All it takes is one look around the grocery store to see that gluten sensitivity is on the rise. Because of the increase in celiac disease, gluten-free foods are more in demand now than ever before. But did you know that even if you don't have celiac disease, you might be gluten sensitive and not even know it?
It's possible – because not even many doctors know you can be gluten sensitive without the telltale gastrointestinal issues that accompany celiac disease.
But if you're suffering from an undiagnosed health problem – or even an "incurable" autoimmune disease – you should consider getting tested for gluten sensitivity. Believe it or not, this "hidden" sensitivity can be at the root of many illnesses – many of them "incurable" autoimmune diseases.
Ultimately, that means that treating these diseases could be a simple as adjusting your diet.
The key to understand this starts with the fairly recent research-backed realization that although gluten sensitivity and celiac disease may overlap, they are not the same illness. Let's cover that first.
Mistaken identity leads to misdiagnosis
Celiac disease – triggered by gliadin, a gluten protein – almost always features very notable gastro-intestinal symptoms, including bloating, gas, diarrhea, abdominal pain, and cramping. In medical school, we were told that celiac disease without gastro-intestinal symptoms was rare to non-existent. We were also told that if an intestinal biopsy that appeared normal meant there was no gluten sensitivity at all.
By contrast, gluten sensitivity (now research-differentiated from celiac disease) often has no gastro-intestinal symptoms at all. To make matters worse, intestinal biopsies in individuals with gluten sensitivity are often normal.
A recent research publicationi summarizes other differences between celiac disease and gluten sensitivity. The researchers wrote: "Unlike celiac disease, gluten sensitivity is not associated with increased intestinal permeability, in fact, [intestinal permeability] was significantly reduced in gluten sensitivity compared with controls."
The researchers pointed out that compared with healthy individuals, certain immune markers (for the technically inclined, IL-6 and IL-21) were elevated in celiac disease but not in those with gluten sensitivity, while another immune marker (TLR 2) was elevated in gluten sensitivity but not in celiac disease.
However, the two problems did share one similarity: lower levels of the immune marker FOXP3 when compared with healthy individuals.
These researchers concluded: "This study shows that the two gluten-associated disorders, celiac disease and gluten sensitivity, are different clinical entities…and it contributes to the characterization of gluten sensitivity as a condition associated with…absence of detectable changes in [the intestinal] mucosal barrier."
Why bother pointing out these differences between gluten sensitivity and celiac disease? It's because even many physicians don't know that it's possible to be sensitive to gluten with minimal if any gut symptoms, so they don't even look for gluten as a relatively common cause of non-gastrointestinal symptoms and illnesses, many of them autoimmune.
The overlooked cause of your autoimmune disease
Decades ago, an article in the Lancet (sorry, can't find the reference) pointed out that the then-new science of white blood cell typing, called "HLA antigens," was finding that certain diseases occurred much more commonly in individuals with certain HLA antigen types. (If you're thinking that this is just a modern, scientific way of documenting and re-stating that illnesses run in families, you're right. Genetically related individuals are much more likely to share many of the same white blood cell types, as they do the red blood cell types A, B, O and AB.)
One group of these "HLA-linked" diseases is almost entirely auto-immune. It includes the following disorders:
- type 1 diabetes
- Hashimoto's thyroiditis
- Graves's disease
- ulcerative colitis
- lupus erythematosis (lupus)
- vitiligo
- Addison's disease
- Sjogren's syndrome
- pernicious anemia
- scleroderma
- chronic auto-immune hepatitis
- dermatitis herpetiformis
- polymyalgia rheumatica
- auto-antibody hemolytic anemia
- celiac disease
(At the time of the Lancet article, "gluten sensitivity" was not yet distinguished from celiac disease.)
The author of this decades-old article pointed out that all but one of these diseases were believed to be auto-immune diseases. He pointed out that the only disease on this list that has an external trigger is celiac disease, which was known since the 1940s to be caused by gluten and gliadin in wheat and other cereal grains. The author then speculated that gluten might actually be the external trigger for all these other illnesses that were originally thought to be of internal origin.
Over the years, I have found that this is often the case. At Tahoma Clinic, whenever we work with an individual with any of these diagnoses, we always include the secretory IgA ("sIgA") anti-gliadin antibody test. (For more details about this test see the August 2011 issue of Nutrition & Healing.)
The sIgA anti-gliadin antibody test is positive in over 90 percent of individuals with any of these problems. Subsequent total elimination of gluten and gliadin, and very often all milk and dairy also, almost always results in major improvements in the health of these individuals.
How to determine if you have an undiagnosed gluten-gliadin sensitivity
How does this relate to whether or not an undiagnosed (or "hidden") gluten-gliadin sensitivity could be to blame for many or even most of your health problems?
Remember that diseases run in families. So, if your family health history includes any of the autoimmune problems listed above, and you are personally having symptoms and health problems that haven't been diagnosed, you may well have undiagnosed gluten-gliadin sensitivity, and should consider having yourself checked with the sIgA anti-gliadin antibody test.
There are also more routine laboratory test clues to undiagnosed gluten-gliadin sensitivity. They all arise from a major effect of gluten sensitivity noted above: the research-proven fact that intestinal absorption of nutrients is "significantly reduced in gluten sensitivity compared with controls."
The first is a measurement included with nearly all routine physical examinations: serum triglycerides. Triglycerides are a type of blood fat. Fats and fat-soluble vitamins are known to be poorly absorbed by individuals with gluten-gliadin sensitivity.
At Tahoma Clinic, our colleague Davis Lamson N.D. pointed out to the rest of the physicians that a fasting serum triglyceride measurement below 50 milligrams per deciliter (normal in most laboratories is said to be 50 to 150 milligrams per deciliter) means gluten sensitivity and gluten-induced malabsorption until proven otherwise. (In my experience, this has been true nearly 100 percent of the time.) Lamson also points out that any individual with both undiagnosed symptoms and health problems and a fasting serum triglyceride below 75 milligrams per deciliter should always be checked for gluten-gliadin sensitivity too, as the probability is high.
Poor intestinal absorption is also to blame for abnormalities in two other tests commonly recommended by practitioners skilled and knowledgeable in natural medicine: the mineral analysis done with a hair specimen, and the fasting plasma essential amino acid determination. If either or both of these tests shows multiple low measurements (three or more of the essential amino acids, five or more of the essential minerals), I'll recommend testing for gluten-gliadin sensitivity. Much more often than not, the test is positive.
Of course, the ultimate proof that gluten sensitivity is the problem is the often-dramatic improvement in previously undiagnosed, chronic symptoms and health problems that always follows the total elimination of gluten-containing foods in these individuals.
Bottom line: Whether you have gastrointestinal problems or not, if you have undiagnosed symptoms or health problems – and if you have one or more of the auto-immune problems listed above in your family – you may have gluten sensitivity. The odds are even higher if your fasting serum triglycerides are below 75, and/or your fasting plasma essential amino acid or hair mineral tests show multiple lower than normal values.
The spreading epidemic of gluten sensitivity
As little as 10 years ago, gluten-free products were hard to find. Twenty years ago, it was almost impossible to find them except in health food stores. Now, it seems gluten-free products are everywhere, even in some convenience stores. Obviously, more and more people are buying gluten-free.
Gluten sensitivity isn't an infectious disease, so why does there appear to be a spreading epidemic?
Although there probably isn't a spreading epidemic of gluten sensitivity itself, there's certainly been a spreading epidemic of a research-demonstrated "trigger" for the problem.
A little-recognized reason for the seeming epidemic of gluten sensitivity can be traced directly to the use and over-use of antibiotics, all beginning in the 1940s.
Mainstream Medicine doesn't understand this at all, and would likely deny even the suggestion. Even many natural medicine practitioners overlook this problem. However, both groups do know that use and overuse of antibiotics has caused many, many Candida albicans (yeast) infections.
In 2003, a group of Dutch researchers reportedii that Candida albicans may stimulate the formation of antibodies to gluten as well as auto-immune antibodies against tissue transglutaminase and endomysium, other types of antibodies found in many gluten-sensitive individuals.
In 2009, another group of researchers reported a single case of chronic candida infection in a four-year-old boy who also was found to have elevated anti-gliadin antibodies. Treatment with anti-fungal patent medicines resulted in improvement in the candida infection, while at the same time the anti-gliadin antibodies declined. Although not a controlled study or even close, this case supports the findings of the research reported in 2003.
In addition to improved diagnostic techniques finding more and more individuals with gluten sensitivity (read more about that on page XX), it appears very likely that the use and overuse of antibiotics leading to many more candida infections has in turn resulted in many more cases of gluten sensitivity also.
A simple solution to an "incurable" disease
In 1989, my wife Holly and I visited the office of Christopher Reading in Dee Why, a suburb of Sydney, Australia. He showed us documentation of over 500 individuals who came to see him with a diagnosis of lupus, a usually-thought-to-be incurable auto-immune disease. With hard work on their own and with Reading's treatment, these individuals eliminated all signs and symptoms of lupus as well as the patent and formerly patent medicines used to treat it.
Mainstream medicine then and now knows of no cure for lupus, but usually tries to control the symptoms with powerful patent and formerly patent medicines, all too frequently including prednisone (a very powerful pseudo-steroid), and methotrexate (an immune-system-destroying, formerly patent medicine often used in cancer treatment). Often, the effects of the patent and formerly patent medicines are as bad as or worse than the damage caused by the lupus itself.
How did over 500 individuals eliminate all signs and symptoms of lupus – and all patent medicines given for it, too – over 20 years ago? Reading had them totally eliminate all gluten, all milk and dairy products, and often other foods to which they were found to be allergic.
The other major part of Reading's treatment included repeated massive (but safe) doses of vitamins and minerals given intravenously.
Despite the success of these 500+ individuals entirely eliminating their lupus over 20 years ago, no researcher or group of researchers have reported any follow-up investigation of Reading's pioneering work.
i Sapone A, Lammers K, et al. Divergence of gut permeability and mucosal gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Medicine 2011;9:23
ii Nieuwenhuizen WF, Pieters RH, Knippels LM, Jansen MC, Koppelman SJ Is Candida albicans a trigger in the onset of coeliac disease? Lancet. 2003 Jun 21;361(9375):2152-4.
Originally published in Nutrition & Healing newsletter; Vol. 8 Issue 12, February 2012. Used with permission.