Celiac Disease is a medical condition where part of the digestive tract (upper small intestine), is attacked, under certain circumstances, and severely damaged by those same white blood cells that normally fight off infections.
The disease, until recently thought to be quite rare, actually affects almost one per cent of the population, although it is recognized that most of those with the condition have not yet been diagnosed. The reason behind the slow diagnoses and recognition of sufferers of the illness, is that it masquerades as several other “common problems”, and there have been no easy-to-use means of telling the difference.
The problems caused by the disease result from a coincidental combination of inherited cell “tissue type” markers (called Human Leukocyte Antigen, or HLA for short) along with our inability to completely digest some parts of the protein found in the grains wheat, barley, rye and oats. The undigested parts of the protein from these grass seeds appear (wrongly), to everyone’s immune system, as evidence that a bacterial infection is taking place. The normal reaction of a healthy immune system is to attempt to eradicate the ‘invaders’.
The early detection of the small, unprocessed bits of protein (called peptide chains, after the name used for the type of chemical bond that fastens amino acids together into long chains) by the immune system white blood cells, takes place inside and near the wall of the small intestine, where giant protein molecules are rapidly “taken apart” by digestive enzymes, being reduced to individual amino acids.
When these “grass seed proteins” aren’t totally reduced to simple amino acid molecules, the remaining short peptide chains are picked up anyway by the cells lining the small intestine (by a process called pinocytosis,) and are ‘presented’ on the outside of the cells (on the opposite side of the intestinal epithelium from the inside of the intestine) and are then mistakenly interpreted by immune system cells that are tasked with preventing food-borne illnesses as evidence of infection. The immune system cells proceed to attack and destroy some of these intestinal epithelial cells (epithelium is skin - outside our bodies, but also inside the respiratory, digestive and intestinal pathways) in a “kill the messenger” process that presumes the cell holding the offensive peptide chain is infected.
Well, if it just stopped there, things wouldn’t be too bad. The epithelial cells re-grow quickly, putting all back to rights in the small intestine. In fact this process goes on all the time, for everyone, with lots of different causes, such as bacterial or viral invaders trying to gain a foothold and make inroads. So it is not really the wrong thing for the immune system to be doing.
But the immune system is very complex, and endlessly resourceful. Which is the basis for the rest of the story – where a couple of coincidences lead to the real trouble. The first interesting factor here is how the immune system avoids attacking cells that belong to its own body – its friends - while the second factor is how the immune system goes after chronic infections – ones that don’t go away quickly. These two factors combine with dire consequences for the unlucky victims of Celiac Disease.
There are tens of millions of “recognition patterns” that are automatically created in everyone’s immune system’s white blood cells as they grow from stem cells in the marrow of our bones. As the bone marrow makes these white blood cells, it sends some of them to the Thymus gland, while others stay for a while in the bone marrow. It is in these two locations that they are trained not to go after ‘self’ cells. The unlucky cells that can’t learn this important lesson are destroyed. So only the properly trained white blood cells can ‘graduate’ from the bone marrow (B cells) or the Thymus (T cells) and go out into the broader circulatory systems - blood and lymph – to stand watch against invaders.
When an infection appears, the immune system’s B cells and T cells (those with the ‘right’ pattern) recognize peptide or polysaccharide fragments from the invader’s cell wall. This triggers a low-level white blood cell attack on the sources of these fragments, and a gradual destruction of the infected cells. If the infection persists for a while, the T cells and the B cells will reproduce, increasing the numbers of ‘recognizers’ available to assist in the war. Eventually, however, the infection is eliminated by the continual attacks by the various immune system cells, almost all of which are directed and stimulated by the pattern recognizers produced by the B and T cells.
After the infection is gone, the winning B and T cells go into reproductive ‘high gear’, setting up quite a large “standing army”, totally prepared to annihilate any similar invaders almost instantly, preventing the invaders from getting a foothold, ever again. They use the version of pattern recognizer that was employed to eliminate the infection to make many more copies of identical pattern recognizers, and then, quite suddenly, they stop reproducing.
This is the same effect we achieve with a vaccination – challenge the immune system with something that looks like an infection, then allow it to be tricked into thinking it “won the battle” and when it prepares its huge army, we have achieved protection without having to suffer all the effects of actually being ravaged by the real disease first.
That is how the process is supposed to work under normal circumstances. In some cases, however, the invaders might have external pieces for which the immune system has no good recognition patterns in store. So the initial response to an invasion would be weak, and insufficient to eliminate the infection right away. But the presence of a partially recognizable fragment drives the B and T cells to keep reproducing anyway, and as they reproduce, another important feature of genetic programming comes into play.
Normally, when cells reproduce, the genetic material that defines their structure and function is copied exactly. There are even special ‘programs’ in the DNA replication machinery that check for the exactness of copying, and whenever they find an error, correct it.
So when B cells and T cells reproduce, they are made as exact duplicates of the previous generation – but scientists have uncovered a special exception in the case of the copying of the part of these cells that is the “pattern recognizer” for invaders. What happens is that the error corrector mechanism gets turned off while copying the pattern. And that allows occasional small changes to slip through. Not every time a cell replicates, but just once in a while. The effect of this small change to the recognition pattern may actually make the pattern a better “fit” to the invader’s external pieces. Engineers call this shifting or diffusion of the target recognizer pattern “fuzzy logic” and have learned how to use it in making better automation systems. In our immune system it provides the ability to adapt when a new pattern is needed.
But the changes that creep in are always quite tiny, and only happen infrequently, so that when a chronic infection is not cleared by the first round of immune system efforts, it may take some time before the pattern shifts enough to match the invader well enough for total eradication.
So a chronic infection is accompanied by continual low-level immune system activity and replication of B and T cells. And the continued replication produces a gradual “spreading out” of the target pattern, making it possible to match up to invader patterns even if there was not a good match to begin with. But where the short term benefits of this gradual shifting of pattern target are good for us, for some people the longer term effect can be bad.
Here is where all the coincidental circumstances befuddle the ”fuzzy logic brilliance” that helps us adapt to fight off all invaders. First, we have an invader that is not an organism, a living thing, but rather is a bit of protein from a seed that is, by chance, used for food. Only recently (around ten thousand years) did we humans start using the seeds from grasses as food. Before that they were not part of a human diet.
These seeds have some protein as part of the store of materials for the baby plant to use. But the protein includes an ‘odd’ amino acid in its peptide chains, called proline. And proline “puts a kink in” any peptide chain. Without proline, the coiling of a protein can be very orderly – coils of coils, even. But these kinks, when near each other, prevent human digestive enzymes from getting a good grip on the chain of amino acids and undoing the peptide bonds to break the protein down into individual amino acids. This leaves “undigested” pieces that are big enough to be interpreted by the immune system cells as antigen – evidence of an infection. Who knew that they might cause us trouble?
Secondly, a chance similarity between the undigested peptide chains from the grass seeds, and one of the inherited types of HLA for a small percentage of the human race. Now each type of tissue in our bodies has three kinds of HLA, and these occur in various combinations, so that every kind of tissue has its own unique cell surface decorations that are recognized by the immune system as ‘self’. And that recognition is trained into the immune system cells in the bone marrow and the Thymus gland.
But what of the unfettered replication of B cells and T cells that takes place in the face of a chronic infection? There is no training to weed out the cells that would go after ‘self’ tissues when they are created by this cloning process and gradually changed by replication-based fuzzy logic. So the result is that any prolonged chronic infection can continually pump out a broader and broader array of patterns for the immune system to attack.
And here the similarity between the grass seed protein fragments and certain HLA patterns allows a shift of the pattern to produce a new line of immune system cells that can attack self cells just because there was a rough similarity between a particular HLA pattern and the indigestible bits of protein from the grass seed.
When a human eats grass seed, the immune system treats the intact short peptide chains as evidence of a chronic infection. When the fuzzy logic of B and T cell replication finally produces a pattern, after a long time, that matches the HLA of a particular type of tissue, the immune system attacks that tissue and destroys it thoroughly.
This is the manner in which autoimmune disorders come about. The production of unfortunate B and T cell patterns is driven through a slow series of random changes to a pattern that was only similar to self HLA.
It might take most of a lifetime to arrive at a close enough match to, say, thyroid producing cells, producing Hashimoto’s Thyroiditis, or it could happen at a fairly young age. It might take many years before a pattern resembling the tissue cushioning and smoothing joint motion was close enough to result in severe arthritis. And the attack on the structural cells holding the villi of the intestinal wall into shape can happen at a young age, or it can wait for many years. Altogether there are over sixty recognized autoimmune disorders.
Is this fuzzy logic stimulated by consuming grass seeds behind all of them? There is not yet proof, but there is growing suspicion. There is a definite relationship between Celiac Disease and consumption of gluten protein from wheat, barley, rye and oats. People who suffer from Celiac Disease experience continued intestinal wall damage until they totally eliminate consumption of those grains and of any products derived from them.
Most people who suffer from Ataxia (an inability to maintain upright posture, generally showing as a sideways tilt) can, when it is noticed early, experience total remission if they eliminate gluten from their diet. This is not Celiac Disease, although some of these people may also have Celiac Disease. When the problem has existed for too long, gluten avoidance is not helpful, and neurologists can see the evidence of brain tissue degeneration using Magnetic Resonance Imaging.
Why would a long undiagnosed Celiac Disease sufferer also have numerous other autoimmune disorders? And quite interestingly, why would optical migraines that were increasing in frequency from age 29 through age 56, (from once a year to three times a day) disappear totally after going gluten-free? Some migraine headache sufferers also experience the same sort of optical phenomena. Is there something inherently neurotoxic in wheat gluten protein peptide fragments? Optical migraines are a phenomena accompanying waves of cerebral cortex surface irritation. Are the peptides causing trouble to neurons, or is it the immune system attacking the neurons?
Why is it that Celiacs can heal when they remove those proteins/peptides from their diet? Apparently the immune system needs the extra challenge of the original driving peptides in order to mount a large enough response to do real tissue damage.
How can the attacked tissue recover? We are not really sure, but there are other examples of amelioration of gluten protein related conditions improving with dietary control. So what about other autoimmune disorders. Will they improve as well when gluten is totally absent? Perhaps.
Some gluten-related problems that have disappeared, in the experience of at least a small number of individuals who became gluten-free while maintaining an open mind about health, include: Ataxia, Dermatitis Herpetiformis, optical migraines, severe bone and joint pain, and Seborrheic Dermatitis. All of these were conditions that were becoming increasingly severe as time passed, yet disappeared over a period of less than six months after going on a gluten-free diet. Perhaps the circle of experiences interviews needs to be expanded.
With elimination of gluten protein from the diet, the immune system ramps up and prepares to annihilate any future invasions (of gluten? Yes.) So that for even minor slip-ups the penalties are severe. And with time, a gluten sensitive individual often progresses on to develop other protein intolerances, presumably as a result of the damage to the intestinal tract preventing complete digestion of many different kinds of proteins. A most common additional intolerance is for milk protein – called casein. Other intolerances include egg and soy proteins.
For one individual, a “gluten-challenge” diet prescribed by inexperienced medical professionals resulted in an incredible experience for this Celiac who had been gluten-free for three years. The effect was profound, and severe enough that the diet was discontinued after two weeks. As a comparative experience, it can shed light on some phenomena that are most likely associated with all who suffer from gluten intolerance.
Apart from the terrible bloating and constant running of the intestines, the most interesting aspect of all of it was the huge fluid production by the mucosal epithelia in the sinuses, mouth, throat and lungs. Presumable it was happening in the digestive tract as well. After cessation of the gluten challenge, these conditions abated only very gradually over several months. A delayed-onset effect was the swelling of various lymph nodes, which also became quite tender, even painful. Radiological examination found the condition to be ‘benign’ – as in not cancer. The nodes took more than a year to recover, and the recovery was still not complete even after several years.
The most unfortunate net effect of this process was a manifold increase in sensitivity to even trace amounts of gluten contamination. This unfortunate effect persists for that individual.
The effect of ingestion of a small amount of gluten, on a very sensitive individual, begins after about ten to eighteen hours. The most immediate result is severe abdominal cramping, forcing the individual to curl up from the intense abdominal pain. This is accompanied by unstoppable bowel urgency and explosive emptying of the gut. Depending on the amount of gluten consumed, this can subside after one episode if the amount was tiny (i.e. one bread crumb) or with a larger dose (i.e. a fugitive crouton hidden in a salad) the reaction can go on for several days.
The worst of the cramping is episodic – after elimination of some of the offending material, the cramps ease for a while, then build again with the same pattern. Someone once described the situation as the small intestine trying to rush out some offensive material, dumping undigested food and digestive fluids into the large intestine, which was only designed for water removal from pretty neutral stuff. So when the large intestine is fed this horrible stuff, of course it reacts with pain and tries to immediately eliminate the offending stuff. Seems pretty basic to me.
The longer term effects include intestinal damage and a reduced ability to process and absorb fats and oils. The obvious sign of this is oil floating on the water in the toilet bowl, even after gut function seems to have returned to ‘normal’.
Most disconcerting of all, is the strong association of Celiac Disease with “other troubles”. These range from numerous other autoimmune diseases/disorders to increased likelihood of certain types of cancer. Apparently there is an eighty times greater probability of having cancer of the small intestine, and an increased likelihood of non-Hodgkin’s Lymphoma. When a Celiac Disease victim is successful at maintaining a total elimination of gluten, these probabilities gradually return to what is normal for the rest of the population. This makes it sound like gluten from wheat, barley, rye and oats actually fits the FDA’s definition of a “carcinogen”. Strange that nobody particularly seems to have noticed.
What to do?
There are a number of organizations that are tackling the issues surrounding the existence of the condition known as Celiac Disease. Some of them are self-serving, looking only to part people from their money. They sell stuff – gluten-free products, publications, newsletters as well as t-shirts, caps and other fund-raising items. Some are looking at the medical aspects of the problem, and are “doing research”. There are some groups looking for a “cure”, and writing research proposals and seeking grants to support their efforts. A few groups are attempting to provide education and “support” for the identified victims of Celiac Disease, and of course this requires fundraising from private sources as well as the public.
But in spite of all this publicity, the vast bulk of the public has never heard of the problem. A few people do know of a relative, friend or coworker who has Celiac Disease. Some of them even seem to be aware of the nature of Celiac Disease. But there is a huge deficit of public awareness, and the incredible lack of understanding of the true nature of the problem. Worst of all, the people who are closest to Celiac Disease organizations also seem to be wearing blinders to the broader nature of gluten intolerance and the other, non-Celiac problems that result from gluten consumption.
What we have is a huge health-care opportunity waiting to be “harvested”. It represents a means to reduce the health care burden we all are paying dearly to support. It is the chance to prevent untold human suffering before it has a chance to happen. It can reduce the need for joint replacement surgeries, it can prevent numerous autoimmune disorders that will otherwise inevitably plague millions who might be spared. It can un-clog hospitals, rein back in the ever growing cost of caring for the elderly. While we can’t reverse all the problems, since some kinds of damage have progressed too far, we can arrest others and cure many of gradually worsening conditions.
There is no guarantee of the magnitude of the savings we might achieve as a society, particularly since the biological mechanisms that have been identified can also be forced into play by other processes – single episode bacterial, viral or fungal infections, and particularly any sort of chronic infection. But from our position of greater understanding today, we can see very great potential in just those areas where there is now certainty about the role of gluten from wheat, barley, rye and oats. There are many millions of people who can be saved from tremendous future suffering.
While there has been a tremendous amount of research into individual conditions and maladies, and tremendous strides have been made in understanding various medical conditions and the underlying causes, there is something important missing. There is no connection being drawn from the problems to the ultimate root causes. There are many independent brilliant research efforts, but there is no good feedback to the public about the meaning of all of this increased knowledge. Who is explaining the meaning of all of this new understanding? Who is applying this new certainty to how the people might change the way we live from day to day.
The worst problem is that we cannot predict exactly what will happen to each individual person. We can say that there is an X per cent probability that you will be stricken with medical condition ABC, and run down a large list of these conditions and the associated probabilities, but it is human nature to think “I am going to live forever. These things will hit the others, but I will be spared.” We cannot walk up to a specific person and tell them accurately “you will suffer severe hip joint degeneration by age 54, requiring replacement surgery.”
What we can do, however, is to begin to pull together all of the newly understood scientific evidence and translate it into a cohesive understandable set of concepts to deliver to the general public in a way that will allow them to make informed, evidence-based, choices about how to live their lives from day to day so that in their futures they do not have to suffer as the previous generations have, because of our ignorance.
The real problem, though, is public incredulity. Even if faced with scientific evidence many people will say it is a bunch of hooey, because a slice of bread never did anything to them. Others react with horror at the thoughts of what believing might mean to them – all the ways things would have to change in their lives – and therefore find the very ideas to be unbelievable. Overcoming disbelief will require a long concerted effort, with a carefully crafted series of messages. But the magnitude of the potential payoff is almost unbelievable.