Although not overtly stated by authors of recent studies on sugar and cancer, links between sugar consumption and cancer proliferation are appearing in the cancer research literature under the guise of pharmaceutical research. Earlier in August I posted about the unique ways in which fructose, but not glucose, contributed to accelerated tumor growth. Research from the Yokohama City University School of Medicine in Japan and the National Cancer Institute in Bethesda recently published their findings concerning the effects of a drug often administered to Type II diabetics, called Metformin, on colon cancer lesions and lung cancer cells, respectively, in the journal Cancer Research Prevention. Metformin was derived from the French lilac plant (Galega officinalis) in France in the 1950s, and entered the US drug market in 1994 as Glucophage, which means “glucose eater.” The drug, later generically released as Metformin, assists in stabilizing blood sugar by limiting the liver’s output of glucose and increasing the use of sugar by muscle tissue. The authors discuss complex protein activation pathways as potential mechanisms of action, but in my view, failed to take a step back and consider the mechanistic process on a more macro level.
Although the authors of these studies did not focus on the previously established findings that Metformin inhibits the formation of Advanced Glycation Endproducts, or AGEs, this is an important avenue to consider. AGEs and reactive oxygen species*, which are both potentially toxic, are formed when we consume and digest sugars. AGEs are produced through a process called glycation, in which a sugar molecule attaches to protein. If blood sugar levels are low, this initial bond can be broken. If blood sugar is high, the process progresses such that these combined AGE molecules bond to each other repeatedly, and sugars continually link proteins together that were never meant to be together (referred to as “cross-linking“). This is problematic, as these proteins (that never should have crossed paths) are now bound together. The A1C test is a direct test of how much glycation is occuring in one’s body, and this measure is generally some 3x higher in Type II Diabetics (who are not receiving treatment).
Understandably, cross-linking introduces cellular changes that were never meant to exist. AGEs have been linked to Type II Diabetes, cardiovascular diseases, Alzheimer’s disease, cancers, neuropathy, and other sensory deficits.
What can we take from this? If metformin inhibits glycation, which decreases the amount of AGEs produced, which in turn leads to fewer incidences of altered gene expression, cross-linking, and other altered cellular properties – all of which are associated with uncontrolled cellular growth (cancer), then perhaps the critical aspect to understand is that metformin inhibits glycation. Hence, it might behoove us to decrease our rates of glycation. How can we do that? One sure way to do this is to decrease dietary carbohydrate (that is, decrease sugar consumption). Of course, the powers that be (Government(s) with research-grant money) would not be huge fans of this interpretation of the data, given the associations between food industries and governments. Perhaps that is why the authors, who would probably like to receive federal/government funding in the future, avoided a straightforward presentation of the logic that follows from their findings.
*Reactive oxygen species are formed when we burn glucose for fuel at the cellular level, and have been associated with a number of diseases, including diabetes. In this process, electrons attach to oxygen atoms, and this renders them able to react with other molecules (they were previously inert). Free radicals are an example of reactive oxygen species. All reactive oxygen species are all called oxidants (hence, lay references to anti-oxidants as being good, as they are thought to neutralize reactive oxygen species).
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