Use Of DHEA By Cancer Explains The "Warburg Effect" ...Increased Cancer Metabolism (New Support of My Cancer Explanation)
Copyright 2017, James Michael Howard, Fayetteville, Arkansas, U.S.A.
I suggest the basis of the findings of San-Millan and Brooks is dehydroepiandrosterone (DHEA). (Carcinogenesis 2017: Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect") Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect. It is known that DHEA increases lactate dehydrogenase (The Journal of Nutrition [1991, 121(12):2037-2043]) and that high LDH "is associated with poorer overall survival in several malignancies, but its link to cancer-specific survival is unclear," (British Journal of Cancer (2015) 113, 1389–1396). In 1994, I first suggested that low DHEA is directly involved in initiation of oncogenes: "An Explanation of Cancer and the Increase in Cancer: High Testosterone, Low DHEA and Breast Cancer," which appeared first in publication: Annals of Internal Medicine 2005; 142: 471-472 . At this point, you should be thinking I have this backward. It is what happens in cancer subsequently to oncogenesis that explains your paper. Once initiated, I suggest cancer increases consumption of DHEA at the expense of the host. DHEA stimulates consumption of glucose. Hence, DHEA increases metabolism of cancer. This explains the "Warburg Effect." DHEA increases glucose transport into cells and "The increased aerobic glycolysis occurs because cancer cells transport glucose into cells at a high rate." other research quotation. Cancer cells increase use of DHEA, and glucose, at the expense of the host, once initiated. The basis of my explanation of oncogenesis caused by low DHEA is low DHEA results in increased cellular surface area because of reduced support of the differentiated state of the cell, that is, cellular adhesion is reduced. Very simply, increased surface area in cells containing oncogenes increases availability of DHEA to stimulate gene activities along with increased glucose availability. If these cells contain oncogenes, the extra DHEA stimulates oncogenesis. Exercise increases DHEA so "Hence, during high-intensity exercise, working muscles display some of the same metabolic characteristics as do cancer cells." San-Millan and Brooks.