Hormonal
Exposure to environmental obesogens (e.g., BPA, PFAS, pesticides) during critical developmental windows programs long-term metabolic dysfunction by hijacking redox signaling (ROS) and endocrine pathways, leading to increased adiposity and insulin resistance later in life.
To mitigate the impact of obesogens, prioritize reducing exposure to environmental chemicals that disrupt hormonal and redox signaling. This includes choosing fresh foods over ultra-processed items (which may contain obesogenic additives or packaging leachates), filtering drinking water, and minimizing the use of plastics (especially for heating food) and harsh household cleaners. While diet and exercise remain important, recognizing the role of environmental factors suggests that reducing exposure to these chemicals is a critical, often overlooked component of obesity prevention.
We propose a combined OBS/REDOX model in which environmental chemicals (in air, food, food packaging, and household products) generate false autocrine and endocrine metabolic signals, including ROS, that subvert standard regulatory energy mechanisms, increase basal and stimulated insulin secretion, disrupt energy efficiency, and influence appetite and energy expenditure leading to weight gain.
Why this rating
The paper is a review/perspective citing animal and in vitro data; human epidemiological data is mentioned but causality is noted as needing more clinical studies.
Source
Obesogens: a unifying theory for the global rise in obesity
Jerrold J. Heindel et al. · International Journal of Obesity · 2024
DOI 10.1038/s41366-024-01460-3
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