Developing Cancer Theories

Over the years, many alternative theories about cancer treatments have existed and some presented in their short runs some intriguing concepts that may yet prove part of a successful cancer protocol. Here are two examples: Dr Asai's development of GE-132 and the other is the use of an apricot kernel extract naturally containing the toxic element, cyanide. The theory for apricot kernels was that only cancer cells contained the enzyme necessary to release the cyanide from it's protective compound form. This would then allow the free cyanide to only kill the cancer cell. It might not really be that specific at only targeting cancer cells as this reference reveals. This aspect that cancer cells produce unique elements formed only in cancer cells and not by normal cells is an avenue Scientists are exploiting to destroy the cancer. Indeed this concept today is at the heart of the direction science is focusing in it's attempt to find a cure, or as the more realistic goal, turning cancer into a disease one could live with that would not spread and kill.

The GE-32 compound uses another cancer theory that says increasing oxygen into the system is not conducive to cancer cell survival (exercise effect). Plus, the Germaniun carrier of this increased oxygen might also play a similar role to cyanide in the apricot kernel reaction. ref  The FDA reviewed both of these theories and ruled the risk of adding toxic substances into the body did not justify any yet to be scientific method proven benefits.  ref

But, the critical aspects these two theories operated under is proving today to yield immense rewards to finding a workable and safe cancer treatment. Any moment now amazing cancer breakthroughs are expected. The just discovered IV vitamin C connection to inhibit HIF-1, an enzyme cancer cells produce to allow them to get enough energy, may be one of these valuable finds. ref  ref  A Turmeric element called curcumin shows natural anti-cancer properties by limiting NF-KB activity, similar to the action of aspirin. They both act to control inflammation.

Another vital link in the cancer arsenal includes the flavonoids from fruits, vegetables, herbs, and teas. The next reference is an easy read and very complete regarding the actions of flavonoids, especially apigenin, to prevent cancer cell growth, a process that includes upregulating DR5. ref ref 

Copied here is definition for what DR5 does to prevent loss of link. "Death receptor 5 (DR5), also known as TRAIL receptor 2 (TRAILR2) and tumor necrosis factor receptor superfamily member 10B (TNFRSF10B), is a cell surface receptor of the TNF-receptor superfamily that binds TRAIL and mediates apoptosis." This means it causes a process that allows cancer cells to die.

TELOMERASE  Another area under research includes the function of telomeres and their control of the lifespan of normal cells. Telomeres participate in a process that destroys normal cells after a regular lifetime, but cancer cells either have a dysfunctional telomere or use an enzyme that stops telomere control of cell lifespan which means they literally exist forever.  ref ref 

There is a fine line to balance this ability to play with the telomere enzyme since it also controls functions in every type of normal cell that must be respected.

Of interest: Another way to increase telomere length, or reduce speed of shortening, is to maintain adequate vitamin D levels. Copied here is a study showing this result on leukocytes. This could mean a slightly longer and possibly healthier life span but is still questionable on influence of cancer cells, but possibly through the control of inflammation.

"Am J Clin Nutr. 2007 Nov;86(5):1420-5.

Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women.

Richards JB, Valdes AM, Gardner JP, Paximadas D, Kimura M, Nessa A, Lu X, Surdulescu GL, Swaminathan R, Spector TD, Aviv A. Twin Research and Genetic Epidemiology, St Thomas' Hospital, King's College, London School of Medicine, London, United Kingdom. brent.richards@kcl.ac.uk

Abstract

BACKGROUND: Vitamin D is a potent inhibitor of the proinflammatory response and thereby diminishes turnover of leukocytes. Leukocyte telomere length (LTL) is a predictor of aging-related disease and decreases with each cell cycle and increased inflammation.

OBJECTIVE: The objective of the study was to examine whether vitamin D concentrations would attenuate the rate of telomere attrition in leukocytes, such that higher vitamin D concentrations would be associated with longer LTL.  DESIGN: Serum vitamin D concentrations were measured in 2160 women aged 18-79 y (mean age: 49.4) from a large population-based cohort of twins. LTL was measured by using the Southern blot method.

RESULTS: Age was negatively correlated with LTL (r = -0.40, P < 0.0001). Serum vitamin D concentrations were positively associated with LTL (r = 0.07, P = 0.0010), and this relation persisted after adjustment for age (r = 0.09, P < 0.0001) and other covariates (age, season of vitamin D measurement, menopausal status, use of hormone replacement therapy, and physical activity; P for trend across tertiles = 0.003). The difference in LTL between the highest and lowest tertiles of vitamin D was 107 base pairs (P = 0.0009), which is equivalent to 5.0 y of telomeric aging. This difference was further accentuated by increased concentrations of C-reactive protein, which is a measure of systemic inflammation.

CONCLUSION: Our findings suggest that higher vitamin D concentrations, which are easily modifiable through nutritional supplementation, are associated with longer LTL, which underscores the potentially beneficial effects of this hormone on aging and age-related diseases."

It is also interesting to note that multiple vitamin consumers have slightly longer telomere length than non-users. This would equate to possibly a little longer life.