"The National Strength and Conditioning Association can’t shut down a suit by its insurer seeking to dodge coverage for an underlying false advertising suit brought by CrossFit Inc. just yet, a California federal court ruled Monday. …The NSCA is currently embroiled in a bitter legal battle with CrossFit over claims that it published a since-debunked 2013 study portraying CrossFit’s exercise regimen as unsafe, despite knowing the study’s findings were bogus."

“If the statement succeeds in its purpose, we will know it because journals will stop using statistical significance to determine whether to accept an article. Instead, journals will be accepting papers based on clear and detailed description of the study design, execution, and analysis, having conclusions that are based on valid statistical interpretations and scientific arguments, and reported transparently and thoroughly enough to be rigorously scrutinized by others.” —Ron Wasserstein, Executive Director, American Statistical Association

"P values, the 'gold standard' of statistical validity, are not as reliable as many scientists assume."

Uffe Ravnskov et al. argue that recent literature suggesting statins reduce heart-disease risk by lowering total (TC) and LDL cholesterol (LDL-C) is flawed, as is the broader belief in the inverse relationship between TC and LDL-C and heart disease. The authors note: “The usual argument in support of the lipid hypothesis is that numerous studies of young and middle-aged people have shown that high TC or LDL-C predict future CVD. This is correct, but association is not the same as causation.” TC or LDL-C may be effective markers for atherosclerotic risk within an untreated (or minimally treated) population, but this does not mean these markers are causal in the disease state.

America is facing a chronic disease crisis. The federal government is fueling that crisis by promoting flawed nutritional advice that contradicts the latest research.

A review of additional scientific literature concerning experiments or studies that challenge the foundation of the somatic mutation theory of cancer, including non-mutagenic origins of metastatic behavior, the absence of gene mutations in cancer cells, the presence of cancer driver genes in some normal cells, and the fallacy of tumor cell growth advantage.