Transformed cells adapt metabolism to support tumor initiation and progression. Specific metabolic activities can participate directly in the process of transformation or support the biological processes that enable tumor growth. Exploiting cancer metabolism for clinical benefit requires defining the pathways that are limiting for cancer progression and understanding the context specificity of metabolic preferences and liabilities in malignant cells. Progress toward answering these questions is providing new insight into cancer biology and can guide the more effective targeting of metabolism to help patients.
Optimal Diet is a dietary model of human nutrition devised and implemented by Dr. Jan Kwasniewski. Lots of fat and low in carbs. Lots and lots of articles collected from various places. He has an out-of-print book: Optimal Nutrition. The book is explained at the Australian Homo Optimus Association website. A thorough analysis is the first post here: Dr. Kwasniewski's Optimal Diet: Sanity, Clarity, Facts.
The WHO trial (so named because the international team of principal investigators contained World Health Organization members) tested the potential of clofibrate, a “pre-statin” cholesterol-lowering agent, to reduce heart attack morbidity and mortality. The investigators ultimately concluded that clofibrate "cannot be recommended as a lipid-lowering drug for community-wide primary prevention of ischaemic heart disease.” Nevertheless, clofibrate remained in use until 2002, when it was pulled for increasing cancer rates. In their review of studies such as the WHO trial, Uffe Ravnskov and David Diamond observe, “Despite the largely disappointing findings from 50 years of cholesterol lower[ing] trials, the indictment and conviction of cholesterol as the causal agent in CVD [cardiovascular disease] has stood the test of time. … [Yet] the grand effort to reduce cholesterol as a strategy to improve health has failed.”
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