Obesity and Cancer

We have argued based upon extensive evidence that obesity is a driver of multiple cancers. A recent paper Kern et al notes:

Obesity promotes the development of numerous cancers, such as liver and colorectal cancers, which is at least partly due to obesity-induced, chronic, low-grade inflammation. In particular, the recruitment and activation of immune cell subsets in the white adipose tissue systemically increase proinflammatory cytokines, such as tumor necrosis factor α (TNFα) and interleukin-6 (IL-6). These proinflammatory cytokines not only impair insulin action in metabolic tissues, but also favor cancer development. Here, we review the current state of knowledge on how obesity affects inflammatory TNFα and IL-6 signaling in hepatocellular carcinoma and colorectal cancers. 

They continue:

During obesity-driven, low-grade inflammation, hepatic NF-κB serves as an antiapoptotic survival factor, which promotes the proliferation of HCC progenitor cells and HCC development. In contrast, hepatic inactivation of IKK2 increases diethylnitrosamine (DEN)-induced HCC burden. In line with this evidence, hepatic NEMO deficiency causes spontaneous progression of TNFα-mediated chronic hepatitis to HCC. This detrimental effect of hepatic NEMO deficiency is potentiated under obese conditions presumably by enhanced liver inflammation and hepatic lipid accumulation. This supports the notion that NEMO acts as a tumor suppressor in the liver. Surprisingly, hepatic NEMO-deficient mice are protected against diet-induced obesity and exhibit improved insulin sensitivity...

There is thus evidence that controlling obesity, not just blood glucose, is a critical task.