Earlier this year I wrote a piece on Early Cancer Indicator | Part I in order to convey the message that cancer doesn’t happen overnight—it’s a process that takes several years to decades to develop well before one is aware. Early detection is important to better control and prevent cancers. When cancer is detected early enough, a person has a higher probability of reversing it (especially if the correct dietary and lifestyle modifications are implemented) and saving themselves thousands of dollars in healthcare spending, innumerable pain and suffering.
Cancer causes its adjacent tissue’s temperature to rise to unhealthy levels as a by-product of accelerated metabolism of disordered, malignant cells. These malformed cells tend to steal nutrients, oxygen, and blood flow away from healthy cells in order to allow the cancer cells to continue rapidly growing (DeBan et al., 1994). Infrared thermal imaging, also called Thermography precisely detects these variances in body temperature in order to detect inflammation and cancer cell growth at any stage of its development. Unlike conventional diagnostic tests like CT and MRI scans, x-rays, and mammograms, they are unable to detect this temperature variances and hence, are unable to easily assess a person’s risk for cancer nor detect early stages of this disease until the cancer has already been growing for many years. These conventional imaging modalities must also use damaging levels of radiation which, in and of itself, cause cancer, and/or contrast iodine dye which harms the kidneys. For these reasons alone, SF Advanced Health has invested in offering thermography to patients for early detection and treatment of cancer in order to continue providing a holistic perspective of this chronic disease.
Today, I want to talk about diet-related cancer risks, specifically long-standing digestive problems that if left untreated can easily progress to cancer. We are going to focus specifically on Celiac disease since it is a hallmark early cancer indicator. Celiac disease’s prevalence rate worldwide is estimated at about 1/150 individuals with the rate increasing every year. (Fasano & Catassi, 2001; Volta et al., 2001; West et al., 2003).
Celiac disease is a permanent autoimmune gastrointestinal disorder triggered by gluten, the storage protein complex in wheat, rye, and barley. Those with a genetic predisposition who carry the HLA-DQ2/DQ8 haplotype along with those at an increased risk for other autoimmune disorders (i.e., diabetes, inflammatory bowel disease, rheumatoid arthritis) are more susceptible to developing celiac disease.
Ingestion of gluten is perceived as a poison by the immune system where it triggers an inflammatory response that ends up killing the cells lining the small intestines and causing “villous atrophy”. T-lymphocytes (a specific type of white blood cells) rush in to “fix” the damage but end up causing more trouble which is seen as cellular “hyperplasia” of the small intestines’ crypts. With a constantly damaged small intestine and an overstimulated immune system, food no longer is properly digested and nutrients are not easily absorbed. Cells begin to starve.
The damage of the small intestine quickly extends into the large intestine. Toxins and pathogenic microorganisms begin leaking out of the gut and into the bloodstream triggering an intense systemic inflammatory response throughout the body damaging healthy tissues. An internal self-destructive reaction has been set off where the body and mind no longer can recognize which foods and drugs are safe versus which ones are poisonous. In other words, this autoimmune reaction causes healthy microorganisms and human cells to be starved and damaged while disordered, malignant cancerous cells steal all of the available nutrients, water, and oxygen and grow out-of-control.
The association between celiac disease and neoplasms is well established. In the 1960s, a population-based study reported a 100-fold increased risk of non-Hodgkin's lymphoma in patients affected by celiac disease (Gough et al., 1962). Recently, this risk has a more conservative value, ranging anywhere from 3-fold (by an Italian study) to 9-fold (by an American study) (Catassi et al., 2002; Green et al., 2003).
Granted, lots of things play into cancer development and progression, but regardless of the actual risk value, it is clear that celiac patients do indeed have a higher risk of developing intestine-specific cancers, like small bowel adenocarcinoma and non-Hodgkin’s lymphoma compared to the general population (Green et al., 2003; Rampertab et al., 2003; Howdle & Holmes, 2004; Silano & De Vincenzi, 2005). Small bowel carcinoma is a rare malignancy that usually arises when a benign tumor turns malignant (Howdle et al., 2003; Freeman, 2004; Catassi et al., 2005). While small bowel carcinoma is a male predominant malignancy, others have found that four out of the five patients affected by this cancer are female (Silano et al., 2007). Since celiac disease is prevalent among women, this finding is further confirmation of the link between small bowel neoplasm and celiac disease. It has also been reported that cancer death rates are significantly higher in those with celiac disease(Corrao et al., 2001; Peters et al., 2003).
The problem is many people who consume gluten do not know they have celiac disease until the disease has progressed significantly. Prolonged delay in the early diagnosis of those with gluten intolerance, sensitivity, and allergy by integrative functional medicine practitioners has led to years of underlying disease and cancer cells overgrowth before pathology is officially detected.
Prolonged period of dietary exposure to gluten hence, causes an aggressive autoimmune reaction which destroys the inner lining of the digestive tract and allows an accelerated overgrowth of cancer cells. Another compounding factor to cancer development in Celiac disease patients is since gluten is a genetically modified crop (GMO) heavily sprayed with carcinogenic pesticides, there is extensive scientific evidence demonstrating that prolonged dietary exposure of the GMO crops corn and soy also accelerates cancer cells growth. These crops are predominantly found in all animal protein (i.e., fish, eggs, poultry, red meat, dairy products) since all animals are fed GMO crops at some point during their lifespan, along with most processed foods and alcohol.
There are lots of reasons linked to genetics and environmental factors which triggers celiac disease and cancer. Diet and lifestyle, when harnessed appropriately, can exert a protective effect towards tumors of the upper gastrointestinal tract in certain people, as was the case when looking at a population of Italians. The Italian based study demonstrated that Italians who ate more healthy foods and lived in more active lifestyles decreased their risk of developing non-hematological malignancies (Corrao et al., 2001).
Conclusion: Having one or more chronic diseases can increase your cancer risk. In this case, severe inflammation in the gut can progress to cancer in susceptible individuals. There is considerable clinical and scientific evidence that the strict compliance to a diet free of gluten (i.e., wheat, barley, rye), corn and soy (which includes all animal protein, a variety of processed foods, and alcohol) is protective against the development and progression of cancer in celiac patients. Since people are often diagnosed with Celiac disease many years after it has already developed, their risk of developing additional malignancies sooner rather than later has exponentially increased.
Unfortunately in conventional modern medicine, celiac disease is not taken seriously until the disease progressives into more severe stages. This is why, from a public health perspective, not much is done for this susceptible population in terms of advanced diagnostic testing. The conversation solely focuses on the removal of gluten, but rarely addresses also removing corn, soy, animal protein, processed foods and alcohols containing high concentrations of these crops. There is also no emphasis on healing protocols for gut repair. The argument goes as follows: “Because the overall risk of developing cancer in celiac populations is uncertain, the evidence does not support the need of serological screening for celiac disease in the general population in order to prevent a malignancy.”
This is a twenty year outdated perspective that needs to be changed ASAP. Gluten (predominantly wheat), corn, soy, animal protein, and alcohol cause a high percentage of gastrointestinal disorders today in most people. The estimated prevalence of non-celiac gluten sensitivity varies between 1% and 13% of the population, which is higher than the prevalence of celiac disease (which is around 1 in 150) (Aziz et al., 2015). So, if you are experiencing digestive problems or suspect you have a “problematic” diet, it may be best for you to first stop consuming wheat, animal protein, and processed foods and alcohol rich in corn and soy for the next three months. Do also consider avoiding these foods if you have a family diagnosed with celiac disease. It’s not worth the alternative risk … You can then consider getting a food allergy IgG/IgA antibody blood test to accurately determine if you have an underlying food sensitivity versus allergy. Do not have food allergy IgE antibody skin testing done (typically done by an allergist) since it does not accurately assess for gut food sensitivities and one’s risk of developing both Celiac disease and cancer.
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Askling, J., Linet, M., Gridley, G., Halstensen, T. S., Ekström, K., & Ekbom, A. (2002). Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpetiformis. Gastroenterology, 123(5), 1428-1435.
Aziz, I., Hadjivassiliou, M., & Sanders, D. S. (2015). The spectrum of noncoeliac gluten sensitivity. Nature Reviews Gastroenterology & Hepatology, 12(9), 516-526.
Catassi, C., Bearzi, I., & Holmes, G. K. (2005). Association of celiac disease and intestinal lymphomas and other cancers. Gastroenterology, 128(4), S79-S86.
Catassi, C., Fabiani, E., Corrao, G., Barbato, M., De Renzo, A., Carella, A. M., ... & Bertolani, P. (2002). Risk of non-Hodgkin lymphoma in celiac disease. Jama, 287(11), 1413-1419.
Corrao, G., Corazza, G. R., Bagnardi, V., Brusco, G., Ciacci, C., Cottone, M., ... & Loperfido, S. (2001). Mortality in patients with coeliac disease and their relatives: a cohort study. The Lancet, 358(9279), 356-361.
DeBan, A. F., Tumey, D. M., Reeves, J. W., McQuain, D. B., Reeves, W. H., Reeves, C. C., & Aboujaoude, E. D. (1994). U.S. Patent No. 5,301,681. Washington, DC: U.S. Patent and Trademark Office.
Fasano, A., & Catassi, C. (2001). Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum. Gastroenterology, 120(3), 636-651.
Freeman, H. J. (2004). Lymphoproliferative and intestinal malignancies in 214 patients with biopsy-defined celiac disease. Journal of clinical gastroenterology, 38(5), 429-434.
Green, P. H., Fleischauer, A. T., Bhagat, G., Goyal, R., Jabri, B., & Neugut, A. I. (2003). Risk of malignancy in patients with celiac disease. The American journal of medicine, 115(3), 191-195.
Gough, K. R., Read, A. E., & Naish, J. M. (1962). Intestinal reticulosis as a complication of idiopathic steatorrhoea. Gut, 3(3), 232-239.
Holmes, G. K., Prior, P., Lane, M. R., Pope, D., & Allan, R. N. (1989). Malignancy in coeliac disease--effect of a gluten free diet. Gut, 30(3), 333-338.
Howdle, P. D., & Holmes, G. K. T. (2004). Small bowel malignancy in coeliac disease. Gut, 53(3), 470-470.
Howdle, P. D., Jalal, P. K., Holmes, G. K. T., & Houlston, R. S. (2003). Primary small‐bowel malignancy in the UK and its association with coeliac disease. Qjm, 96(5), 345-353.
Peters, U., Askling, J., Gridley, G., Ekbom, A., & Linet, M. (2003). Causes of death in patients with celiac disease in a population-based Swedish cohort. Archives of internal medicine, 163(13), 1566-1572.
Rampertab, S. D., Forde, K. A., & Green, P. H. R. (2003). Small bowel neoplasia in coeliac disease. Gut, 52(8), 1211-1214.
Silano, M., & De Vincenzi, M. (2005). Small bowel malignancy at diagnosis of coeliac disease. Gut, 54(4), 565-566.
Silano, M., Volta, U., Mecchia, A. M., Dessì, M., Di Benedetto, R., De Vincenzi, M., & Collaborating Centers of the Italian Registry of the Complications of Coeliac Disease. (2007). Delayed diagnosis of coeliac disease increases cancer risk. BMC gastroenterology, 7(1), 8.
Volta, U., Bellentani, S., Bianchi, F. B., Brandi, G., De Franceschi, L., Miglioli, L., ... & Tiribelli, C. (2001). High prevalence of celiac disease in Italian general population. Digestive diseases and sciences, 46(7), 1500-1505.
West, J., Logan, R. F. A., Hill, P. G., Lloyd, A., Lewis, S., Hubbard, R., ... & Khaw, K. T. (2003). Seroprevalence, correlates, and characteristics of undetected coeliac disease in England. Gut, 52(7), 960-965.