Celiac disease made the “What's In” list for the decade 2010 in the Washington Post's “Ranking What's Out, What's In.” The number of people diagnosed with the disorder seems high enough to call it “epidemic.” Everyone is talking about it. Celiac disease has had top billing on the popular daytime talk show The View. Co-host Elisabeth Hasselbeck is increasing awareness by talking about her struggles with the disease. More than two million people in the US have celiac disease. An estimated one in one hundred children has the disease, yet the majority of those afflicted are not diagnosed. The symptoms at any age can range from severe—diarrhea, vomiting, and weight loss—to vague, such as an upset tummy, bloating, being out of sorts, or even none at all.
That is the problem! Years may go by with celiac disease undiagnosed, which puts your health, including bone health, in jeopardy. Gluten, which is found in wheat, rye, and barley, is toxic to the bowel. In the small intestine, little mini fronds called “villi” provide increased surface area for absorption of nutrients. Villi means “shaggy hair” in Latin. Basically, the shaggy hair gets a bad buzz haircut with celiac disease. The villi become damaged and inflamed nubs. This damage and inflammation in the small intestine leads to poor absorption of vitamins and nutrients that are vital for your health.
The treatment for celiac disease (also referred to as gluten sensitivity or intolerance) is a strict gluten-free diet. I mean strict! Gluten is hidden in hundreds of common food products that you would not suspect. No soy sauce on your sushi! Just an eighth of a teaspoon of gluten is enough to harm your intestine. You have to be a true sleuth and become familiar with what you can and can't eat. This is a huge lifestyle and nutrition change that is socially challenging.
In the past, this diet was extremely difficult to manage. Now “gluten-free” has gone mainstream. My local supermarket has a gluten-free section; other supermarkets offer lists of gluten-free products available in their stores. Labels are explicit: “No gluten ingredients used” or, conversely, “Made on equipment that processes wheat.” Even so, you still need to be savvy and informed about what to eat. That is the reason Hasselbeck put together her New York Times bestselling book The G-Free Diet.
First, celiac disease needs to be diagnosed.
CELIAC DISEASE: HIDDEN CAUSE OF LOW BONE MASS AND FRACTURES
A number of studies have identified the presence of celiac disease without obvious symptoms in middle-aged women with low bone density. These findings have led to the use of screening blood tests for celiac disease in the evaluation of people with low bone density. The tests look for proteins, called autoantibodies, that react against the body's own tissues. The common markers have long technical names: antiendomysial antibodies, antigliadin antibodies, and tissue transglutaminase. Your doctor may include one or more of these tests to detect celiac disease.
Osteoporosis is more common in people with celiac disease than in the general population. At the time of diagnosis, low bone density is common in both children and adults. Before starting a gluten-free diet, osteoporosis may be present in up to one-third of adults with celiac disease. Typically, bone density increases about five percent during the first year of adhering to a gluten-free diet. However, bone density tends to remain lower than the average range. Early reports showed that the association of celiac disease with osteoporosis was found in up to 20 percent of postmenopausal women evaluated for osteoporosis. These reports tended to be from specialty clinics. Later reports from more general populations found much lower rates. Approximately 2 to 3 percent of women were reported to have the combination of previously undetected celiac disease and osteoporosis.
The fracture risk in patients with celiac disease varies across different study populations. Overall, fractures are more common among patients with celiac disease than in the general population. Specific risk factors for fracture include: young age at the onset of celiac disease, failure to follow a gluten-free diet, undernourishment, and low vitamin D and calcium intake.
Low vitamin D is common in celiac disease. Low bone mass and high fracture risk may be due to the intestinal inflammation itself, which is triggered by gluten, and the reduced absorption of calcium and vitamin D. The exact mechanism of bone loss in celiac disease has not been fully worked out.
A blood test for celiac disease should be considered as part of your evaluation if you have been diagnosed with low bone mass or a recent fracture. Celiac disease should also be considered as a possible cause if you have a low calcium level measured in a twenty-four-hour urine test or bone loss despite therapy with an osteoporosis medicine.
Based on screening guidelines, bone density evaluation (DXA scan) is recommended for adults with celiac disease.
INFLAMMATORY BOWEL DISEASE: CROHN'S DISEASE AND ULCERATIVE COLITIS
Despite the name, inflammatory bowel disease also causes health problems outside of the digestive system. Low bone mass is a common finding in inflammatory bowel disease (IBD)—Crohn's disease and ulcerative colitis. The frequency of low bone mass ranges from 11 percent to a high of 78 percent. This wide range is a result of the populations studied and the large variation of the diseases. The location, extent, and severity of the diseases all play a role in its effect on bone, as does drug treatment, especially steroids. Some studies indicate that Crohn's patients are at higher risk than those with ulcerative colitis, while other studies found no bone mass differences between the two groups.
Fracture risk is estimated to be 20 to 40 percent higher than for the general population. Fracture rates increase with age, and postmenopausal women are at the highest risk. Fractures do not necessarily correlate with bone density. In one study, over half of those with fractures had normal bone density. Bone density measurements need to be considered in association with risk factors.
Risk factors for low bone mass and fractures include the general risk factors for osteoporosis, in particular older age, being female, and being underweight. Other factors related to inflammatory bowel disease include steroid use, surgical removal of parts of the small intestine, vitamin D deficiency, and activity and duration of the inflammatory process. Onset of the disease before age eighteen, during the phase of large bone mass gains, may prevent attaining optimal peak bone mass and height.
The rate of bone loss is highest in postmenopausal women. Bone loss rates of 3 to 6 percent a year are reported for the spine during periods when the diseases are active. After remission for longer than three years, the rate of bone loss appears to follow average bone loss for age and gender. Bone loss is most closely related to steroid use. A high lifetime dose of steroids is associated with low bone mineral density at the hip and spine. Steroids, even in low doses of less than 7.5 mg of prednisone, may accelerate bone loss. Use of intermittent high-dose steroids may cause greater bone loss than long-term low doses.
However, the effect of steroids is difficult to separate from disease activity. Those with severe disease are more likely to receive steroid treatment. Even before the use of steroids, patients with inflammatory bowel disease have lower than normal bone density. Certain inflammatory factors, called cytokines, are overproduced. These are thought to contribute to bone loss as well.
Inadequate vitamin D along with poor absorption of calcium is a big problem in Crohn's disease. Since Crohn's disease commonly affects the part of the small intestine where vitamin D and calcium are absorbed from the gut, this is not surprising. Those with a history of surgery to remove part of the small intestine are at particularly high risk for vitamin D deficiency. Testing of vitamin D levels is essential in order to know how much supplementation is needed for maintenance of adequate vitamin D levels.
Poor nutrition as a result of chronic inflammation of the digestive system can have an additional impact. During flares, getting enough calories is a challenge and absorption of nutrients may be decreased. Frequently, patients lose weight, including muscle mass. Bone loss is associated with the weight loss, which may be rapid during an acute flare. The good news is that a return of bone is possible after successful treatment of the disease.
Increased awareness of the risk of low bone mass and fractures is essential in the management of inflammatory bowel disease regardless of the cause of bone loss. The American Gastroenterological Association's guidelines published in 2003 recommend assessment of risk factors and use of bone density (DXA) in select high-risk patients. I would add that there is a need to evaluate all inflammatory bowel patients to prevent fractures in the future. All will benefit from awareness about general bone health measures.
Recent advances in the management of inflammatory bowel disease have provided more treatment options. These include both steroid and nonsteroidal drugs. Entocort® (budesonide) is a steroid that acts locally in the intestine and has been in use for some time. Due to its inactivation in the liver, Entocort is less harmful to the bone and has limited general effects. Other combinations of biologic agents (monoclonal antibodies) and immunosuppressive drugs are being investigated, which may one day provide “steroid-free” treatment and remission.
|
The Bare Bones
|