Refined Sugar Promotes Cancer
A preponderance of research has concluded that eating too much refined sugar is linked to a greater risk of cancer.
Cancer and refined sugar
Unfolding research led by Harvard Medical School professor Dr. Lewis Cantley has determined that refined sugar stimulates the growth of cancer cells into tumors, and then larger tumors.
The discovery was broadcast by CBS’ 60 Minutes, in a piece that also highlighted research led by Dr. Robert Lustig. Dr. Lustig conducted other research on sugar toxicity.
Dr. Cantley, a professor of cell biology at Harvard, has been documenting how cancer cells are able to grow and multiply. He finds that when blood sugar spikes from eating refined sugars, insulin levels also climb. This spike in blood glucose and insulin promote the cancer cells to develop insulin receptors, which allow them to become increasingly active and aggressive by utilizing glucose. Without this spike in blood sugar, the research shows, cancerous cells can be more easily knocked out by the immune system.
Two decades of research has illustrated that we all produce cancer cells on an ongoing basis. But feeding these cells with glucose promotes the growth of tumors into full-blown cancers.
Most of this was highlighted in the 60 minutes piece. The story gets even more interesting, however, as we consider some of Dr. Cantley’s more recent findings.
The fact is, cancer cells are adapting and changing rapidly in the body to accommodate themselves. How do they do this?
Cancer cells utilize enzyme
Dr. Cantley and his associates have found that cancer cells utilize an enzyme called phosphoglycerate dehydrogenase, or PHGDH. PHGDH is a substrate derived from phosphate and glucose developed during the glucose energy cycle. PHGDH apparently allows the tumor cells to modify the positions of carbon atoms among their genetic structures.
This alteration of carbon atoms allows the cell to mutate and adapt, allowing them to grow stronger and evade the body’s immune system.
Dr. Cantley and his research teams have found PHGDH active within the gene regions of cancer cells. Their increased expression has been found in breast cancer cells, melanoma cells and others.
Another interesting finding by Dr. Cantley and his teams is that cancer cells are able to begin their alteration of the normal glucose energy cycle when a critical enzyme, pyruvate kinase M2, is blocked by reactive oxygen species (also called ROS). This means that the ability of the cancer cells to alter the normal sugar conversion process requires using free radicals – produced when we eat unhealthy foods or are exposed to toxins.
As Dr. Cantley stated in his article in the journal Science last December, “control of intracellular reactive oxygen species (ROS) concentrations is critical for cancer cell survival.”
“Control” comes in the form of reducing ROS by increasing antioxidant intake and reduced toxin exposure.
Free radicals and sugar
One of the most available ROS comes from low-density lipoproteins, which oxidize readily to become ROS. This means that the cancer cells are using LDL-cholesterol radicals and other free radicals – along with spiked glucose levels – to help them grow into larger tumors.
Dr. Cantley’s research provides the linch pins that connect the high-fat, highly-processed and overly sugary western diet to the rapid growth of cancer in modern society. For this reason, lung cancer is associated with increased junk foods in the diet. This is probably why cancer incidence is growing in children. On the other hand, eating more foods with flavanols reduces the risk of cancer according to other research.
Learn about a high-antioxidant, anti-carcinogenic diet:
Garcia-Cao I, Song MS, Hobbs RM, Laurent G, Giorgi C, de Boer VC, Anastasiou D, Ito K, Sasaki AT, Rameh L, Carracedo A, Vander Heiden MG, Cantley LC, Pinton P, Haigis MC, Pandolfi PP. Systemic Elevation of PTEN Induces a Tumor-Suppressive Metabolic State. Cell. 2012 Mar 5.
Anastasiou D, Poulogiannis G, Asara JM, Boxer MB, Jiang JK, Shen M, Bellinger G, Sasaki AT, Locasale JW, Auld DS, Thomas CJ, Vander Heiden MG, Cantley LC. Inhibition of pyruvate kinase M2 by reactive oxygen species contributes to cellular antioxidant responses. Science. 2011 Dec 2;334(6060):1278-83.
Mullarky E, Mattaini KR, Vander Heiden MG, Cantley LC, Locasale JW. PHGDH amplification and altered glucose metabolism in human melanoma. Pigment Cell Melanoma Res. 2011 Dec;24(6):1112-5.
Wang Z, Chatterjee D, Jeon HY, Akerman M, Vander Heiden MG, Cantley LC, Krainer AR. Exon-centric regulation of pyruvate kinase M alternative splicing via mutually exclusive exons. J Mol Cell Biol. 2011 Nov 1.
Locasale JW, Grassian AR, Melman T, Lyssiotis CA, Mattaini KR, Bass AJ, Heffron G, Metallo CM, Muranen T, Sharfi H, Sasaki AT, Anastasiou D, Mullarky E, Vokes NI, Sasaki M, Beroukhim R, Stephanopoulos G, Ligon AH, Meyerson M, Richardson AL, Chin L, Wagner G, Asara JM, Brugge JS, Cantley LC, Vander Heiden MG. Phosphoglycerate dehydrogenase diverts glycolytic flux and contributes to oncogenesis. Nat Genet. 2011 Jul 31;43(9):869-74.