THE CELIAC ICEBERG
The “Celiac Iceberg” may not simply illustrate the problems and issues associated with diagnosis and disease prevalence, but may represent the need for a paradigm shift in how we view both CD and wheat consumption among non-CD populations. First let us address the traditional view of CD as a rare, but clinically distinct species of genetically-determined disease, which I believe is now running itself aground upon the emerging, post-Genomic perspective, whose implications for understanding and treating disease are Titanic in proportion.
Despite common misconceptions, monogenic diseases, or diseases that result from errors in the nucleotide sequence of a single gene are exceedingly rare. Perhaps only 1% of all diseases can be considered to fall within this category, and Celiac disease is not one of them. In fact, following the completion of the Human Genome Project (HGP) in 2003 it is no longer accurate to say that our genes “cause” disease, any more than it is accurate to say that DNA is sufficient to account for all the proteins in our body (which it is not!). Despite initial expectations, the HGP revealed that there are only 30,000-35,000 genes in human DNA (genome), rather than the 100,000 + believed necessary to encode the 100,000 + proteins found in the human body (proteome).
Within the horizon of this new perspective even classical monogenic diseases like Cystic Fibrosis (CF) can be viewed in a new, more promising light. In CF many of the adverse changes that result from the defective expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene may be preventable or reversible, owing to the fact that the misfolding of the CFTR gene product has been shown to undergo partial or full correction (in the rodent model) when exposed to phytochemicals found in turmeric, cayenne, and soybean.5 Moreover, nutritional deficiencies of seleniun, zinc, riboflavin, vitamin e, etc. in the womb or early in life, may “trigger” the faulty expression or folding patterns of the CFTR gene in Cystic Fibrosis which otherwise might not have undergone epigenetic activation.6 This would explain why it is possible to live into the late seventies with this condition, as was the case for Katherine Shores (1925-2004). The implications of these findings are rather extraordinary: epigenetic and not genetic factors are primary in determining disease outcome. Even if we were to exclude the possibility of the reversible correction of certain monogenic diseases, the basic lesson from the post-Genomic era is that we can’t blame our DNA for causing disease, rather, it may have more to do with what we choose to expose our DNA to.
What all of this means for CD is that if the genetic susceptibility locus, HLA DQ, does not determine the exact clinical outcome of the disease7, or, if the HLA genes are activated not as a cause, but as a consequence of the disease process8, we may need to shift our epidemiological focus from viewing this as a classical “disease” involving the passivity of a subject controlled by aberrant genes to viewing it as an expression of a natural, protective response to the ingestion of something that the human body was not designed to consume.9
New insights into the genetic differences between humans and diverse species such as mouse, rat, chicken and turkey who share leptin genes, indicate that the seeds of cereal grasses were not introduced into the human diet until as recently as 500 generations ago. Within this context arguments against eating wheat take on greater relevance.
People with celiac may actually have an advantage over the unafflicted because those who are “non-symptomatic” and whose wheat intolerance goes undiagnosed or misdiagnosed for lacking classical symptoms may suffer in ways that are equally or more damaging, but expressed more subtly, or in distant organs. Within this view Celiac disease would be redefined as a protective (healthy?) response to exposure to an inappropriate substance, whereas “asymptomatic” ingestion of the grain with its concomitant “out of the intestine” and mostly silent symptoms, would be considered the unhealthy response insofar as it does not signal in an obvious and acute manner that there is a problem with consuming wheat.
WGA is glycoprotein classified as a lectin and is known to play a key role in kidney pathologies, such as IgA nephropathy. In the article: “Do dietary lectins cause disease?” the Allergist David L J Freed points out that WGA binds to “glomerular capillary walls, mesangial cells and tubules of human kidney and (in rodents) binds igA and induces IgA mesangial deposits,” indicating that wheat consumption may lead to kidney damage in susceptible individuals.10
The mucous coats the offending substance, preventing its absorption and facilitating safe elimination via the gastrointestinal tract. From this perspective the HLA-DQ locus of disease susceptibility in the Celiac is not simply activated but utilized as defensive adaptation to continual exposure to an inappropriate substance. In those who do not have the HLA-DQ locus, an autoimmune destruction of the villi will not occur as rapidly, and exposure to the universally toxic effects of WGA will with all likelihood go unabated until silent damage to distant organs precipitates into the diagnosis of a seemingly non-wheat consumption related classical disease species.
These same sulfur-to-sulfur bonds are found in hair and vulcanized rubber products, which we all know are difficult to decompose and are responsible for the sulfurous odor they give off when burned. There will be 676 million metric tons of wheat produced this year alone, making it the primary cereal of temperate regions and third most prolific cereal grass on the planet. This global dominance of wheat is emblemized by fact that the Food & Agricultural Organization (FAO) – which is the United Nation’s international agency for defeating hunger. – uses a head of wheat as its official symbol. Any effort to indict the credibility of this “king of grains” will prove challenging. As Rudolf Hauschka once remarked, wheat is “a kind of earth-spanning organism.” It has vast socio-economic, political, and cultural significance. For example, in the Catholic Church, a wafer made of wheat is considered irreplaceable as the body of Christ.
The medical justification for these classifications may be secondary to economic and cultural imperatives that require the inherent problems associated with wheat consumption be minimized or occluded. In all probability the Celiac genotype represents a surviving vestigial branch of a once universal genotype, which through accident or intention, have had through successive generations only limited exposure to wheat. The Celiac genotype, no doubt, survived through numerous bottlenecks or “die offs” represented by a dramatic shift from hunted and foraged/gathered foods to gluten-grain consumption, and for whatever reason simply did not have adequate time to adapt or select out the gluten-grain incompatible genes. The Celiac response may indeed reflect back to us what was once a species-wide intolerance to a novel new food source: the seed storage form of the monocotyledonous cereal grasses which our species only began consuming 1-500 generations ago at the advent of the Neolithic transition (10-12,000 BC). Let us return to the image of the Celiac iceberg for greater clarification.
The iceberg metaphor is an excellent way to expand our understanding of what was once considered to be an extraordinarily rare disease into one that has statistical relevance for us all, but it has a few limitations. For one, it reiterates the commonly held view that Celiac is a numerically distinct disease entity or “disease island,” floating alongside other numerically distinct disease “ice cubes” in the vast sea of normal health. Though accurate in describing the sense of social and psychological isolation many of the afflicted feel, the Celiac iceberg/condition may not be a distinct disease entity at all. Although the HLA-DQ locus of disease susceptibility on chromosome 6 offers us a place to project blame, I believe we need to shift the emphasis of responsibility for the condition back to the disease “trigger” itself: namely, wheat and other prolamine rich grains, e.g. barley, rye, spelt, and oats, and without which the typical afflictions we call Celiac would not exist. Within the horizon of this view the “Celiac iceberg” is not actually free floating but an outcropping from an entire submerged subcontinent, representing our long-forgotten (cultural time) but relatively recent metabolic prehistory as hunters-and-gatherers (biological time), where grain consumption was with all likelihood non-existent, except in instances of near-starvation.
Wheat presents a special case insofar as wild and selective breeding has produced variations which include up to 6 sets of chromosomes (3 genomes worth!) capable of generating a massive number of proteins each with a distinct potentiality for antigenicity. Common bread wheat (Triticum aestivum), for instance, has over 23,788 proteins cataloged thus far.13 In fact, the genome for common bread wheat is actually 6.5 times larger than that of the human genome! 14
Thankfully we don’t need to rely on our intuition, or even (not so) common sense to draw conclusions about the inherently unhealthy nature of wheat. A wide range of investigation has occurred over the past decade revealing the problem with the alcohol soluble protein component of wheat known as gliadin, the glycoprotein known as lectin (Wheat Germ Agglutinin), the exorphin known as gliamorphin, and the excitotoxic potentials of high levels of aspartic and glutamic acid found in wheat. Add to these the normal anti-nutrient content found in grains, phytates, enzyme inhibitors, etc. and you have a substance which we may consider the farthest thing from wholesome.
1) WHEAT GLIADIN CREATES IMMUNE MEDIATED DAMAGE TO THE INTESTINES
In a study published in GUT in 2007 a group of researchers asked themselves the question: “Is gliadin really safe for non-coeliac individuals?” In order to test the hypothesis that an innate immune response to gliadin is common in patients with Celiac disease and without Celiac disease, intestinal biopsy cultures were taken from both groups and challenged with crude gliadin, the gliadin synthetic 19-mer (19 amino acid long gliadin peptide) and 33-mer deamidated peptides. Results showed that all patients with or without Celiac disease when challenged with the various forms of gliadin produced an interleukin-15-mediated response. The researchers concluded: “The data obtained in this pilot study supports the hypothesis that gluten elicits its harmful effect, throughout an IL15 innate immune response, on all individuals [my italics].”15
2) WHEAT GLIADIN CREATES INTESTINAL PERMEABILITY
3) WHEAT GLIADIN HAS PHARMACOLOGICAL PROPERTIES
I believe a strong argument can be made that the agricultural revolution that occurred approximately 10-12,000 years ago as we shifted out of the Paleolithic into the Neolithic era was precipitated as much by environmental necessities and human ingenuity, as it was by the addictive qualities of psychoactive peptides in the grains themselves. The world-historical reorganization of society, culture and consciousness accomplished through the symbiotic relationship with cereal grasses, may have had as much to do with our ability to master agriculture, as to be mastered by it. The presence of pharmacologically active peptides would have further sweetened the deal, making it hard to distance ourselves from what became a global fascination with wheat.
The Roman appreciation for wheat, like our own, may have less to do with its nutritional value as “health food” than its ability to generate a unique narcotic reaction. It may fulfill our hunger while generating repetitive, ceaseless craving for more of the same, and by doing so, enabling the surreptitious control of human behavior. Other researchers have come to similar conclusions. According to the biologists Greg Wadley & Angus Martin: “Cereals have important qualities that differentiate them from most other drugs. They are a food source as well as a drug, and can be stored and transported easily. They are ingested in frequent small doses (not occasional large ones), and do not impede work performance in most people. A desire for the drug, even cravings or withdrawal, can be confused with hunger. These features make cereals the ideal facilitator of civilisation (and may also have contributed to the long delay in recognising their pharmacological properties).” 17
4) WHEAT LECTIN (WGA) DAMAGES OUR TISSUE.
There is evidence that WGA may cause increased shedding of the intestinal brush border membrane, reduction in surface area, acceleration of cell losses and shortening of villi, via binding to the surface of the villi18 WGA can mimic the effects of epidermal growth factor (EGF) at the cellular level, indicating that the crypt hyperplasia seen in celiac may be due to a mitogenic reponse induced by WGA.19 WGA has been implicated in obesity and “leptin resistance” by blocking the receptor in the hypothalamus for the appetite satiating hormone leptin.20 WGA has also been shown to have an insulin-mimetic action, potentially contributing to weight gain and insulin resistance.21 And as we discussed earlier, wheat lectin has been shown to induce IgA mediated damage to the kidney, indicating that nephropathy and kidney cancer may be associated with wheat consumption.
5) WHEAT PEPTIDES EXHIBIT MOLECULAR MIMICRY
6) WHEAT CONTAINS HIGH LEVELS OF EXCITO-TOXINS
For hyper-linked references to the footnotes in this article please visit the following link.
Sayer Ji is the founder of greenmedinfo.com
This is one of the most well written and comprehensive papers written on the topic of celiac disease, gluten sensitivity, and the genetic aspects of this far reaching problem. Thank you Sayer for all of your research and hard work. Educators like yourself are invaluable. If you are a visual learner, watch this video.