Hormonal
Low-dose exposure to persistent organic pollutants (POPs) increases the risk of type 2 diabetes (T2D), primarily through mechanisms involving beta-cell dysfunction and mitochondrial toxicity rather than solely through insulin resistance.
You cannot completely avoid environmental pollutants like PCBs or pesticides, but you can manage their impact. Focus on healthy lifestyle behaviors like regular exercise and calorie restriction, which help eliminate POPs and improve mitochondrial function, thereby reducing your risk of developing type 2 diabetes.
Low dose persistent organic pollutants (POPs) have emerged as a new risk for type 2 diabetes (T2D)... as POPs can directly reduce insulin secretion of beta cells, the role of POPs may be more prominent in the development of beta-cell dysfunction-dominant T2D rather than insulin resistance-dominant T2D.
Why this rating
The paper is a review of review articles and observational studies; it cites consistent human epidemiological data and in-vitro/in-vivo experimental evidence, but notes inconsistencies and research gaps.
Source
Persistent Organic Pollutants and Type 2 Diabetes: A Critical Review of Review Articles
Yu‐Mi Lee et al. · Frontiers in Endocrinology · 2018
DOI 10.3389/fendo.2018.00712
More from this paper
- Adipose tissue acts as a double-edged sword regarding POPs: it protects organs by sequestering POPs when healthy, but releases them into circulation during uncontrolled lipolysis (common in obesity or weight loss), increasing toxicity to other organs.Good
- POPs act as mitochondrial toxins at low doses, causing mitochondrial dysfunction which is a more plausible mechanism for T2D development than endocrine disruption alone.Good
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