I try to stay on the cutting edge of research as it relates to celiac disease and gluten sensitivity. Occasionally a study emerges that just doesn’t seem to ‘add up’ when compared to other studies and just good common sense.
Often it turns out that the study is perfectly valid, but the problem lies in the conclusions others are drawing from the study. In other words, it’s the interpretation that is at fault. My reason for bringing this up is that there is much data available on the Internet and such erroneous conclusions and interpretations could be confusing or even discouraging for the individual with gluten intolerance who is working so hard to remain gluten-free and restore their health. Therefore, I’d like to shed some light on this area.
Just yesterday I read about a study evaluating mortality incidence in celiac patients as it relates to healing of their small intestine. This was presented in Alimentary Pharmacology and Therapeutics. The goal of the researchers was to determine if persistent villous atrophy was associated with increased mortality.
The researchers discovered that in over 7,000 celiacs, “persistent villous atrophy is not associated with increased mortality in coeliac disease”.
Hmm… The ‘interpretation’ of this study that I came across seemed to insinuate that it therefore didn’t really matter if a celiac healed their small intestine or not, because their risk of death was unchanged, regardless. Obviously that doesn’t make sense to those of us who are more aware of the ‘truth’. But for someone newer to the disease, such an analysis could be downright depressing.
Let’s analyze some earlier research that hopefully will shed light on this more recent study.
In 2009 a large study presented in JAMA entitled “Small intestinal histopathology and mortality risk in celiac disease” demonstrated a moderate increase in mortality in several different celiac and gluten sensitive populations. The researchers found that the risk of mortality increased by:
- 75% for patients with mild inflammation of the small intestine at a median follow-up of 7.2 years
- 35% for patients with latent celiac disease (defined as gluten sensitivity due to the presence of no villous atrophy) at median follow-up of 6.7 years
- 30% for patients diagnosed with celiac disease and showing positive for villous atrophy at a median follow-up of 8.8 years
The increased death rate was found to be primarily from diseases such as heart disease, cancer, and respiratory diseases, the most common causes of death in celiac.
Another study from 2003 published in the Archives of Internal Medicine, entitled Causes of Death in Patients with Celiac Disease in a Population-Based Swedish Cohort, also found increased mortality rates amongst celiacs, with this study showing significant increases – 2-fold on average.
Specifically they found an increase for a wide array of diseases, including:
- Non-Hodgkin’s lymphoma
- Cancer of the small intestine
- Autoimmune diseases, including rheumatoid arthritis
- Diffuse diseases of connective tissue
- Allergic disorders such as asthma
- Inflammatory bowel diseases, including ulcerative colitis and Crohn’s disease
- Diabetes mellitus
- Disorders of immune deficiency
The authors of this study concluded that the elevated mortality risk for all causes of death combined reflected, for the most part, disorders characterized by immune dysfunction. That certainly makes sense considering gluten attacks the nervous system of susceptible individuals.
Thus we are pretty clear that celiac disease increases mortality. While it might seem counterintuitive that the most recent 2013 study revealed that inflammation of the small intestine shows a higher mortality risk than does villous atrophy, a seemingly more serious condition, let me offer an explanation.
Inflammation of the small intestine is a serious condition. The small intestine is, after all, where 80% of the immune system is housed. It is also the organ that turns food into fuel and literally feeds the 10 trillion cells in the body. So perhaps the moral of the story is that ‘any’ problem with the small intestine is a serious one and must be addressed comprehensively.
Let’s review the possible interpretations of the 2013 study:
- The cynical one: It doesn’t seem to make any difference if you heal your small intestine or not, because your incidence of death will remain the same. (False in my opinion.)
- The more intelligent one: It is critical that you not only heal the small intestine of any villous atrophy but one must also handle any inflammation, leaky gut, etc. Why? Because anything less than a normal operating small intestine, appears to increase your risk of dying.
I know that there’s a lot of information out there. Some of it can seem confusing. Do realize that some reporters and news agencies like to make unusual conclusions simply to foster conflict. Accurate analysis is sometimes less important than a lively discussion.
Please know that I am here for you to act as a translator, if you will, for studies and comments that don’t seem quite right.
I hope you found this informative. If your health is not at the level you desire, consider contacting us for a free health analysis – call 408-733-0400. Our destination clinic treats patients from across the country and internationally so you do not need to live locally to receive help.
To your good health,
Dr Vikki Petersen, DC, CCN
Founder of HealthNOW Medical Center
Co-author of “The Gluten Effect”
Author of the e-Book: “Gluten Intolerance – What you don’t know may be killing you!”
Alimentary Pharmacology & Therapeutics. 2013 Feb;37(3):332-9. doi: 10.1111/apt.12164. Epub 2012 Nov 28. Mucosal healing and mortality in coeliac disease.
Lebwohl B, Granath F, Ekbom A, Montgomery SM, Murray JA, Rubio-Tapia A, Green PH, Ludvigsson JF.
JAMA 2009;302 (11):1171-1178. Small intestinal histopathology and mortality risk in celiac disease. Ludvigsson JF, Montgomery SM, Ekbom A, Brandt L, Granath F.
Archives of Internal Medicine 2003;163(13):1566-1572. doi:10.1001/archinte.163.13.1566. Causes of Death in Patients With Celiac Disease in a Population-Based Swedish Cohort. Ulrike Peters, PhD, MPH; Johan Askling, MD; Gloria Gridley, MS; Anders Ekbom, MD, PhD; Martha Linet, MD