Sayer Ji

The Dark Side of Wheat: New Perspectives on Celiac Disease & Wheat Intolerance Part 1 of 3

by Sayer Ji on March 15th, 2010


The globe-spanning presence of wheat and its exalted status among secular and sacred institutions alike differentiates this food from all others presently enjoyed by humans. Yet the unparalleled rise of wheat as the very catalyst for the emergence of ancient civilization has not occurred without a great price. While wheat was the engine of civilization’s expansion and was glorified as a “necessary food,” both in the physical (staff of life) and spiritual sense (the body of Christ), those suffering from celiac disease are living testimony to the lesser known dark side of wheat. A study of celiac disease may help unlock the mystery of why modern man, who dines daily at the table of wheat, is the sickest animal yet to have arisen on this strange planet of ours.

THE CELIAC ICEBERG

Celiac disease (CD) was once considered an extremely rare affliction, limited to individuals of European origin. Today, however, a growing number of studies indicate that celiac disease is found throughout the US at a rate of up to 1 in every 133 persons, which is several orders of magnitude higher than previously estimated.

These findings have led researchers to visualize CD as an iceberg. The tip of the iceberg represents the relatively small number of the world’s population whose gross presentation of clinical symptoms often leads to the diagnosis of celiac disease. This is the classical case of CD characterized by gastrointestinal symptoms, malabsorption and malnourishment. It is confirmed with the “gold standard” of an intestinal biopsy. The submerged middle portion of the iceberg is largely invisible to classical clinical diagnosis, but not to modern serological screening methods in the form of antibody testing. This middle portion is composed of asymptomatic and latent celiac disease as well as “out of the intestine” varieties of wheat intolerance. Finally, at the base of this massive iceberg sits approximately 20-30% of the world’s population – those who have been found to carry the HLA-DQ locus of genetic susceptibility to celiac disease on chromosome 6.

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.

IT IS NOT THE GENES, BUT WHAT WE EXPOSE THEM TO

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 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. 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).

The “blueprint” model of genetics: one gene → one protein → one cellular behavior, which was once the holy grail of biology, has now been supplanted by a model of the cell where epigenetic factors (literally: “beyond the control of the gene”) are primary in determining how DNA will be interpreted, translated and expressed. A single gene can be used by the cell to express a multitude of proteins and it is not the DNA itself that determines how or what genes will be expressed. Rather, we must look to the epigenetic factors to understand what makes a liver cell different from a skin cell or brain cell. All of these cells share the exact same 3 billion base pairs that make up our DNA code, but it is the epigenetic factors, e.g. regulatory proteins and post-translational modifications, that make the determination as to which genes to turn on and which to silence, resulting in each cell’s unique phenotype. Moreover, epigenetic factors are directly and indirectly influenced by the presence or absence of key nutrients in the diet, as well as exposures to chemicals, pathogens and other environmental influences.

In a nutshell, what we eat and what we are exposed to in our environment directly affects our DNA and its expression.

Within the scope 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 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 might otherwise have avoided epigenetic activation. This would explain why it is possible to live into one’s 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 exclude the possibility of reversing 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.

CELIAC DISEASE REVISITED

What all of this means for CD is that the genetic susceptibility locus, HLA DQ, does not determine the exact clinical outcome of the disease. Instead of being the cause, if the HLA genes are activated, they are a consequence of the disease process. Thus, we may need to shift our epidemiological focus from viewing this as a classical “disease” involving a passive 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.

If we view celiac disease not as an unhealthy response to a healthy food, but as a healthy response to an unhealthy food, classical CD symptoms like diarrhea may make more sense. Diarrhea can be the body’s way to reduce the duration of exposure to a toxin or pathogen, and villous atrophy can be the body’s way of preventing the absorption and hence, the systemic effects of chronic exposure to wheat.

I believe we would be better served by viewing the symptoms of CD as expressions of bodily intelligence rather than deviance. We must shift the focus back to the disease trigger, which is wheat itself.

People with celiac may actually have an advantage over the apparently unafflicted because those who are “non-symptomatic” and whose wheat intolerance goes undiagnosed or misdiagnosed because they lack the classical symptoms and 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.

It is possible that celiac disease represents both an extreme reaction to a global, species-specific intolerance to wheat that we all share in varying degrees. CD symptoms may reflect the body’s innate intelligence when faced with the consumption of a substance that is inherently toxic. Let me illustrate this point using Wheat Germ Agglutinin (WGA), as an example.

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. Indeed, a study from the Mario Negri Institute for Pharmacological Research in Milan Italy published in 2007 in the International Journal of Cancer looked at bread consumption and the risk of kidney cancer. They found that those who consumed the most bread had a 94% higher risk of developing kidney cancer compared to those who consumed the least bread. Given the inherently toxic effect that WGA may have on kidney function, it is possible that in certain genetically predisposed individuals (e.g. HLA-DQ2/DQ8) the body – in its innate intelligence – makes an executive decision: either continue to allow damage to the kidneys (or possibly other organs) until kidney failure and rapid death result, or launch an autoimmune attack on the villi to prevent the absorption of the offending substance which results in a prolonged though relatively malnourished life. This is the explanation typically given for the body’s reflexive formation of mucous following exposure to certain highly allergenic or potentially toxic foods, e.g. dairy products, sugar, etc? 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 a defensive adaptation to continual exposure to a harmful 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 likely go unabated until silent damage to distant organs leads to the diagnosis of a disease that is apparently unrelated to wheat consumption.

Loss of kidney function may only be the “tip of the iceberg,” when it comes to the possible adverse effects that wheat proteins and wheat lectin can generate in the body. If kidney cancer is a likely possibility, then other cancers may eventually be linked to wheat consumption as well. This correlation would fly in the face of globally sanctioned and reified assumptions about the inherent benefits of wheat consumption. It would require that we suspend cultural, socio-economic, political and even religious assumptions about its inherent benefits. In many ways, the reassessment of the value of wheat as a food requires a William Boroughs-like moment of shocking clarity when we perceive “in a frozen moment….what is on the end of every fork.” Let’s take a closer look at what is on the end of our forks.

Next week: Part 2 Our Biologically Inappropriate Diet

--------------------------- Author Information: Sayer Ji Website: http://www.greenmedinfo.com Research archive: www.sayerji.com LinkedIN URL: http://www.linkedin.com/pub/b/606/799 Twitter URL: http://twitter.com/greenmedinfo Email Sayer Ji


3 Responses to “The Dark Side of Wheat: New Perspectives on Celiac Disease & Wheat Intolerance Part 1 of 3”

  1. Vicky says:

    There are many species of wheat, some contain more gluten than others. As the breeding has been refined for bread and dough making it has been bred to contain increased amounts. Now it is therefore more toxic…

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