Why does obesity promote cancer?

open access

Special Issue

Why does obesity promote cancer? Epidemiology, biology, and open questions

 Keywords: obesity, body mass index, insulin, inflammation, DNA damage

  
Abstract

The association between obesity and/or metabolic syndrome and an elevated mortality from cancer has been confirmed by an astonishing number of studies across nations and ethnicities, such that obesity is now recognised to be among the most prominent cancer risk factors worldwide.

Despite this overwhelming evidence and the societal impact of obesity, we know surprisingly little about the underlying molecular mechanisms. This knowledge gap is a major obstacle to the implementation of effective lifestyle change policies. As the scientific community is insecure on what messages it should deliver, administrators are uncertain as to what exactly to recommend, and consumers are confused about whom to believe. This leaves the field flooded with pseudo-scientific recommendations that are hard to eradicate.....

Gynaecological cancers (note: nothing on ovarian cancer)

Conclusion

The discourse on obesity and cancer has become dominant in public debate. Some aspects of this issue are clearly established beyond any reasonable doubt, namely the impact of obesity prior to diagnosis on specific cancer risks and on survivor outcome. Other aspects, such as the exact molecular mechanisms and the extent to which lifestyle changes can modify risk, still await definitive proof. Ultimately, the debate revolves on how much we can modify our cancer risk by intervening on the most basic of animal activities: nutrition. Some might find it tempting to dismiss this debate on the grounds that cancer risk (especially for those cancers where a single environmental factor cannot be identified) is mostly determined by ‘bad luck’, an un-escapable randomness in our stem cells’ DNA mutation accumulation rate [52]. It is clearly not so, but it is also true that our understanding of how nutrition impacts on cancer is far from complete. This creates fertile ground for the proliferation of pseudo-scientific recommendations and bogus ‘super healthy’ nutritional supplements. Likely, some mechanisms and specific lifestyle interventions may have stronger impact on specific cancers. It is also likely that an individual’s genetic makeup may influence response to diet, as we find variable genetic predisposition to specific cancers and genetically determined differences in metabolism. In the wave of medicine personalisation, it is not hard to imagine a future in which lifestyle plans will be tailored to individual risk profile and metabolism.