Volume 16, Issue 63 (8-2026)
NCMBJ 2026, 16(63): 1-17 |
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Tahmasebi Fard Z. Obesity and Environmental Obesogens as Synergistic Factors in the Development and Progression of Hormone-Dependent Cancers. NCMBJ 2026; 16 (63) :1-17
URL: http://ncmbjpiau.ir/article-1-1844-en.html
URL: http://ncmbjpiau.ir/article-1-1844-en.html
Department of Biology, RO. C, Islamic Azad University, Roudehen, Iran
Abstract: (16 Views)
Background and Aim: Hormone-dependent malignancies, including cancers of the breast, prostate, endometrium, ovary, and thyroid, rank among the most prevalent cancers worldwide. Obesity significantly accelerates hormonal carcinogenesis by inducing hyperleptinemia and leptin resistance, reducing adiponectin levels, promoting insulin resistance, and enhancing the conversion of androgens to estrogens in adipose tissue. Environmental obesogens such as bisphenol A, phthalates, dioxins, and PM2.5 exert synergistic effects with obesity through disruption of sex hormone receptors, activation of the AhR signaling pathway, and induction of oxidative stress, thereby aggravating leptin resistance. Chronic urban stress further amplifies these disruptions via the hypothalamic–pituitary–adrenal (HPA) axis. This review aims to elucidate the shared mechanisms by which obesity, environmental obesogens, and chronic stress contribute to the development of hormone-dependent cancers.
Material and methods: This scoping review was conducted according to PRISMA-ScR guidelines. A systematic search was performed in PubMed, Scopus, Web of Science, and SID databases from January 2019 to November 2025 using relevant keywords including obesity, leptin, adiponectin, obesogens, endocrine-disrupting chemicals, BPA, phthalates, PM2.5, and hormone-dependent cancer. Of 1,284 identified articles, 72 studies satisfied the inclusion criteria and were incorporated into the narrative synthesis.
Results: The findings show that obesity can increase the risk of hormone-dependent cancers up to sevenfold. Environmental obesogens synergize strongly with obesity by disrupting sex hormone receptors, activating the AhR pathway, and inducing oxidative stress, which worsens leptin resistance. Chronic urban stress further potentiates these alterations along the HPA axis.
Conclusion: The complex interaction between obesity and environmental obesogens constitutes a common pathogenic axis driving hormone-related cancers. Targeted interventions emphasizing weight reduction and reduced exposure to environmental pollutants may play a crucial role in preventing disease progression and improving clinical prognosis.
Material and methods: This scoping review was conducted according to PRISMA-ScR guidelines. A systematic search was performed in PubMed, Scopus, Web of Science, and SID databases from January 2019 to November 2025 using relevant keywords including obesity, leptin, adiponectin, obesogens, endocrine-disrupting chemicals, BPA, phthalates, PM2.5, and hormone-dependent cancer. Of 1,284 identified articles, 72 studies satisfied the inclusion criteria and were incorporated into the narrative synthesis.
Results: The findings show that obesity can increase the risk of hormone-dependent cancers up to sevenfold. Environmental obesogens synergize strongly with obesity by disrupting sex hormone receptors, activating the AhR pathway, and inducing oxidative stress, which worsens leptin resistance. Chronic urban stress further potentiates these alterations along the HPA axis.
Conclusion: The complex interaction between obesity and environmental obesogens constitutes a common pathogenic axis driving hormone-related cancers. Targeted interventions emphasizing weight reduction and reduced exposure to environmental pollutants may play a crucial role in preventing disease progression and improving clinical prognosis.
Keywords: Leptin, Adiponectin, Environmental Obesogens, Hormone-Dependent Cancers, Endocrine Disruptors.
Type of Study: Research Article |
Subject:
Physiology
Received: 2026/07/25 | Accepted: 2026/08/1 | Published: 2026/08/1
Received: 2026/07/25 | Accepted: 2026/08/1 | Published: 2026/08/1
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