Table 1.

Obstacles to prevention of obesity-associated cancers

Obstacles to disrupting obesity promotion of cancer
1. Multiplicity of obesity-driven extracellular hormone and growth factors promoting tumor cell growth, for example, insulin, IGF-1, leptin, estradiol, etc.
2. Multiplicity of obesity-driven extracellular inflammatory factors, for example, IL-1β, IL-6, TNF-α, etc.
3. Receptor hybridization, cross-talk and multiplicity, for example, IR, IGF receptor, leptin receptor, etc.
4. Multiplicity and cross-talk among intracellular pathways activated by obesity mediators, for example, PI3K–Akt–mTOR, JAK2–STAT3–MAPK, NANOG–SOX, and EGFR–Notch1–Survivin.
5. Multiplicity of cellular targets, for example, cancer cells, cancer stem cells, tumor microenvironment, vascular endothelium, etc.
Obstacles to obesity control
6. Genetic programming for energy storage
7. Abundance of high-energy density foods
8. Poor adherence to caloric restriction
9. Inadequate sleep
10. Sedentary lifestyles and proliferation of energy saving devices
11. Built environment impediments to physical activity
12. Cost and accessibility of exercise equipment and programs
13. Absence of effective pharmacologic interventions
14. High cost and consequences of bariatric surgery