk.

You are now forewarned about blindly accepting a doctor’s offer to just write you a prescription for such medication without looking further into the possible causes of your heartburn as well as the risks of simply treating your symptom with a medication. This is especially important since the medication may actually worsen a known complication of an underlying undiagnosed problem that can be simply treated by diet decreasing your risk of osteoporosis. Subscribe to this blog to receive automatic updates of new posts offering information and insights from the Food Doc so that you are kept up to date
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Gluten-free flours:Gluten-free substitutes for wheat include tapioca

Today I used Tapioca flour to coat an oven bag for our turkey. Tapioca is a gluten-free starch derived from dried cassava tuber or root. The cassava plant is a woody tropical shrub cultivated primarily in Brazil, Thailand, Nigeria, Zaire, and Indonesia. It is also known as yucca or manioc.

Tapioca flour is an excellent substitute for gluten containing wheat flour in cooking when a light texture is needed, for example in pancakes and waffles. Tapioca flour can be used to thicken foods such as puddings (tapioca pudding), sauces or gravies. In baking it can provide a bit more stickiness lacking in gluten-free baking.

The cassava tuber contains about 30% starch but very little protein. The tuber can be prepared like a potato but similarly should not be eaten raw. Toxic cyanogenic glucosides in raw cassava tubers are rendered non-toxic with cooking.

The origin of the word tapioca comes from the Tupi-Guarani language of Brazil, the largest producer of Cassava. From tipi, meaning residue, and ok, meaning to squeeze out, we get tapioca. This is traditionally the roots are grated then squeezed or pressed to remove the sap. The residue is then further dried. Dried roots can be milled into flour that is gluten-free.


Bob’s Red Mill pure tapioca flour or all-purpose gluten free baking flour made from tapioca, garbanzo, potato, sorghum and fava flour, both work well for cooking. Bob’s Red Mill stone grinds gluten-free flours in a dedicated facility that is free from wheat and other gluten containing grains. The production line is separate from other lines and they batch test regularly using an ELISA gluten testing process that detects any gluten down to 20 parts per million. They report they are also dairy and casein free.




For one of two smaller turkeys we roasted, I applied high heat safflower oil to coat the surface prior to inserting in an oven bag coated with 1 tablespoon of tapioca flour. To the other, for those in the family who are not casein sensitive, melted organic salted butter was used to baste the surface before cooking in a separate oven.

Though maintaining a gluten-free diet can be a challenge that is necessary for those with celiac disease, it can be done and should be considered for many others who are gluten sensitive. Alternative flours exist for baking and the benefits of gluten-free lifestyle can be life changing for many individuals. For more information be sure to subscribe to this blog to receive regular updates from the Food Doc, the food allergy and food intolerance expert doctor. You may find some of Bob's Red Mill gluten-free products at the Food Doc amazon affililiate store or by visiting their website www.bobsredmill.com directly.





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Celiac disease with negative endomysial antibody not only exists but may be longstanding, more severe and associated with higher risk of lymphoma

A new report Finland not only confirms others studies showing celiac disease can be present in absence of a positive anti-endomysial antibody (EMA) but also this may be associated with longstanding, undiagnosed, more severe and complicated disease with a higher risk of lymphoma and death.

Celiac disease occurs with negative endomysial antibody:
Twenty two people without IgA deficiency, a cause of false negative EMA, were confirmed to have celiac disease by small intestinal biopsy that not only had classical changes but deposits of tissue transglutaminase IgA (tTG) in the intestinal tissue not found in people without celiac disease.

Endomysial antibody negative celiac patients are older and more often men:
The EMA negative patients were not only on average older (median age 55 versus 40 for EMA+) but more commonly men (59%) compared with the usual women predominance seen in celiac disease.

Endomysial antibody negative celiac patients have higher death rate:
During follow up 27% or six of twenty-two patients with negative EMA blood test diagnosed with celiac disease died during the follow up. Because these patients were on average older at time of their diagnosis it is presumed they had been undiagnosed and untreated for longer time than those who had a positive blood test.

Endomysial antibody negative celiac patients get lymphoma:
Three of the twenty-two with negative EMA had enteropathy-associated T cell lymphoma (EATL), a known complication of untreated, undiagnosed longstanding celiac disease. Two had an earlier small bowel biopsy that was consistent with celiac disease but was the diagnosis was overlooked because their EMA was negative.

Endomysial antibody negative celiac patients have severe intestinal damage:
The biopsies of EMA positive and EMA negative patients were not significantly different. Patients with negative EMA had advanced intestinal damage (Marsh III, partial to total villous atrophy) just as often as the blood test positive patients.

Duodenal biopsies testing for TG2 deposits may be done in future:
This study demonstrates that transglutaminase (TG2) is present in intestinal tissue in celiac disease but not in patients without celiac disease. Because these deposits can be detected when celiac blood test are negative or biopsy is equivocal, this testing may be useful in seronegative celiac disease instead of subjecting the patient to potentially dangerous gluten challenge or delay in diagnosis and instituting timely treatment with gluten-free diet. Without testing for TG2 in intestinal biopsy diagnosis of celiac disease may not be correctly made and gluten-free diet started early enough to prevent an increased risk of lymphoma and early death.

Duodenal biopsy indicated for symptoms or family history:
This study would support an approach that any patient with symptoms or signs of celiac disease should undergo an upper endoscopy with small biopsy regardless of EMA blood test results especially if they are a relative of celiac patient and/or DQ2 or DQ8 positive.

Endomysial antibody negative blood tests do not rule out celiac disease:
A negative EMA blood test does not rule out celiac disease but instead may result in delay in diagnosis and treatment. This delay in diagnosis and treatment may increase risk of more complications including lymphoma and death.

Celiac disease misperceptions may be a threat to your life:
This study further illustrates the expanding knowledge as well as misperceptions about celiac disease. Doctors who have told patients that they either don't have celiac disease or don't need a small bowel biopsy because of a negative endomysial antibody test should shudder. If you have been told you do not have celiac because you have a negative EMA despite having suggestive symptoms or a family history of celiac I recommend you have a small bowel biopsy. If you already have but were told that biopsy was not diagnostic or because your EMA was negative you don't have celiac disesase, I suggest you ask your doctor to reconsider the possibility. This is especially true if you are HLA DQ2 and/or DQ8 positive. Your life may be at risk.

Stay tuned as the Food Doc reviews another important article in the same December 2006 issue of Gut as this article also concluding that positive blood tests are not required for diagnosis of celiac disease and adding that mild biopsy findings of intraepithelial lymphocytosis without villous atrophy can result in malabsorption severe enough to result in anemia and osteoporosis.

Reference:
Salmy TT. Endomysial antibody negative coeliac disease: clinical characteristics and intestinal autoantibody deposits. Gut 2006;55:1746-1753.


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Bacteria causing the leaky gut resulting in colitis

A mouse colitis model study has demonstrated that live fecal bacteria not only induce a defect in the intestinal barrier (a leaky gut) but also intestinal inflammation and injury. Bacteria cell products or protein components could induce intestinal barrier defects or trigger a leaky gut, but without live bacteria, could not cause intestinal inflammation or colitis. Only live bacteria could cause colitis.

Loss of tolerance to proteins of normal bacteria residents in the gut, or endogenous gut flora, plays an important role in intestinal inflammation. However, it is not known why some bacteria do and others do not cause intestinal inflammation.

Oral tolerance to some bacteria appears to develop just as tolerance to certain foods occurs. Loss of tolerance may be due to a variety factors. Factors specific to an individual may include their immunogenetic make-up, underlying or pre-existing gut injury, an immune affecting event or infection, and certain combinations of bacteria, yeast, and food proteins.

When tolerance is lost, inflammation can result that may perpetuate gut injury. The resulting increasingly leaky gut leads to further intolerance. The cycle becomes self perpetuating, as on auto pilot, resulting in an autoimmune process that is difficult to break.

It may be that until altered gut flora is restored to normal and/or certain food protein exposures limited or eliminated, that this cycle continues. Medications like steroids can reduce the inflammation but not necessarily reverse the self-perpetuating process that occurs in Crohn’s disease, for example.

However, the concept of antibiotic use to kill the "bad" bacteria that have altered the normal gut flora, followed by probiotics is gaining steam. This approach is being advocated to prevent the development of irritable bowel syndrome as well as colitis and Crohn’s disease after infection or gastroenteritis. The concept of elimination of foods that are known for or suspected to be causing injury when interacting with altered bacteria and/or yeast levels bacteria in the gut is also receiving more attention.

This makes sense. The presence of antibodies to bacteria and yeast components in Crohn’s disease are indication of loss of tolerance to endogenous flora. The presence of antibodies to gliadin and the specific proteins endomysial and tissue transglutaminase indicates a loss of tolerance to gluten in celiac disease.

In both instances, the presence of these specific antibodies indicate a loss of intestinal barrier function, or leaky gut, that allows foreign bacteria and food proteins to come in contact with the genetically predisposed gut immune system. Once activated, the immune system has difficulty shutting down. Instead this self-perpetuating cycle of injury, inflammation and leaky gut continues, often fueled by bad gut bacteria levels and ongoing food protein stimulation.

The billion-dollar question may be how do you protect the gut from injury and activation of an altered gut immune response? Is it by taking probiotics regularly? Is it by avoiding certain foods? As the food doc, I offer these ideas as food for thought as we continue to explore together the links between the leaky gut, bacteria, and food.

Reference: Sydora BC et. al. “Bacterial antigens alonecan influence intestinal barrier integrity, but live bacteria are required for initiation of intestinal inflammation and injury. Inflammatory Bowel Disease. 2006;12(6):429-436.


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Cow’s milk protein intolerance or dairy allergy and the red belly button sign.

Redness of the belly button (umbilicus) is a diagnostic sign of cow’s milk protein intolerance (CMPI). This unusual but very specific physical sign was present in almost 10% of Italian children confirmed with CMPI. The red umbilicus sign was seen in children with gastrointestinal (GI) symptoms as well as those with respiratory and dermatological symptoms of food intolerance. The redness went away on an elimination diet (ED) and reappeared on food challenge. This was not seen in children without food intolerance.

Prior to diagnosis and ED trial, the red belly button appeared after or at the same time as milk allergy symptoms in 90% in whom it was observed. The redness disappeared before the end of the second week of the ED, usually by five days, but reappeared within 24 hours when cow’s milk protein was re-introduced. On challenge the red belly button sign often reappeared before the main symptom(s) of CMPI.

Though uncommon, parents and doctors should remember this highly specific but odd sign of cow's milk and other food protein intolerance. If your child has a red belly button, think food allergy or intolerance. If tests for food allergy or intolerance are negative or non-diagnostic, I recommend an elimination diet trial followed by re-challenge. A food symptom diet diary should be recorded before after the ED.

You can now tell your doctor that a positive red umbilicus sign is highly suggestive of food intolerance! Subscribe now to the food doc blog to become your own food allergy expert and health advocate.


Reference: Iacono G., et. al. The “Red Umbilicus”: A Diagnostic Sign of Cow’s Milk Protein Intolerance. Journal of Pediatric Gastroenterology and Nutrition 2006:42(5); 532-534.

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Celiac and gluten sensitivity: Duodenal intraepithelial lymphocytes significantly increased compared with esophagitis and gastritis

Intraepithelial lymphocytes (IEL’s), are increased in number in the intestinal villi in celiac disease. Though not specific for celiac disease (CD), increased IEL’s are accepted as the earliest sign of gluten intolerance in the gut. Most pathologists either report the number of IEL’s per 20 intestinal lining cells (enterocytes) or per 100 enterocytes.

For more than 30 years >40 IEL’s/100 enterocytes was considered the diagnostic threshold for CD. That number has been reduced to >30/100. More recent studies have indicated it may need to be lowered to >20-25/100.

Helicobacter pylori bacteria infection, giardia parasite infection, cow’s milk protein sensitivity, and viral infections have all been reported to be associated with increased duodenal IEL’s. Though not well established, it is believed that the number of IEL’s in these conditions may not be as high as in CD.

A recent study of biopsies of the esophagus, stomach, and duodenum of 46 people without evidence of CD reached several conclusions. Though there may be a slight increase IEL’s in esophagitis and gastritis, the difference in IEL numbers is not significantly different in normal biopsies of the esophagus and stomach. Though general ranges of duodenal IEL's found in active esophagitis (2-13, average 8.8), active gastritis with Helicobacter pylori infection (2-13, average 7.2) and chronic gastritis without H. pylori infection (4-20, average 10.2) was very similar to those with negative esophagus, stomach and duodenal biopsies (2-18, average 6.7) the average number of IEL's was slightly higher, though not statistically significant.

I believe this study is important because it argues against attributing more than 20-25 IEL’s/ 100 enterocytes to other inflammatory processes in the esophagus or stomach. It also supports the findings of other studies that have found that >20-25 IEL’s/100 is a sign of gluten sensitivity and possibly early CD.

In the context of elevated gliadin antibody levels I believe that >25 IEL’s more likely than not indicates gluten sensitivity though not necessarily CD. Strict criteria for diagnosing CD require a positive specific CD blood test such as endomysial antibody or tissue transglutaminase antibody and >30 IEL’s/100 enterocytes and/or evidence of villous atrophy on small intestinal biopsy.

For more information about IEL’s, including illustrative biopsy photos, see my website www.thefooddoc.com and earlier posts on this blog.

Reference:

Yousef MM, Yantiss RK, Baker SP and Banner BF. Duodenal Intraepithelial Lymphocytes in Inflammatory Disorders of the Esophagus and Stomach. Clinical Gastroenterology and Hepatology 2006;4:631-634.


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Lactose intolerance and hidden Celiac disease

Several studies have shown high incidence of lactose intolerance in Celiac disease. A study published in Digestion in 2005 confirmed that many lactose intolerant people also have undiagnosed Celiac. Almost a quarter of people had lactose intolerance as the only sign of hidden Celiac disease. All the lactose-intolerant people that did not get better with lactose avoidance had Celiac disease. I agree with their conclusion. All people suffering from lactose intolerance should be screened for Celiac disease. I would also include all people labeled as having IBS.

Lactose is milk sugar. A disaccharide or combination of the two simple sugars (monosaccharides) glucose and galactose, lactose digestion requires the intestinal enzyme lactase. Lactase is found on the tips of the villi of enterocytes, or small intestine lining cells, where it is vulnerable to injury. See my diagram, microscope slides, and explanation of villi on this blog and my website www.thefooddoc.com. Lactose intolerance resulting from small bowel injury or abnormal gut bacteria is termed acquired or secondary lactose intolerance. Though there are many causes of small bowel injury, two of the most common are viral gastroenteritis, or “stomach flu”, and food intolerance. Lactase function can be also be impaired by abnormal bacteria levels in the small intestine known as small bowel bacterial overgrowth (SBO). Lactase enzyme levels also diminish with age.

Primary or congenital lactase enzyme deficiency is present in up to 80% of black Latinos, nearly 100% of Asians and Native Americans, but 15% of Caucasians of Northern European ancestry. Most of the latter are not lactose intolerant unless they have small bowel injury or SBO. Lactose intolerance in these individuals should raise the suspicion of Celiac disease (Celiac Sprue, non-topical Sprue and gluten sensitive enteropathy).

In my experience as a food allergy and intolerance expert, many lactose intolerant people as well as individuals labeled as IBS, are undiagnosed gluten sensitive individuals. After a gluten-free diet and associated gut healing they can tolerate dairy much better and many have improvement or resolution of IBS type symptoms. This is also my personal experience. In medical school, I diagnosed myself as having irritable bowel syndrome (IBS) and lactose intolerance.

Though, my blood tests for Celiac disease are negative I carry the major gene predisposing to Celiac, HLA DQ2, and have elevated stool antibodies to gliadin and tissue transglutaminase (www.enterolab.com). With a gluten-free diet my “IBS” resolved and my lactose tolerance dramatically improved. However, since I am intolerant to the milk protein, casein, I generally avoid dairy products. Casein or milk protein intolerance and milk or dairy allergy are distinctly different conditions from lactose intolerance.

If you have been diagnosed with IBS or lactose intolerance you should tested for Celiac disease.
Below I have included some helpful diagnosis codes.

References:
Ojetti, V. et. al. High prevalence of Celiac disease in patients with lactose intolerance. Digestion 2005;71:106-110.

Heyman, M. Lactose intolerance in infants, children and adolescents. Pediatrics September 2006;118(3):1279-1286.

ICD9 diagnosis codes:
Lactose intolerance 217.3
Celiac disease/gluten sensitivity 579.0
Irritable bowel syndrome 564.1
Milk allergy V15.02
Other food allergies, not specified V15.05

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Osteoporosis? Get screened for celiac disease.

I frequently encounter younger and younger women as well as more men who have been diagnosed as having osteoporosis or osteopenia. Osteoporosis is a progressive decline in bone density. The bones are weakened and the brittleness predisposes to fractures from even minor falls or trauma. Sometimes, even opening a window, lifting or being hugged can result in spine fractures. Bone density normally declines with age, especially in women who undergo menopause who are not receiving estrogen supplementation. However, accelerated osteoporosis occurs from poor absorption of calcium such as when the gut is damaged or injured. In pre-menopausal women Celiac disease is a common yet often unrecognized cause of osteoporosis from gut injury resulting in malabsorption.

Often I see patients for routine screening colonoscopy at age 50 and I note that they are on fosamax or other medications for osteoporosis. Many also list thyroid hormone medication. When I inquire about these medications, they don't seem to think it is that unusual, just part of getting older, Yet, on further questioning, most admit to chronic gastrointestinal symptoms like bloating, gas, and diarrhea, usually resulting in a diagnosis of irritable bowel syndrome. Few of them have ever been screened for celiac disease. Why is this? Most physicians and certainly most patients are unaware of the associations of hypothyroidism, irritable bowel syndrome or osteoporosis with celiac disease. A survey of primary care physicians published in 2005 confirmed that less than half (45%) were aware that osteoporosis was a manifestation of celiac disease. Only 13% were aware of the association of diabetes with celiac and less than a third knew symptoms of celiac could begin in adulthood. It is no wonder that though 1/100 in people have celiac disease, the majority remain undiagnosed and suffer for an average of 13 years before diagnosis, usually too late to fully reverse a variety of associated autoimmune, musculoskeletal, and neurologic conditions.

Amagan and colleagues published in 2005 results of screening of almost 100 pre-menopausal women with idiopathic osteoporosis. They found 10-20% had blood tests positive for Celiac disease or gluten sensitivity. Since 1% of people have Celiac disease, most undiagnosed, a ten to twenty times incidence of Celiac disease in individuals with osteoporosis is observed. This justifies the recommendation that all women who have unexplained osteoporosis and all pre-menopausal women with premature osteoporosis should be screened for Celiac disease.

If you are a man or a woman under 50 with osteopenia or osteoporosis, I recommend you ask your doctor to screen you for celiac disease. If you have any gastrointestinal symptoms, fatigue, history of infertility, type I diabetes, thyroid disorder, rheumatoid arthritis, headaches, neuropathy, anemia, or skin problems you should also be screened.

References:
Amagan O et.al. Clin Rheumatol. 2005 (3):239-43
Zipser, et.al. J Gen Intern Med. 2005; 20(7):644-46.

Osteoporosis Resource:
National Osteoporosis Foundation
www.nof.org

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Gluten-free expresso chocolate cookies

After recovering from a busy call weekend I decided to write a lighter note about gluten-free cookies. Many of us who have celiac disease or are gluten sensitive struggle with missing such pleasures as a good cookie. Pamela's products make several gluten-free and casein-free foods that can be ordered online and delivered to your home. The expresso chocolate chunk cookies are great, especially when dunked in coffee! And they can be ordered in boxes containing individual wrapped packets of two cookies each as well as boxes containing 12 cookies each. Pamela's products are formulated and produced to be wheat-free and gluten-free though produced in a facility that also makes products containing other food allergens such as peanuts, tree nuts, milk, eggs and soy.




The expresso chocolate chunk cookies are one of my gluten-free indulgences when I am not worrying about my fat intake or being strictly casein-free. Nearly half of their delicious calories are fat calories and two cookies contain only 1 gram of fiber. Since they do potentially contain traces of milk protein I limit my intake as I am also casein sensitive.

Though I advocate avoiding packaged foods as much as possible, I am like most of you, a realist. I work a busy schedule, have small children and a spouse who are following a gluten-free diet. We all tire of only fresh fruits and vegetables, lean meats and fish without a snack or dessert. However, as a physician who is gluten sensitive, married to a physician with celiac disease, and daily diagnosing and treating people with Celiac disease, I am comfortable recommending this particular product to you.

I plan to periodically intersperse with my reviews of the latest scientific research with reviews particular foods or products, recipes, and diagnostic tests that I am personally comfortable with, as feel can relate to your struggle because it is also my struggle.

The website www.thefooddoc.com is continuing to be developed in it's final premier form and should launch soon as well. It will include several web based applications including a symptom assessment tool, online diet diary, info wizard and a virtual office. I hope all of you, from over 35 countries, who have been kind of enough to e-mail me your support or inquiries will continue to check in to the food doc blog and the website for helpful information. Stay tuned as I prepare to launch a podcast in the very near future and begin recording some short videos that will be available online soon too.

You may see that this blog has some ads and an amazon store link. These generate some revenue that helps to fund the website so I can continue to bring free quality content to the public as a physician while continuing to actively provide direct patient care.
Yours truly,

Dr. Scot Lewey
"the food doc"
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