11 January 2024 | Jerrold J. Heindel, Robert H. Lustig, Sarah Howard, Barbara E. Corkey
The article proposes a unified model to explain the global rise in obesity, integrating four existing models: the Energy Balance Model (EBM), the Carbohydrate-Insulin Model (CIM), the Oxidation-Reduction Model (REDOX), and the Obesogen Model (OBS). The EBM focuses on the balance between energy intake and expenditure, while the CIM emphasizes the role of insulin in energy storage. The REDOX model highlights the impact of reactive oxygen species (ROS) on metabolic signaling, and the OBS model suggests that environmental chemicals can interfere with hormonal signaling, leading to adiposity. The authors propose a combined OBS/REDOX model where environmental chemicals generate false metabolic signals, including ROS, which subvert regulatory mechanisms, increase insulin secretion, disrupt energy efficiency, and influence appetite and energy expenditure, leading to weight gain. This integrated model incorporates data from all four models and provides a rationale for future preventative efforts, focusing on reducing exposure to environmental chemicals. The article also discusses the developmental origins of obesity and the potential for transgenerational epigenetic inheritance.The article proposes a unified model to explain the global rise in obesity, integrating four existing models: the Energy Balance Model (EBM), the Carbohydrate-Insulin Model (CIM), the Oxidation-Reduction Model (REDOX), and the Obesogen Model (OBS). The EBM focuses on the balance between energy intake and expenditure, while the CIM emphasizes the role of insulin in energy storage. The REDOX model highlights the impact of reactive oxygen species (ROS) on metabolic signaling, and the OBS model suggests that environmental chemicals can interfere with hormonal signaling, leading to adiposity. The authors propose a combined OBS/REDOX model where environmental chemicals generate false metabolic signals, including ROS, which subvert regulatory mechanisms, increase insulin secretion, disrupt energy efficiency, and influence appetite and energy expenditure, leading to weight gain. This integrated model incorporates data from all four models and provides a rationale for future preventative efforts, focusing on reducing exposure to environmental chemicals. The article also discusses the developmental origins of obesity and the potential for transgenerational epigenetic inheritance.