Research
Energy balance
POPs act as mitochondrial toxins at low doses, causing mitochondrial dysfunction which is a more plausible mechanism for T2D development than endocrine disruption alone.
POPs may damage your mitochondria, the energy powerhouses of your cells, contributing to diabetes. You can counteract this by improving mitochondrial function through exercise, calorie restriction, and eating plant-based foods rich in phytochemicals.
GoodSupportsHIGH confidence
Considering the complexity of EDC mixtures, other mechanisms might be more plausible as an explanation for the consistent findings about POPs relating to T2D in human studies. In fact, many environmental chemicals are known as mitochondrial toxins... Evidence is accumulating that low dose POPs can induce mitochondrial dysfunction and/or reduce oxidative phosphorylation capacities.
Why this rating
Based on accumulating evidence from experimental studies showing mitochondrial impairment by low-dose POPs.
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
narrative_reviewCited 94×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- 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.Good
- 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
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